Aquatic Ape Theory

Discussion in 'Human Science' started by LIGHTBEING, Aug 22, 2002.

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  1. spookz Banned Banned

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    musings

    *There are two ways in which a new idea in science is rejected: one is by direct confrontation and attempts to refute it, the other is by turning a blind eye to it and hoping that