What is evolution?

the standard answer we seem to be getting over the forum seems to be the change in gene frequency in a population over time.

This is a very unsatisfactory basis for the concept of evolution, mainly because it is just the dogma of restricted biological discipline: population biology.

If we look back in history then we see that at some point developmental biologists and population biologists started to disagree on the question if evolution could be satisfactory explained. The developmental biologist saw that there was currently something missing. The population biologist did amazing work with Drosophila and such and saw no problem.

But the time seems right that there should be a union of both disciplines in this respect. From a developmental viewpoint the dogma of change in gene frequency is pointless. They are not interested in studying the change as such. They study how an individual is made, which is only partly based on genetics. In developmental biology it is the 'arrival' of the fittest that counts, not the 'survival'. An individual is not the content of its genome, rather it is a life cycle, which is governed partly by the genome. At all stages during its life the individual must be able to survive. From a single cell, to a blastula, a gastrula, an intermediate larval stage to the adult, to the aging adult, all are different stages with different requirements. None is more important than the other. All need to be survived.


any thoughts on this matter, or are we all happy with the current viewpoints?

Can you explain why "change in gene frequency in a population over time." is not a satisfactory definition of evolution… not that I disagree with your argument but I don’t think you have explained what is wrong here in detail.

Whoa! Excellent topic, which will generate a lot of heat. This touches on a large difference of opinion between strict Neo-Darwinists, like Mayr, and inconoclasts like Gould. The definition, which I agree may be out-dated in this new age of evo-devo, is predicated upon the presumption that evolution proceeds gradually and that small differences in gene frequencies between populations of species add up over time to eventual speciation and further differentiation.

Gould, in his book Ontogeny and Phylogeny, as well as papers published with Eldridge (punctuated equilibrium), reject this gradualistic view of evolution and speciation.

The 2 views of evolution and speciation are not mutually exclusive, therefore, I agree the current definition is not sufficient. However, even new 'arrivals,' in addition to 'survivals' can be measured using measurements of gene frequency (I apologise for the awkward wording).

Do you have alternatives in mind for definitions?

Random genetic drift leaning towards creatures that survive and breed better in the situation they are in. After all, dead creatures can't breed.

One argument:


genetic changes do not always mean phenotypocal changes.


This is a developmental phenomenon. The nature of developmental processes is that they are to a high degree 'buffered'. There can be an accumulation of many mutations without any phenotypical (which means visible in the organism) change. But after some time of accumulation or under different conditions there can be selection for these genetic changes.

Originally posted by spuriousmonkey
One argument:

genetic changes do not always mean phenotypocal changes.
Would it be more true to say that genetic changes very, very rarely mean phenotypical changes?

It may sound daft, but one question I can't figure out is why anything cares about surviving. There doesn't seem to be a appropriate mechanism. I've never seen this problem addressed except by Stuart Kaufman in relation to organised complex systems, when he wonders what it is that explains why dynamic systems are dynamic in the first place. Is there an answer?

I hope that isn't a silly question. You guys seem to know what you're talking about.

Originally posted by spuriousmonkey

From a single cell, to a blastula, a gastrula, an intermediate larval stage to the adult, to the aging adult, all are different stages with different requirements. None is more important than the other. All need to be survived.

Of course some stages are more important than others. When an organism reaches sexual development and passes on its genes, it doesn't need to be around any more. Once it can no longer do this, it has no function within the population and has no impact on evolution of the species. Organisms that cannot reproduce are not needed by the population.

one needs to be careful not to invoke group selection. post reproductive characteristics are blind to natural selection (old age and diseases associated with it) however this is not because they aren't needed by the 'population.'

illustration of what i mean, say there's a deleterious gene that only expresses itself in old age (post reproductive age), natural selection can never weed it out because it doesn't affect offspring till post reproductive stage, i.e. the fitness of those with the gene is equal to the fitness of those without it. it's maintained in the population indefinately.

Originally posted by Canute
Would it be more true to say that genetic changes very, very rarely mean phenotypical changes? very true, and a good point.

Originally posted by Canute
It may sound daft, but one question I can't figure out is why anything cares about surviving. There doesn't seem to be a appropriate mechanism. I've never seen this problem addressed except by Stuart Kaufman in relation to organised complex systems, when he wonders what it is that explains why dynamic systems are dynamic in the first place. Is there an answer?

I hope that isn't a silly question. You guys seem to know what you're talking about. can't say I understand your question unless it's about the obvious fitness advantage of passing genes on to the next generation.

Originally posted by paulsamuel
post reproductive characteristics are blind to natural selection (old age and diseases associated with it) however this is not because they aren't needed by the 'population.'

I don't disagree. But you can't say that post-reproductive organsims are as important to the population as those that can reproduce. Your example didn't really address this. I can't think of an example where a non- or post-reproductive organism is as important to the evolution of the population as one that can pass on its genes.

Originally posted by paulsamuel
can't say I understand your question unless it's about the obvious fitness advantage of passing genes on to the next generation.
Yeah, it's a very naive question in a way. I'm asking why entities use their fitness advantage, why they bother. It's not meant as a trick question, it's something I can't figure out. Evolutionary theory seems to take it for granted that things compete for survival but there must be a reason.

Even in the best computer models of evolutionary competition the software entities have to be programmed to compete, their competitive 'instinct' doesn't evolve in any way. I'm wondering what drives that competition in real life.

Why would they need to be programmed to compete? A creature swimming around in a pool sees a bit of food or a potential mate and it goes right up to get it without thinking about anything else. When you have too creatures going after one piece of food you have instant competition. One who happens to be faster will be more likely get the food or the mate so it will have more children and now you have instant evolution.

would phenotypic plasticity be relevant to this topic?
for instance..

Dr. Stan Boutin, from the Department of Biological Sciences at the University of Alberta in Edmonton, has been studying a North American red squirrel population in Canada's southwest Yukon for almost 15 years. The squirrels, faced with increasing spring temperatures and food supply, have advanced the timing of breeding by 18 days over the last 10 years—six days for each generation. His findings appear on First Cite and will appear in the journal Proceedings of the Royal Society London B next month.

if that aint evolution what is?

:D

oh
i forgot to mention..lamarck rules!

:D

Originally posted by Clockwood
Why would they need to be programmed to compete?
A creature swimming around in a pool sees a bit of food or a potential mate and it goes right up to get it without thinking about anything else. When you have too creatures going after one piece of food you have instant competition. One who happens to be faster will be more likely get the food or the mate so it will have more children and now you have instant evolution.
Yes but why do they bother? In software models of competition the virtual entities have to be told to compete. They don't do it naturally.

Originally posted by spuriousmonkey
One argument:
genetic changes do not always mean phenotypocal changes.


very true. However, would you agree that there is even less systematic (ie repeatable through generations and multiple offspring in the same generation) phenotypocal change without an associated genetic change?

Originally posted by canute
It may sound daft, but one question I can't figure out is why anything cares about surviving. There doesn't seem to be a appropriate mechanism. I've never seen this problem addressed except by Stuart Kaufman in relation to organised complex systems, when he wonders what it is that explains why dynamic systems are dynamic in the first place. Is there an answer?
I think that the reason for the drive to survive is clear enough: those who don't have a strong desire to survive won't fight as hard to do so, and will therefore be less likely to survive. therefore, will be less likely to pass on their genes.

Originally posted by spookz
would phenotypic plasticity be relevant to this topic?
for instance..

Dr. Stan Boutin, from the Department of Biological Sciences at the University of Alberta in Edmonton, has been studying a North American red squirrel population in Canada's southwest Yukon for almost 15 years. The squirrels, faced with increasing spring temperatures and food supply, have advanced the timing of breeding by 18 days over the last 10 years—six days for each generation. His findings appear on First Cite and will appear in the journal Proceedings of the Royal Society London B next month.

if that aint evolution what is?

:D

I'll suggest that the squirells are genetically evolved to breed when the conditions are right (as are all living things). The breeding date have been moving up not for evolutionary or phenotypic plastical reasons, but because theur environment is changing. They are sticking to their plan- "screw when there's enough food int he fridge, and the lawn is warm" it's those two "when's" that are driving the change. lengthen the winter, and reduce the food supply, and the breeding season will shift back to its original time frame.

Originally posted by Canute
Yes but why do they bother? In software models of competition the virtual entities have to be told to compete. They don't do it naturally.

you answered your own question.

Even the most intricate software models cannot begin to simulate the 'real world' with 100% accuracy.

The entities in the virtual world has no 'limbic system' , these virtual entities have no 'urges' to procreate and to survive.

They will exhibit none of these attributes until we program them to do so.

So computer models are false. There's something else at work. Or is it just an infinite regression of genetic programming?

Originally posted by Canute
Yes but why do they bother? In software models of competition the virtual entities have to be told to compete. They don't do it naturally. Computer models have to be told everything, they don't do anything naturally.

Competition is a behaviour we can observe. It is genetically selected for from the moment that ONE organism happens to have a competetive behaviour. Those that do not have it will loose and disappear. The competitive trait is bound to appear anywhere several creatures are sharing a limited ressource.

This also fits observations: The dodo, alone without competition on an isolated island with plenty of food ressources, was unable to cope when "competition" arrived, in this case in the shape of attrition from hunting. Had humans not killed off the dodos, they might have died out due to animal species introduced in their environment by humans (rats, cats, crows, parasites).

Hans

Originally posted by Canute
So computer models are false. There's something else at work. Or is it just an infinite regression of genetic programming?

I wouldn't say that computer models are false.
I would say that it is difficult to take into account ALL of the variables, interactions, and parameters at play in a particular system.

Just look at the Pharmecutical industry.
They spend millions on R&D trying to predict how a drug will behave in the human body. (a closed system)

They use math models, computer simulations, and even trial tests on actual humans they still cant get their stats over 70%.

i dont see the validity in the comparison tho
computer models are programmed. all you got to do is keep track of the code from the first line to the last. stuff is either on or off. in the case of the human body, i doubt if anyone claims we have a complete understanding of anatomy

Originally posted by copper
Of course some stages are more important than others. When an organism reaches sexual development and passes on its genes, it doesn't need to be around any more.

why are our grandparents around then?

Hmm. Not what I meant but never mind. I might post it as a thread sometime.

Originally posted by spuriousmonkey
why are our grandparents around then?

because we, as humans, have alot of cultural information that needs to be passed on for survival. Information which isn't passed on in the genes.
If all of our survival mechanisms were included in our genetic code, then I bet we wouldn't have grandparents around. Just like most non-social animal species.

You are absolutely right, but if I may add to that that it is in the genes to have them around. Otherwise they wouldn't be.

you are absolutly right.

Originally posted by spuriousmonkey
why are our grandparents around then?

Only beacuse we're afraid to die. We have them around becuase we've become a compassionate species with high importance on family. That is something that is environmental (we learn it from our parents). It is absolutely not genetic.

As for imparting "cultural information" on to the next generation, I think that has a minimal (if any) effect on the evolution of a species.

If you think of species other than humans there is really no reason to keep around older individuals. If fact, they're usually the first ones to be picked off by predators.

Originally posted by copper
It is absolutely not genetic.



couldn't 'compassion' have a genetic component? Possibly a combination of genes that we havent considered?

I mean, if a species treasures its older members, and those older members then impart crucial knowledge that will then allow for greater success in mating/survival, then isnt that valid?

I suppose, but that would be like saying personality is genetic, right? Which I believe is not. However, I'm not up on my "twins separated at birth" psycological profiles. Has anyone done studies to see if they have similar personality traits? I seem to remember that maybe they do (laughs, hobbies, etc). But I think, overall, the most important traits for survival are instictual. Those for sociailly acceptable behavior (i.e. keeping our elders around) are learned.

this isnt exactly my area of specialised knowledge, but...

"couldn't 'compassion' have a genetic component?"
"I suppose, but that would be like saying personality is genetic, right?"
"Those for sociailly acceptable behavior (i.e. keeping our elders around) are learned."

i was under the distinct impression that we have a capacity for empathy and compassion, and it is present from the earliest ages (and we also have a capacity for nastiness etc.) We also have the need and desire for interpersonal contact and groups and so on, such that I thought all that was instinctive, therefore genetic, and the keeping your elders going is due to those feelings and instincts acting upon the social set up. Ie your genes provide the scaffolding, and culture and personal experience flesh it all out.

Originally posted by guthrie
this isnt exactly my area of specialised knowledge, but...

"couldn't 'compassion' have a genetic component?"
"I suppose, but that would be like saying personality is genetic, right?"
"Those for sociailly acceptable behavior (i.e. keeping our elders around) are learned."

i was under the distinct impression that we have a capacity for empathy and compassion, and it is present from the earliest ages (and we also have a capacity for nastiness etc.) We also have the need and desire for interpersonal contact and groups and so on, such that I thought all that was instinctive, therefore genetic, and the keeping your elders going is due to those feelings and instincts acting upon the social set up. Ie your genes provide the scaffolding, and culture and personal experience flesh it all out.
I think that's probably wrong. 'Compassion' and 'empathy' have never been observed, and they have no place in neo-Darwinist theory. However observable behaviour that might be conjectured to arise from compassion or empathy is allowed.

back to topic then:

gradualism vs punctuated equilibrium.

a hot topic creating many flaming debates. That is from a population biology perspective.

Within the developmental biology perspective the problem doesn't really appear to be that great. As we have mentioned before we can have an accumulation of mutations because of the modularity of developmental systems. This can at one point facilitate fast and large changes in the morphology. Also it is claimed that mutations in regulatory genes can also create large changes. It seems therefore that we have the best of two worlds that can explain fats changes in morphology.

In the end it is however not about who is best...population biology or developmental biology. There are currently trying to get together and make a new baby. The baby hasn't quite been born yet though, so we could discuss what the baby might look like. It could be a real ugly one.

genetic changes do not always mean phenotypocal changes. If Elevation of blood sugar as in diabetes is a phenotypocal change or a genetic change. Can high BS be a responsible factor for genetic changes. Don't relate insulin changes along with it.

Now, elevation of insulin as in diabetes is a phenotypocal change or genetic change. Can high insulin be a responsible factor for genetic changes. Now don't relate blood sugar with it.

Originally posted by Kumar
If Elevation of blood sugar as in diabetes is a phenotypocal change or a genetic change. Can high BS be a responsible factor for genetic changes. Don't relate insulin changes along with it.

Now, elevation of insulin as in diabetes is a phenotypocal change or genetic change. Can high insulin be a responsible factor for genetic changes. Now don't relate blood sugar with it.

i think you are mixing up your terminology once again. Diabetes is an acquired disease, not an evolutionary adaptation or an example of polyphenism.

Frankly, In Diabetes two changes takes place in type2. First, the blood sugar increases, second, the insulin secretion in blood also increases side by side. Now which of these two will be the responsible factor which can cause additional genetic manifestations/hereditory inheritance or additional polyphenism. Sugar or Insulin?

go to your own thread please with this stuff. This has got nothing to do with this thread.

You are right, sorry. Please give reply in that tread as it is very important. I am weak in language specially technical language.

A confusing group of terms (directed, adaptive, selection-induced, Cairnsian) describing mutations has spread in the scientific literature. As I see it, two basic areas can be distinguished: (1) an increase in the beneficial mutation occurring in stressed organisms; and (2) the imposition of a specific selection on large numbers of organisms in order to find and amplify certain novel mutations. The first aspect is most important to the evolution/creation discussion, the second to the pharmaceutical industry.

In the September 1997 issue of Scientific American, Tim Beardsley reviewed the current Adaptive Mutation situation. The possibility that living organisms possess the ability to select for beneficial mutations when stressed has challenged the conventional notion that mutations are purely random events and overwhelmingly harmful. The starting point was a 1988 article by Cairns et al. In those experiments, bacteria deprived of the ability to utilize lactose were plated onto media with only that food source available. Cairns reported a significant increase in the occurrence of mutations that restored the lactose utilization ability compared with the same bacteria living with other sugars available.

The most conservative explanation is that cells may simply sustain higher rates of random mutations (hypermutation) under stress. This may be for no other reason than that the resting bacteria experience a breakdown of their normal biochemical processes. Therefore, rare beneficial mutations will numerically occur more often. A more radical explanation is that the genetic tool box of cells selectively mutates portions of its DNA with a much higher likelihood of achieving beneficial results. A debate of these issues can be found in Science. In my opinion, the weight of evidence seems to be on the side of non-random mutation (shades of Lamark!)

Hey everyone, this is my first post here so, huzzah for me.

First, development is important to the evolution of morphologies, but this is only really a matter of the power of selection on the contributing genes. So development doesn't appear to play any direct role in heritable change other than through selection. And so I don't really see how development is integral to defining evolution, though I'm happy to hear any newer, better definitions :)

I do agree population genetics has created a narrow definition of evolution though, but because it is based purely on genes, rather than including all the rest of the inherited material. At the time that population genetics was developed, pretty much nothing was known of molecular biology. We have a better idea now, inherited material not only comes in neat packets that give rise to phenotypic traits but also functions in the control and structure of material itself. I think the definition should be broadened to include all of the inherited material, perhaps something simple like: the changes in heritable material present in the offspring of a parent population.

A great idea. It allows some space for what we don't yet know.

Originally posted by skyederman
Hey everyone, this is my first post here so, huzzah for me.

First, development is important to the evolution of morphologies, but this is only really a matter of the power of selection on the contributing genes. So development doesn't appear to play any direct role in heritable change other than through selection. And so I don't really see how development is integral to defining evolution, though I'm happy to hear any newer, better definitions :)


when scientists first started using the word evolution, they were actually referring to the development of an organism and not at all to the process of descent with modification as charles darwin postulated. Even darwin only mentions the word evolution only once in his book on the origin of species i think.

Evolutionary developmental biology strives to explain the diversity of life. Population biology strives to explain the distribution of genetic information in a population. Population biology cannot explain the evolution of a straucture such as an eye. Evo-devo can. Development can tell you how a duck got webbed feet or how a bord got feathers. Development is at the origin of any phenotypical change. There is no gene for webbed feet after all.

Spurious

"There is no gene for webbed feet after all."

Can you explain that a bit.

Ducks have webbed feet because a gene that is already expressed in this area has extended its expression domain (or chickens lost it, depending who was first, the chicken or the duck).

In this case gremlin, a BMP inhibitor, is expressed in the interdigital space (the space between your toes) in ducks, but not in chickens. This prevents the apoptosis (regulated cell death) of the cells between the digits. Hence the duck never loses the tissue between its toes.

You can similate this by putting a bead loaded with gremlin protein inthe interdigital space of the foot of a chicken embryo. This mimicks the effect of gremlin in the duck. There is no apoptosis and you end up with a chicken with webbing between the digits where the bead was placed.

The question then becomes how this expression pattern was changed, and although we do not know exactly, developmental biology has the theories to explain this. Which are tested and proven in other systems.

in conclusion, there is no specific gene for webbed feet. We are dealing with a slight alteration of an existing system, with rather beneficial consequences if you are fond of a pond.

and of course, this cannot be measure in terms of gene frequency. This is on the level of combinatorial control of gene expression.

Thanks. Does this mean that inhibitors are not part of the gene?

no gremlin is a gene that codes for a protein. This protein inhibits the action of the BMP gene.

But this doesn't mean that ducks have a different gene for gremlin than chickens. If you would put the coding region of the gremlin gene of a chicken into a duck, the duck would still produce webbed feet.

That confused me. Gremlin (is it really called that?) is a gene, but you say ducks and chickens have the same genes. Sorry to be thick. Do they both have the gene but it is not expressed as a protein in a chicken for some reason?

Development is at the origin of any phenotypical change. There is no gene for webbed feet after all.

There's no webbed feet without genes though ;)

[edit] So how would you define evolution?

Originally posted by skyederman
There's no webbed feet without genes though ;)


there are no webbed feet without an egg either.

there are no male crododiles if it is too hot either.

Originally posted by Canute
That confused me. Gremlin (is it really called that?) is a gene, but you say ducks and chickens have the same genes. Sorry to be thick. Do they both have the gene but it is not expressed as a protein in a chicken for some reason?

gremlin is expressed in both chick and duck in many different organs and at many different time points.

What is important is the alteration of temporal and spatial expression, not the gene itself. What we are looking for are changes in enhancer sites and changes in modulation of upstream signals.

I'm still not quite with you. Are you saying that the mechanisms that determine when and where gremlin will be expressed in ducks is not genetically determined? Or are you saying that there is no gene for webbed feet because they are caused by a complex of interacting genes? Or am I missing the point?

Originally posted by Canute
Or are you saying that there is no gene for webbed feet because they are caused by a complex of interacting genes?

correct. Although the basis is genetic, i doubt we could measure this meaningfully in terms of changes in gene frequency. We because we do not know what we should measure, if we do not understand the development. Development gives us therefore a window on evolution.

Ah, got it. Thanks.

A question we could ask is whether evolutionary genetics provide a sufficient theory of morphological change?

Any question about a definition has two aspects -
1) simply the linguistic act of deciding what a specific word means
2) the act of deciding what the essence of some general idea is

The basic idea of evolution, in a non-biological sense, is the set of changes in a system that take it from one state to another. The essential problem that I think spurious monkey wants to highlight is that there is something unsatisfying about defining it simply as change without any consideration of what type of change will occur. A directionality perhaps.

In a biological sense I think the discussion should be overlayed strongly by statistical mechanical/thermodynamical conceptions.

To make an example if one has two chambers, one containing gas and one not, separated by divider and removes the divider the gas will expand and fill both chambers. The reverse will not occur, there are statistical reasons why the process will move in one direction when considering the possible paths available to the molecules (the exceedingly small number of paths leading the molecules to return to a single chamber are negligible among the multitude of paths where they remain filling the two chambers).

By the same token if one considers the set of mutations that occurs in a species over time there is an inherent directionality. We will never retrace the path we have so far followed or one close to it. Even though we know there is a set of molecular operations that could take us on that path.

The reason is close to a creationist confusion regarding irreducible complexity (though I shudder to get anyone started on this topic). Once a component that has been added to a genetic system, for instance a duplicated gene, has acquired some new useful function, it is difficult to imagine it being removed.

This increase in complexity is similarly tracked on the morphological level, as in the case of Williston's law (the number of serially homologous elements tends to decrease while the individual elements tend to become more different and specialized). As each component becomes more specialized it becomes more difficult to do without it. One must follow a very specific set of molecular changes to remove elements and maintain function, whereas the system is more robust to adding elements which then are the object of selection until they become an integral component of the system.

In the long run evolution is about the choice of what path is taken on the road to increasing complexity. Not in a conscious sense - although one could argue populations lead to a certain amount of democracy in weighting various choices. The road most traveled to success for a single individual helps set the path of the population.

I would like to make a sidenote that it is not truly difficult to make developmental changes. It is just difficult to make them for certain structures. The developmental importance of these structures is reflected in the concept of bauplan and phylotypic stage.

If we look at the phylotypic stage we may note that it is possible to make enormous changes in development before and after this stage. The important structures that hardly change (such as the notochord) function to instruct other structures, organs and tissues.

Do you mean it's not difficult to have mutations that change development? Or ones that change development and are workable evolutionarily?

Also how would you define difficult? There are obviously a large fraction of mutations possible in each protein that don't even alter the protein generated in addition to the buffering you mentioned in the actual developmental processes. Do you mean difficulty defined as some fraction of mutations that alter development? Or more like the fraction of such changes that are viable? or ...

I must admit I'm also curious as to whether I was on the right track to answering your question in my previous response ... were you trying to get at a metric of evolution beyond simple changes in frequency. Fixation of duplications being one possibility from my response (which hallmarks arrival of a qualitatively different individual).

Of course one experimental issue with this definition is that one would need full genome sequences to identify such changes and most evolutionary studies currently sample from single genes. Then again duplicated genes could be found if one makes intelligent use of reduced stringency screening processes. Still the exact quantification procedure is much more ill-defined when one is forced to look at the greater range of possibilities when dealing with more complicated global changes.

Originally posted by scilosopher


I must admit I'm also curious as to whether I was on the right track to answering your question in my previous response ... were you trying to get at a metric of evolution beyond simple changes in frequency. Fixation of duplications being one possibility from my response (which hallmarks arrival of a qualitatively different individual).
.

I meant that changes in gene frequencies is a really unsatisfactory definition of evolutin. Even darwin did better than that with his descent with modification. It left more room open.

We could know exactly how a gene frequency changed and still not know anything about evolution. A favourite quote would be that ontogeny does not recapitulate phylogeny, but ontogeny creates phylogeny. The developmental process is therefore a means to make evolutionary change possible. It should be at the center of evolutionary thought.

I knew you meant that (indeed Williston's law has strong similarity to descent with modification). What I tossed out was a very general conceptual framework regarding for thinking about sets of genes and their inter-dependencies. SInce evolution occurs on the level of the organism one clearly has to start thinking about how the elemental building blocks of genes fit together into functional systems.

Development is certainly a good system for doing so since it elaborates spatially and the end goal is fairly apparent. For a detailed metric concerning effects on development, people need to experimentally determine and then compare complete gene networks in different organisms.

Other biological systems are reasonable as well though. I'd be interested if anyone has made an evolutionary comparison of transcriptional or other networks in bacteria where it's considerably more feasible (I don't think development is a necessary part of moving forward, just considering networks/systems that have a specific function). In development, it's certainly a goal of many like Tautz and Carroll, but it's not that easy and it's not surprising with the paucity of data that it hasn't taken over the evolutionary field. There aren't enough instances to do any interesting stats on relative rates of evolution.

If you have access to development check out:
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9716530&dopt=Abstract

I also recommend reading stuff by CH Waddington (a bit old, but he had many intelligent thoughts on the matter). If you have any good refs on people working on this subject, I'd be interested as well.

For tooth development Jukka Jernvall is on the cutting edge of evo-devo

Salazar-Ciudad, I. & Jernvall, J. (2002) A gene network model accounting for development and evolution of mammalian teeth. Proceedings of the National Academy of Sciences, U.S.A. 99: 8116-8120.

for a evo-devo model on tooth shape

and because I know Isaac and nobody reads his crap volentarilyI will also recommend his review article.
Salazar-Ciudad, I., Jernvall, J. & Newman, S. A. (2003) Mechanisms of pattern formation in development and evolution. Development 130: 2027-2037

Let me introduce myself, this is my own shit:
Development 130, 1049-1057 (2003)
Root or crown: a developmental choice orchestrated by the differential regulation of the epithelial stem cell niche in the tooth of two rodent species
Mark Tummers* and Irma Thesleff

but that is not really relevant here, although the article contains the word evolution.

Originally posted by scilosopher
SInce evolution occurs on the level of the organism one clearly has to start thinking about how the elemental building blocks of genes fit together into functional systems.


this might be pointless because development is highly modular. functions can be adapted and switch and to accomplish the same structure different modules can be used in quite related species. I was looking myself at the stem cell compartment of the tooth in mice and voles and noticed for instance that the WNT ligands (one of the major signaling families) are not expressed similarly. This project has never reached an advanced status but possibly different WNTs take over the function of another WNT in the same tooth in vole and mouse. Or because I actually did not find any subsitute for certain patterns yet, another signaling pathway may have taken over the role completely. And that to create a tooth which is the same in shape and function in both instances. This is just a personal example, but I am sure it is not the only one.

What is therefore then the point in looking at elemental building blocks of genes? They don't necessarily exist in this fashion. A similar functional system can arise by different developmental means, using different genetic 'blocks'.

Thanks for the refs. They look interesting ... I should get a chance to read the papers sometime next week. A bit busy this week (presenting my thesis proposal tomorrow to my advisory committee). My name's Mark as well ... but I haven't published anything I'm too proud of, let alone relevant.

Maybe I should have emphasized "fit together into functional systems". One certainly has to evaluate things on the network or system level, but how the components fit together is critical for this purpose.

Presumably there are a large number of ways a system can be organized while maintaining the same function (just as you say). All networks with the same function can be called instances of a single "meta-network". In evolution you move both between instances of a meta-network and more interestingly, you occasionaly move between functionally different meta-networks.

If one can count the number of instances of two meta-networks (or estimate their size somehow) and the number of paths between specific instances of each of the two meta-networks (under some survivability constraint), then one will begin to understand the evolution of such meta-networks. You definitely need to sample the networks at a reasonable scale because the numbers are combinatoric and there is a large flexibility in the number of ways instances can occur.

This of course is very experimentally laborious. Particularly depending on the level of resolution with which one understands the network (quantitatively vs qualitatively). Using modeling and sampling techniques would certainly be helpful, but it's unclear one could make good models at this point. Therefore one needs both research into understanding the molecular details of example systems, like Eric Davidson, and sampling of systems in related organisms (of which you seem more aware).

Doesn't evolution happen at the level of populations? Once you're an organism, your evolution's done.

Except in Star Trek, where people evolve spontaneously.

"Hey Sam, wanna go out?"
"Nah, I thought I'd stay home and evolve."

Every organism is a data point in the statistical sampling that leads to improvement at the population level.

The reproductive success of each individual is a measurement that leads to information at the population level in terms of what works well.

You require a reproductive chain of individuals to evolve - it's not like individuals bud off of a population and then the two go there separate ways. Each individuals contribution back to the population is very important. They aren't two separate entities.

That is so, but individuals cannot EVOLVE, they can only be SELECTED UPON. Generally when you're a multicellular organism, genetic adaptation only happens once - when you're conceived.

Everything after that is about environment, luck, and the success of your design. If you chance to reproduce, then your offspring also get to adapt - once. Evolution is really a name that humans apply post hoc, when some pressure is put on a population and some of them don't die.

I agree that creating metanetworks describing functional components of organisms would be experimentally laborious - that's probably an understatement. The workings of the nuclear DNA itself, with inhibitors and activation sites and so on, is fiendishly complicated, and I understand that the protein interactions which result from them are vastly more difficult to understand.

The biggest problem, most likely, is that our understanding of organic genomes (our own, for instance), is pretty bad. People still refer to non-coding regions as if we were sure that they didn't do anything... if you go on a gene-by-gene basis we share most of our genetic code with chimps, and also with blowfish and probably some species of mold. Trying to break down an organism into all of its functional components (including those that aren't expressed, but can be with minor mutations, like the human sixth finger / gills / other "junk DNA" like that) would be an Herculean task even for simple organisms.

Okay, I see you're working off a direct quote - I meant selection occurs at the level of the organism. My point was to say evolution selects at the level organism not the gene.

Although I wasn't claiming it - it is easy enough to argue that individual humans do evolve. It is one of our strengths - we learn a lot as we grow up and become more "fit". Of course if you define evolution to require change in DNA that is not the case. There are also examples of organisms that undergo different development paths depending on their environment and in a certain sense they are also evolving.

I generally think it's important to try to understand what people mean and not worry so much about how they word things.

I apologize; I hadn't realized that you were using the broader sense of "evolution" meaning change of any kind.

When we are talking about natural selection in populations your examples are poor; a tadpole changing into a frog, or a person learning to use an abacus, do not relate to the selection of their children when they are removed from the picture - the frog's offspring will be born tadpoles, not frogs - the abacus user's child will not be born knowing how to use an abacus. Somatic adaptations - of any kind - are not passed on to the offspring.

Social adaptations can be passed on from one person to another, but the capacity to inherit social adaptations from another person (technology or whatever) is only dimly related to your genetic relation to them - you can learn how to unscrew a jar as easily from a gorilla as you can from your own parents.

Most people try to stick to genetic information as the medium for the passing down of adaptations, because fairly simple and predictable circumstances can easily wipe out the passing down of things like social adaptations - if the child is isolated from the parent, then none of their "evolution" is passed along except for whatever genetic adaptation was inherited by the child. No amount of evolution is meaningful in the sense of population adaptation if the gain is wiped out between generations.

I actually wasn't using evolution to mean change of any kind. My point was about language and context and how easy it would be for me to argue with you if I chose to misinterpret your words.

If you read the posts I think you'll agree that I wasn't talking about changes of any kind, that was my example of misinterpretation and how silly it is. I should have been more clear and labelled it that way.

Is there some reason you want to attack me? I come here to chat informally about interesting ideas and don't understand why you're being so antagonistic.

You seem like a smart enough fellow - why don't you contribute by putting forward interesting ideas instead of attacking the wording of other people's?

Originally posted by scilosopher


This of course is very experimentally laborious. Particularly depending on the level of resolution with which one understands the network (quantitatively vs qualitatively). Using modeling and sampling techniques would certainly be helpful, but it's unclear one could make good models at this point. Therefore one needs both research into understanding the molecular details of example systems, like Eric Davidson, and sampling of systems in related organisms (of which you seem more aware).

the model used in the Jernvall paper that can accurately predict tooth shapes actually throws all the inhibitors and activators on one heap. Therefore the question may arise if individual patterns of inhibitors and activators are that important. It is the combined effect that will eventually predict shape. This also explains why some activators can be exchanged for others in one system between 2 species. This is hardly a quantifiable effect in the sense you are aiming at ...probably. I don't know.

this might be in line with what you are looking for


Science, Vol. 302, Issue 5643, 249-255, October 10, 2003

A Gene-Coexpression Network for Global Discovery of Conserved Genetic Modules

Joshua M. Stuart,1* Eran Segal,2* Daphne Koller,2 Stuart K. Kim3

To elucidate gene function on a global scale, we identified pairs of genes that are coexpressed over 3182 DNA microarrays from humans, flies, worms, and yeast. We found 22,163 such coexpression relationships, each of which has been conserved across evolution. This conservation implies that the coexpression of these gene pairs confers a selective advantage and therefore that these genes are functionally related. Manyof these relationships provide strong evidence for the involvement of new genes in core biological functions such as the cell cycle, secretion, and protein expression. We experimentallyconfirmed the predictions implied bysome of these links and identified cell proliferation functions for several genes. By assembling these links into a gene-coexpression network, we found several components that were animal-specific as well as interrelationships between newly evolved and ancient modules.

I've read that paper ... my meta-terminology is a bit of a rip off from there actually. If you haven't read any of Uri Alon's papers I recommend them when it comes to evaluating genetic networks statistically. They haven't got the data to do direct cross species comparisons though.

Although they get at group of co-regulated genes, they know nothing about the structure of the regulatory networks generating them (ie gene A regulates targets 1 .. n). I think that's of primary importance. It is certainly a good first step and interesting work though.

I was looking at fig 1. I noticed that compared to flies and worms the human species only uses a small subset of genes for development Which seems a bit strange, because we don't have that much more genes than a fruitfly, and all these genes are conserved. In fact, vertebrates usually have more duplicated genes.

I recall from bio that certain base sequences are more vulnerable to mutation than others - that having to do with the chemical properties thereof.

It might be possible that the forms of these highly important cell regulatory genes tend to protect them from mutation, and so they have been passed along relatively unchanged because of their importance. The less protected forms of the cell regulators might have been weeded out by mutation.

Am I correct in thinking the Stuart extract says that genes can form interdependent pairs which can sometimes become structurally stable and can be transmitted across generations?

Or does he just say that within stable and 'fit' sets of genes pairs of genes tend to be structurally complimentary to each other?

Or did he say something else completely?

who is stuart?

Stuart Kim - the last author on that Science Article.

As a very morbid side-note, I had lunch with him when he visited my school and he told us that they had some C elegans on the Columbia. Apparently NASA doesn't report much on the negative health effects of being in space, but there are a number. So they were looking into whether it would be a good model organism and wanted to see simply if they would survive the trip. They did.

Originally posted by spuriousmonkey
who is stuart?
I should have said Stuart et al, authors of the extract you posted.

I'm going to try to read the Jernvall paper this weekend, but I think it's quite reasonable to group all activators together and all repressors together. However grouping activators and repressors together would be a bit odd.

As far as the oddity in number of human genes involved in development, I would imagine it's a reflection of the annotation. Human development isn't directly studied so even if human genes are involved in development and studied in human they would probably be clasified functionally, like "transcription" or "signaling".

From re-skimming the paper and my recollection, the point of the Stuart paper is that genes that are involved in the same pathway or protein complex need to be expressed together. So over evolution their correlation in expression is maintained, whereas some genes are coexpressed for more indirect reasons in a single organism. Therefore one gains information about genes with conserved co-expression to genes of known function. They never really comment on protein structure.

I hadn't noticed/recalled the first author's last name was Stuart ... sorry about the tangential morbid anecdote.

Bigbluehead,
Sorry if I was a bit testy ... was a bit stressed out regarding my thesis proposal defense yesterday. Clarity in communicating science is important and you were just enforcing the proscribed nomenclature. Not to mention the fact I probably wasn't that clear. My committee had some issues with my clarity yesterday themselves.

n a CpG (meaning the sequence CG rather than the CG basepair) the C is typically methylated, which increases the probability that a C will change to a T. This methylation is suppressed around transcription start sites which leads to a high local enrichment of CpG in these regions. This sequence is relatively rare everywhere else. So far as I know this is the only sequence specific mutation mechanism.

Generally, important genes mutate more slowly because of selection, not their specific sequence. Actually ubiquitously expressed genes, genes with many targets, and genes with many interaction partners all mutate more slowly because they have more constraints on their sequence, structure, and/or function. This is quite independent of CpG islands. If anything the large number of constraints might make instances of CpG in these genes more long lived not less, though I've not heard anything on this topic. Not really my area. Paul Samuel certainly would know more about that kind of thing.

Scilosopher! I spend most of my time here arguing social reform with and2000x and Galt; your "testiness" is like a gentle caress. I'm often too argumentative, and it was good of you to point it out.

The example (CpG) you mentioned here is the one I recalled from my Bio classes - I probably should have looked it up again before mentioning it, since it's been a little more than a year since I was in school.

So... now I have to clarify for myself... given the content of the Stuart paper, were you referring to meta-networks as mappings of relations of functional expression by looking at the related genes?

(I ask because I previously thought you were referring to mapping the functional expressions of an organism by picking them out individually. I had not realized you might be referring to the kind of relation mentioned in this paper, which would make for a quite different experiment...)

I mainly stole the phraseology of "meta" to describe an element of functional redundancy across a range of species, with potentially different molecular characteristics.

When I referred to networks I meant the regulatory links between factors (such as the protein from gene A activates transcription of gene B or the protein from gene X activates the protein from gene Y by phosphorylation).

The expression patterns generated by a network would therefore be a function of the regulatory interactions and the initial state of the system (including the distribution of various cell types expressing various different molecules).

I didn't intend to imply any experimental similarity between the Stuart paper and what I was suggesting. I meant mapping the functional interactions/regulatory links through a combination of misexpression, genetics, and biochemistry. All these are necessary to determine the various effects of molecules and more importantly the direct interactions responsible for those effects.

For instance removing a transcriptional repressor P can lead to LOSS of expression of gene R that is not even a target of that molecule. This could make one think P was an activator of R, when it is neither an activator or is R a target. Alternatively P could have been repressing Q, a direct repressor of R. Upon loss of P, Q is no longer repressed and therefore is expressed and can repress R.

Therefore one has to hunt down the molecular details of regulatory effects beyond a genetic description on effects upon expression patterns (although w/double mutants and detailed staging one can figure much out, but that's much more tricky and molecular handles make such inferences more straightforward to demonstrate).

I read your friend Isaac's paper. I can see why no one voluntarily reads his stuff. His writing might be even less clear than mine.

It was interesting, it'd be nice if they measured some of the parameters they picked and showed they were in the right range. Still I think the work goes in the right direction.

I hope more for molecular insight into the actual mutations that lead to change, but that is certainly asking a lot. It would be really cool if they could demonstrate molecular compensation between different factors such as SHH and FGFs between mouse and vole or something along those lines.

The other concern with modeling is related to your comment on how there are many different ways to achieve a certain result. Just as molecular details can change and maintain the same macroscopic pattern, models differing from the true details can yield results consistent with what is known from experimental work. Although certain approaches may work, they may never be used in evolution because they are overly sensitive to parameter choice and therefore are difficult to establish.

i knew this would be a productive discussion.

Congrats on your successful proposal defense, scilosopher.


Re: microarray analyses and discovery of co-evolving genes (I am assuming that co-expressed genes will also be coevolving although I'm not sure of the validity of this assumption yet);
I'm pretty sure there are many people who are using this technique to identify, not only gene pairs that are co-expressed, but also genes involved in entire metabolic pathways, including their regulation? I would think that these genes would evolve as a unit and not merely as individual genes. I therefore think that a modular view of evolution for these genes is an excellent research approach.
co-expression, in itself, may indicate functional linkage, but there are many situations in which genes that are not functionally linked would co-express. However, that Stuart et al. found this coexpression across multiple phyla, suggests strongly that these genes are functionally linked, which I find to be an incredibly important discovery.

Re: the gene conservation across evolutionary time;
Sci-Phi is right, important genes are conserved through natural selection. I think structural protection of DNA from mutation, in eukaryotes, like methylation, are somatic cell adaptations to protect those genes or regulatory sites within the life and cell proliferation of the organism.

To get back to the original topic; although I agree that 'change in gene frequency' is not a fully descriptive definition of evolution, it is at least fully accurate.

Originally posted by paulsamuel
To get back to the original topic; although I agree that 'change in gene frequency' is not a fully descriptive definition of evolution, it is at least fully accurate.

the definition 'change in morphology' is also fully accurate.

Wouldn't preadaptive changes (someone mentioned them just recently I think) represent a change in gene frequency (or allele frequency or whatever) without necessarily representing a morphological change?

I think the morphology view is hard to argue for. There is the potential for many functional changes that could impact fitness that wouldn't effect morphology. For example alterations in metabolic pathways have no effect on morphology, but would affect fitness and should certainly be considered in evolution.

By the same token it isn't clear that gene frequency is completely satisfactory either. Alterations in arrangement of genes could facilitate downstream changes that are of large functional significance. Although this would presumably have an impact on allele frequency, it is the first point of change with functional consequence.

Further there are some clear examples of epigenetic changes that have hereditable consequences. Most of those studied constitute switches that cycle between two states, but it would be relatively difficult to study one time epigenetic mutations (of course so far as I know Jacob-Krutzfeld and prion diseases in general are a one way event).

Pragmatically the ability to isolate genes by PCR and the fact that DNA sequence can be read as a discrete measure of type for any population makes it a very good choice for an evolutionary metric. By the same token evolutionary studies in the absence of understanding the functional impact of the changes noted are of only academic interest.

I think it's good to encourage studying evolution in the context of change in morphology or system function, but I do not see any other measure that has nearly as many pragmatic advantages as something DNA based. By the same token with increased genome sequencing, I think other types of changes are worth study (ie arrangement, repeat sizes and distributions, cooccurance of allele pairs, and the like which all can be done with PCR on a population level ... and may be for all I know).

(thanks paulsamuel)

Monkey, do you mean morphology with respect to protein conformation, or with respect to the phenotypic expression of the entire organism?

Originally posted by spuriousmonkey
the definition 'change in morphology' is also fully accurate. not necessarily. a population can have gene frequency changes with no consequent morphological changes. This is evolution.

a population can also have genotypic change without phenotypic change. This is evolution.

Originally posted by scilosopher
I think the morphology view is hard to argue for. There is the potential for many functional changes that could impact fitness that wouldn't effect morphology. For example alterations in metabolic pathways have no effect on morphology, but would affect fitness and should certainly be considered in evolution.


I'm merely pointing out the emptyness of the statement that the change in gene frequency is fully accurate. Lots of things are fully accurate, but not necessarily satisfactory. Morphology is a fully accurate description of evolution. In a way it is more accurate than the genotypic change because we actually have some historic record even of the morphological change, although not complete (fossil record). The historic record for genotypic change is very sparse.

so let us not bullshit around with clinging to straws. We need to examine the core of evolution.

You can certainly argue that various metrics of evolution have their own advantages. Like morphology and the fossil record or DNA based changes which I mentioned some advantages of in my last post.

Our working conception of evolution must be oriented towards metrics in order to do science. That's a pragmatic necessity. Our theoretical conception is more free of this constraint, but is somewhat academic until one can experimentally address the theoretical subtleties that lie outside our working conception as defined by various experiments.

Ideally evolution in my mind should seek to determine the primary causal material (ie within the organisms "design") and contextual (ie within the environment) changes that alter the fitness of individuals within a poplation. We obviously have a very poor grasp of environment in many cases simply due to the complexity of factors that are important. We also have sever limitations on what measurements we can make.

Often in science, as in this case, the important thing to do is see what straws you can get your hands on and make intelligent use of them. By the same token if the availability goes from straws to hay, so to speak, one is an idiot to stick to looking at things only at the level of the straws as you're accustomed. It's equally stupid to ignore what you know from your past work and ignore what you've learned from looking at straws or try to take on too much.

It's clear that morphology can sometimes be deceptive without using molecular markers and examining mechanism, even when dealing with spatial aspects of evolution. The important thing to do is develop integrative approaches, not say "change in allelle frequency is fully accurate" or "change in morphology is fully accurate".

The only thing that's a fully accurate depiction of evolution is tracing the path of every atom since the beginning of life. We can't do that. Things have to be coarse grained at a certain level, when you're dealing with something as complex as biology (and possibly the various levels studied hierarchically and mentally integrated). I personally think you shouldn't say A is better than B, rather A can guide us in this way and B in that and the best way to proceed is get information X from A and then fill in Y from B.

It's also a good way to avoid wasting time arguing ... put forward what is learned from what and then it will become clear that certain information is more useful in understanding various different questions.

spuriousmonkey said:
We need to examine the core of evolution.

But evolution is only a description of a series of relatively unrelated processes, it's more of a pattern than it is a force. A multidisciplinary approach may be the only hope in studying it completely. Genetics and morphology, as you say, aren't as... uh... bijective(?) as they could be in our present study of them. Given that we aren't able to relate them in a one-to-one manner, a study of evolution would seem to require both.

Originally posted by spuriousmonkey
a population can also have genotypic change without phenotypic change. This is evolution.

I'm merely pointing out the emptyness of the statement that the change in gene frequency is fully accurate. Lots of things are fully accurate, but not necessarily satisfactory. Morphology is a fully accurate description of evolution. In a way it is more accurate than the genotypic change because we actually have some historic record even of the morphological change, although not complete (fossil record). The historic record for genotypic change is very sparse.

I agree that the definition 'gene frequency' is not fully descriptive, and thus not fully satisfactory, but I cannot agree that morphology is an acurate descriptor because there are evolutionary changes that are not manifested in phenotype.

Also, one of the reasons why DNA sequence phylogenetics are so powerful is because of the paucity of the fossil record (evolutionary relationships can be examined with NO fossil record). So, it seems to me, your argument, that morphology is the more accurate description because of the fossil record, is contrarian (i.e. it actually argues the opposite point, that morphology cannot be the more accurate description because of the incompleteness of the fossil record).

Originally posted by BigBlueHead
spuriousmonkey said:


But evolution is only a description of a series of relatively unrelated processes, it's more of a pattern than it is a force. A multidisciplinary approach may be the only hope in studying it completely. Genetics and morphology, as you say, aren't as... uh... bijective(?) as they could be in our present study of them. Given that we aren't able to relate them in a one-to-one manner, a study of evolution would seem to require both.

studies of evolution do use both, but rarely simultaneously. comparative morphology is a powerful tool in studying evolution, and it was the only tool evolutionary biologists had before the 1960's.

i didn't say that.

Originally posted by paulsamuel
I agree that the definition 'gene frequency' is not fully descriptive, and thus not fully satisfactory, but I cannot agree that morphology is an acurate descriptor because there are evolutionary changes that are not manifested in phenotype.

Also, one of the reasons why DNA sequence phylogenetics are so powerful is because of the paucity of the fossil record (evolutionary relationships can be examined with NO fossil record). So, it seems to me, your argument, that morphology is the more accurate description because of the fossil record, is contrarian (i.e. it actually argues the opposite point, that morphology cannot be the more accurate description because of the incompleteness of the fossil record).

evolutionary relationship is not the same as evolutionary history. You can also make a nice evolutionary relationship scheme based on morphology.

but we are still digressing. I shall repeat myself.
I'm merely pointing out the emptyness of the statement that the change in gene frequency is fully accurate. Lots of things are fully accurate, but not necessarily satisfactory. Morphology is a fully accurate description of evolution. In a way it is more accurate than the genotypic change because we actually have some historic record even of the morphological change, although not complete (fossil record). The historic record for genotypic change is very sparse.

hence let us not get overy excited by the 'accurate nature' of change in gene frequncy. We might be able to measure it (similarly we can measure morphological traits rather accurately) rather accurately, but that doesn't mean that we know what it means.

I don't think lots of things are fully accurate (except semantically depending on various definitions). Every measure and explanation is approximate and rough. The details are way beyond our experimental and theoretical abilities right now.

The question is what would you find a satisfactory measure for understanding evolution?

Personally I think people should take well studied networks in a given organism and study them in well separated organisms. Try to bootstrap themselves as much as possible off what is known in the original organism. For an interesting paper that takes that approach see:

Regulation of the Tribolium homologues of caudal and hunchback in Drosophila: evidence for maternal gradient systems in a short germ embryo.

Wolff C, Schroder R, Schulz C, Tautz D, Klingler M.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9716530&dopt=Abstract

It seems that evolution discussions may restart Lamarck-Darwin battle, eh? I'm doubting that natural selection is the only way of evolution, considering that there are now just plain too many specieses (or should I say: distinct speciese?) for natural selection to be true..... Help.

Did Lamarck posit a higher rate of development/speciation? Haven't read his stuff...

Natural selection isn't supposed to explain how you get new variants. I haven't read Darwin's stuff myself (started once and never quite got through it), but my understanding is that he gave no force for generating variants to be selected upon, and rather presumed their existence.

So the number of species that exist is something apart from Darwin's theory of natural selection. I don't think Lamarck is a rational alternative. Genetics has lead to the understanding that variants are generated by imprecise maintanance and copying of existing DNA as well as its "shuffling" in the recombination process during sperm and egg production.

To get evolution one needs a balance of variants and consistency. Too inconsistent and a species doesn't maintain it's past abilities, too consistent and it doesn't have variants that can handle new or changing conditions.

Lamarck, as I recall, also doesn't have a very good explanation for sympatric speciation, that is, why two groups of creatures that are originally in the same population will evolve to be different enough from one another that they can no longer interbreed... Lamarck's ideas, as I recall, only related to positive pressures on the population. I could be wrong though.

One example I got about Lamarck vs Darwin was on girraffes.......

Lamarck: "In the past, all giraffes were short-necked. When food on the ground went scarce, they ate leaves on trees. When trees got taller or put their leaves higher, giraffes grew their necks so that they still could eat."
Anti-Lamarck: "Look, dinos extinct....."

Darwin: "There were a lot of giraffe specieses on earth, but primarily, there were those with long necks and those with short necks. As food was starting to grow at taller places, short-necked giraffes died from starvation, and the long-necked kept living."
Anti-Darwin: "Hello...... we can relate nowadays bird with achaeoptheryx......"

Yes, but the reason that I brought up the speciation example is that Lamarck's theory doesn't very well explain why two populations, when they evolve different characteristics, sometimes speciate - that is, can no longer interbreed.

If I understand Lamarck correctly, interbreeding between any two animals should only be prevented by mechanical problems (too big vs. too small), because there isn't any pressure for the reproductive systems of the two populations to change.

evolution is the change in gene frequency over time:

that seems a bit a daunting prospect for elucidating the problem of the evolution of viruses.

An expert was telling me that they had 50 genomes sequenced of a certain virus type, but it was expected that there would be at least something like 10*30 ( to the power of 30). He wasn't very hopeful that they would ever be able to sequence the lot, or even a significant part of them.

Why would you need to sequence them all - because they coninfect and work together?

Otherwise, unless there is another type of envrionmental effect, what's wrong with just sampling them?

I'm not sure what you mean by type, but one doesn't need to sequence each and every unique genome of a species, genus, what have you to get a reasonable estimate of the change in gene frequency (or any other DNA based metric).

Of course you'd be more likely to might miss out on pairwise correlations in changes, but you have to start somewhere.

he seemed to think so. He is appraoching the problem from the other side. Extremely conserved structures.

anyhoo...the problem with the DNA phages was that they were all mosaics. You couldn't make a tree anymore because of this. It is a world wide web of phages. they can all exchange and often seem totally unrelated until you happen to see an intermediate. But there are too many phage genomes to sequence as I said earlier. 10*30 is quite a big number. That is a conservative estimate btw.

Although I would agree that to get an accurate measure of a small rate, or to sample rare events, one would need to sequence many examples.

Alternatively one could look at highly diverged species and make guesses about what changes are most likely and come up with a stringent PCR based approach (presumably the genomes are combinations of a much smaller number of mutations if the structures are quite highly conserved).

However it sounds like he's not doing the best job picking a research topic.

i guess that is why they made him a professor.

this is a nice little article by him:

Res Microbiol. 2003 May;154(4):231-6.
Do viruses form lineages across different domains of life? Bamford DH.

The scarce characterisation of the viral world has hampered our efforts to appreciate the magnitude and diversity of the viral domain. It appears that almost every species can be infected by a number of viruses. As our knowledge of viruses increases, it appears that this myriad of viruses may be organised into a reasonably low number of viral lineages including members infecting hosts belonging to different domains of life. Viruses belonging to a lineage share a common innate "self" that refers to structural and assembly principles of the virion. This hypothesis has a few consequences. All viruses are old, maybe preceding cellular life, and virus origins are polyphyletic, as opposed to the idea of a monophyletic origin of cellular life.

The polyphyletic aspect of the story is quite nice and could be considered 'revolutionary' if you are a bit conservatively minded.

Perhaps it would be best to examine viral genomes in a very isolated organism which doesn't tend to come into contact with others very often... shame that it's so hard to get to those deep-sea vent creatures.

A virus that infects a monocultural organism, like a high-altitude plant or an archaebacterium, might provide the least complex set of data.

Unfortunately my school doesn't have an online subscription to Res Microbiol.

Also for some reason after your post "i guess that is why they made him a professor." my web browser (mozilla on linux) won't display the sciforums website. It still loads on other machines in the lab though. So I might not have much to say for a bit though not due to a lack of interest.

(EDIT - it was a stupid XFree86 update, I just had to reboot)

Originally posted by BigBlueHead
Perhaps it would be best to examine viral genomes in a very isolated organism which doesn't tend to come into contact with others very often... shame that it's so hard to get to those deep-sea vent creatures.

A virus that infects a monocultural organism, like a high-altitude plant or an archaebacterium, might provide the least complex set of data.

apparently it doesn't really matter where you collect these kind of viruses

After reading the Bamford paper I must say, I'm not sure if his main conclusion is reasonable. Granted he did point out that he was aiming to be "unorthodox and, perhaps, provocative", but I guess what he provoked in me was some disbelief.

His main point about polyphyletic origins of virsuses, is based largely on the fact that structurally homologous viruses infect all domains of life. Viruses evolve very fast - as he himself points out in very the necessity to look at structure to see the lineal relation. Why then is it not more likely that viral lineages split before Bacteria, Archea, and Eukarya than there were multiple events that lead to completely unrelated viruses?

I've never studied virology, so maybe the point that viruses may have existed before the split of the main domains of life into the three groups is not a well recognized issue. If so, I find that strange because it would have been a basic assumption of mine.

Anyways, viruses are very interesting evolutionarily for many reasons - coevolution with hosts (or hosts immune responses even), they evolve on timescales that allow one to actually follow the evolutionary process, they have very compact and finely tuned developmental programs, and their whole genome can be manipulated to form alternative points for starting evolutionary experiments.

While I find some features of the paper interesting they do not seem to be the ones he focuses on. Perhaps it is because he is being unorthodox and the field's orthodox focus has aimed at the more interesting features of viral evolution and attributes. I find it very unfortunate that most scientists are more interesting to speak to about a subject than they can discuss in papers, I'd probably find it quite interesting to speak with him in person ...

Originally posted by spuriousmonkey

From a developmental viewpoint the dogma of change in gene frequency is pointless. They are not interested in studying the change as such. They study how an individual is made, which is only partly based on genetics. In developmental biology it is the 'arrival' of the fittest that counts, not the 'survival'.


Genetics reflects design (which does not imply a designer, necessarily) and for me, measuring the adaptation of a creature is more important than measuring a statistical change in DNA.

Craig said:
Genetics reflects design (which does not imply a designer, necessarily) and for me, measuring the adaptation of a creature is more important than measuring a statistical change in DNA.

However, if you believe in preadaptive changes, a series of relatively invisible genetic changes can end in a sudden (evolutionarily speaking) change; DNA changes, even those with no direct appearance, can still have a drastic effect on an organism's phenotype. Morphological changes (the apparent adaptations) are important, but determining the rate and mechanism of genetic change can help to predict/understand the morphological changes.

Preadaptive change is part of adapation. Create 100 beasts, each with a different way of doing task A, and then unleash them on reality. The ones that aren't killed represent an optimized methodology for task A.

True, but preadaptive change is not an adaptation until the situation arises where it is useful; a morphological assay of a population may miss preadaptive changes, and so the morphological approach is not a sufficient description of evolution.

Originally posted by BigBlueHead
True, but preadaptive change is not an adaptation until the situation arises where it is useful;
I don't know anything much about this, and my apologies if I've misunderstood, but if what you say is true then wouldn't it mean that it is entirely a matter of luck who survives best, and also which adaptions survive best?

That is, if adaptions only becomes useful after environmental change then it would be a matter of luck which members of a species happened to have some non-useful features capable of becoming considered as advantageous 'adaptions' after the change.

That's convoluted. What I'm struggling to say is that if before the change features are not useful then surely they cannot become 'adaptions' just because, by luck, the environment changed to make them so?

Canute

I think the idea in preadaptive change is that certain adaptations to do task "A" better also make it more likely that you'll do task "B" better even though you've never had to do task "B" before. Therefore preadaption is to some extent the evolution of more generically favorable systems - ie robust to more environmental perturbations and the like.

I too have little familiarity with pure evolutionary science/though though and may have misunderstood or misremembered the idea.

If that's true then I'm going right off adaptionism. Can someone give the official line on when a 'spandrel' becomes a selected for trait?

I'm not sure what you are looking for....

genetic assimilation.

genetic information exists but is not selected for. The organism is place in a new environment and selection takes place for this previously 'hidden' genetic information. The phenotype changes accordingly. We place the organism back to the original environment, and the phenotype persists, despite the presence of new selective pressure.

example:

limnea. They produce elongated shells in deep water. When placed in shallow water a new phenotype appears that deals better with the new situation; shorter shells. When put back into deeper water the shells remain short.

Spurious

No that's not quite it.

BBH said "True, but preadaptive change is not an adaptation until the situation arises where it is useful..."

In this case surely preadaptive change is not adaptive at all. It is just happens to seem adaptive later, because of environmental change.

Surely adaptionism requires that adaptions are selected for at the they time that they happen? Otherwise they're not adaptions, they're just non-useful mutations.

Canute

Canute: Adaptations are selected for at the time that they happen, but the mutation that permits the adaptation has to happen before that. Adaptation is a description of the combined process of mutation and selection.

But didn't you you say that expressions of genetic mutations weren't useful until after the environment had changed, (and were thus 'preadaptions' until then) at which time they became adaptions? This seems tautological to me.

That's why Dawkins called his book The BLIND Watchmaker.

Maybe, I've read it but forgotten his argument. How would he have answered my point?

It seems to me that pre-adaption means non-adaption, as the metaphor of spandrels suggests. If a feature is not useful it cannot be selected for but is there by pure chance. Even if the environment changes to make it useful I don't see how that alters the fact that it arose by chance.

To put it another way if my son had been born with a beak this mutation would have been not only useless but positively survival-threatening. However if the environment changed and suddenly we all had to live on bird food it would be quite useful. Would we then call it an adaption derived from a preadaption?

That's about right. Mutations pretty much can't happen at the time of selection for multicellular organisms, because the mutation has to have an adaptive significance and also be present in the reproductive organs. Mutations generally happen within the gametes and are inherited by the offspring by that mechanism. As such with human beings there can be as much as a 30-40 year lag between mutation and selection, depending on how long you wait to have children.

I think I see what you're saying here and it makes sense. But a few more questions to make sure I'm getting this right.

Originally posted by BigBlueHead
That's about right. Mutations pretty much can't happen at the time of selection for multicellular organisms, because the mutation has to have an adaptive significance and also be present in the reproductive organs.
(I assume you mean mutation of phsyical features here).

I agree that mutations can't happen at any particular time, since they can't by definition, but I don't quite understand what you're saying here. Are you saying that a mutation of phenotype has to have an adaptive significance before it can be considered to be an adaption?

Mutations generally happen within the gametes and are inherited by the offspring by that mechanism. As such with human beings there can be as much as a 30-40 year lag between mutation and selection, depending on how long you wait to have children. [/B]
If I get you right the mutation is random, the 30-40 years is the preadaption stage, then the mutation becomes an adaption because it suddenly becomes useful in some way.

Wouldn't the time lag have to be shorter than this, otherwise he (let's assume it's a he) does his mating in the pre-adaption period and isn't any better than his competitors at passing on his genes?

Also, how is the mutation selected for here? There has been no change of environment to make it useful.

This is a pretty interesting and instructive topic. Essentially, we are asking about non-adaptive origins for adaptive characterisitics, wheather we call them spandrels, preadaptations or exaptations. Exaptations do not need to be neutral characterisitics (i.e. nonadaptive). They can be and are adaptations that are shared for a new function. Feathers, e.g., were thought to derive for warmth but also were used for flight.

But if feathers were useful for warmth wouldn't they have been an adaption? They were exaptations in terms of wings, but that's just a point of view taken in hindsight.

My problem with all this is that if an adaption only becomes useful with a change of environment than in what sense are they adaptions? Surely they are just useless mutations that by chance become useful.

well, the (legitimate) problem is that adaptations do not arrive whole, de novo when needed. These morphological characteristics are thought to derive gradually over time. However, how does natural selection refine partial characters. One answer could be that these 'adaptations', as we see them, had other adaptive functions while evolving. For example, feathers for warmth before being co-opted for flight as well. These questions abound in evolutionary biology, and I'll bet, if you pick up any Evolution issue (the scientific journal) over the last 20 years, you'll find at least one article addressing this, at least in a tangential way. Alternatively, there is the hypothesis that denies that these charactersitics have to evolve gradually from which derives the 'hopeful monster' theory and which is addressed by some 'evo-devo' researchers.

paulsamuel, I am not very informed about evolutionary theories, but
what is your take on "Beak of the Finch," the book that won the
1995 Pulitzer Prize by Jonathan Weiner? I have not read the book,
but saw a documentary on TV about Rosemary and Peter Grant's
work a few years ago. I'm sure you are aware of their study of the
quickly changing beak sizes of Darwin's finches to reflect the changing
food supply. Does that represent evolution and natural selection
or something else?
http://www.2think.org/tbotf.shtml

Interesting. Darwin seems also to have felt that mutations do not occur entirely at random (although their precise effect might be near random) and that they might be (quantitively at least) an immediate response to environmental change. (Or have I read this wrong).

“Although each modification must have its proper exciting cause, and though each is subjected to law, yet we can so rarely trace the precise relation between cause and effect, that we are tempted to speak of variations as if they spontaneously arose. We may even call them accidental, but this must be only in the sense in which we say that a fragment of rock dropped from a height owes its shape to an accident.” (V ii Darwin’ Notebooks on the Transmutation of Species) 'Darwin' – Jonathon Howard – OUP 1982 p70

canute, I don't think anyone considers Darwin an expert on mutation. He was pretty much in the dark as to the basis for the generation of diversity ...

paulsamuel, what do you think about the CH Waddington hypothesis about selection for sets of alleles that alter biological function. The current incarnation of the idea is demonstrated in the Rutherford and Lindquist paper on hsp90:

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12101404&dopt=Abstract

The mechanism they suggest involves both cryptic variation and the possibility for selecting sets of alleles rather than single alleles. The basic idea is that hsp90 a chaperone (meaning it helps avoid misfolded proteins) masks certain allelic variants that bias a pathway towards a different behaviour. If you have multiple variants that encourage this behavior hsp90 can no longer mask the effect (possibly because the alleles are in a protein complex and mutually stabilize eachother). Therefore a population can harbor many mutations that alone have no effect and through sex rapidly generate the set that gives the improved phenotype.

I guess as a molecular biologist I feel uncomfortable speaking about things so abstractly that one looses site of mechanism and such ...

http://www.sqwark.com/Epigenetics.htm

http://en2.wikipedia.org/wiki/Epigenetic_inheritance

Most epigenetics says nothing about acquired characters being passed on. In fact most known epigenetic inheritance only involves cycling through states which clearly would not result in contributing information to speed evolution.

The fact that it would be useful if such information could be passed on does not mean it will be. In fact the nervous system is evidence of an alternative approach to passing on acquired characters. It allows you to teach your children. Indeed it is particularly powerful as acquired knowledge can be passed to others than your own progeny.

Originally posted by scilosopher
canute, I don't think anyone considers Darwin an expert on mutation. He was pretty much in the dark as to the basis for the generation of diversity ...

I'm aware of that. But I think he had a point.

Canute,
I'm not aware of any mechanism of mutation that could give biased mutations (other than in the immune system and generation of antibody variation). While I would not rule out the possibility that such systems could exist, random mutations should do the trick assuming a large enough population anyhow.

Therefore to me all his statement says is that he's not ignoring causality and physical law. At what height the rock happened to be dropped from has to be random to hold the analogy to mutation.

spookz,

epigenetics is not lamarckianism, epigenetics is about the control of genes and protein production, epigenetic factors can turn genes off, on or throttle productions levels depending on signals they receive (internal or external). Epigenetic factors are not or have not been linked to permanent genetic changes from one generation to the next. You can not acquire a epigenetic factor by demand and give it to your progeny.

Originally posted by scilosopher
Canute,
I'm not aware of any mechanism of mutation that could give biased mutations ...etc. [/B]
I didn't feel that he was claiming this. Rather he was saying that the rate of mutations (or their clustering) might be affected by environmental factors (climate change or city living perhaps). Whether he also speculated whether to some very general extent the category of mutation that occured could be affected by changes in living conditions he doesn't make clear here.

I don't enough about it to form a strong view, but it seems a reasonable enough idea.

Regards
Canute

Fair enough. That more mutations happen under stressfull conditions (ie. when things aren't working out so well), is not that diffidult to imagine as a simple reduction in available energy (as during hunger) could clearly encourage mutation as mutation repair requires energy.

However I do not read any of the nuances you put forward into the passage above. Still you've given rise to the first mechanistic hypothesis as to why mutation may be higher at certain times and it has a natural correlation to when you'd want them. Though in multicellular organisms it isn't clear the timing would work out right (hungry mom has baby with more mutations than normal sounds like it would cause problems as much as evolution).

bah
even though i know next to nothing about this stuff, i sniff blood!:mad:

Hmm. I thought that there'd be some objection to that idea. Is there actually any research on the correlation between sudden (ish) environmental change and mutation rates?

Sppokz, I think you're sniffing something other than blood if you think epigenetics provides the potential for passing on acquired traits. Particularly in most organisms which separate their reproductive cells and somatic cells very early. All of the cool epigenetic regulation of chromatin can't be involved, which makes it very hard to imagine any meaningfull passing of acquired characters ...

Canute - nothing I know about or I would have mentioned ... maybe paulsamuel knows something?

quite possible!:)

blind cave fish

the mexican tetra fish lives in both caves/underground pools and streams/ponds. the former are blind and without pigmentation. eye development starts the usual way..rudimentary lens and optic cup. within 24 hrs however the cells die, cornea/iris does not develop. eyeball sinks and is covered by skin.

now it is known that shit atrophies without use. how is tho that the tetra passes on this degradation to its offspring.

dont plants do this kinda stuff all the time? if they do, how and why are we so special?

(pdf link p15) (http://philsci-archive.pitt.edu/archive/00000546/)

there is more...butterfly wing morphology(p17) and geomyoid rodents (p19)

thoughts on this? on evo devo as a whole?
thanks

Originally posted by scilosopher
Most epigenetics says nothing about acquired characters being passed on.

most? what epigenetics says stuff about acquired characteristics?

gee
i decided to skim a bit and....Alternatively, there is the hypothesis that denies that these charactersitics have to evolve gradually from which derives the 'hopeful monster' theory and which is addressed by some 'evo-devo' researchers. (dr paul)

Originally posted by spookz
gee
i decided to skim a bit and....Alternatively, there is the hypothesis that denies that these charactersitics have to evolve gradually from which derives the 'hopeful monster' theory and which is addressed by some 'evo-devo' researchers. (dr paul)

That not what I said, my answer does not conflict with that statement. Again epigenetics only deals with genes that control the function of other genes, epigenetics does not go against Darwinism.

:confused: the quote was attributed to paulsamuel.

epigenetics does not go against Darwinism.

why are some making a big stink about it? there is no controversy?

edit: just ignore posts. i respect you guys too much to screw this thread up:)

Honestly yes there is no controversy, scientist are just very excited about epigenetics because of new break-throughs in understanding it. Some things in epigenetic goes against the central dogma (like RNA only genes) a major revolution in thought. but epigenetic still obey the laws of heredity.

Originally posted by copper
I don't disagree. But you can't say that post-reproductive organsims are as important to the population as those that can reproduce. Your example didn't really address this. I can't think of an example where a non- or post-reproductive organism is as important to the evolution of the population as one that can pass on its genes.

Man is the only exception. All important things for mankind (except children) man create in post-reproductive period.

since when is epigenetics a new idea?

it was a reaction to preformatism. It's a dusty part of history.

While the idea of epigenetic inhereitance might be dusty what is understood about it is quite new and cutting edge. Chromatin, imprinting (and it's importance in reproductive cloning), and the like are very interesting active areas of research. Indeed there may be the potential for epigenetic inheritance for all we know on germ plasm and the epigenetic state of certain genes. This could allow fast regulatory change in early developmental programs.

(spookz - I wouldn't claim all since I'm not completely on top of the field. I think there may be some examples from Susan Lindquist with yeast PSI that switching between prion states is favoured during cellular stress (due to titration of chaperones), which then is passed to progeny. I guess that counts as an acquired character, though it does exist in a latent form in the DNA.)

very nice sci. excellent attitude. a pox on the other retards

A fascinating example of epigenetic inheritance is available if one looks to the reptile world. While the sex of human offspring is determined genetically, in turtles two mechanisms exist: both a genetic mechanism and an epigenetic mechanism. Turtles are sex-typed at the time of fertilization but can have their sex reversed if the temperature during a specific phase of their development is appropriate to induce the change. Specifically, high temperatures are feminizing and lower temperatures are masculinizing. The temperature of a nest is often dictated by the mother's choice of nesting sites (Sura, 1995)

While the existence of phenotypic plasticity based on epigenetic inheritance does not necessarily point up the inheritance of the manifested phenotype there is a po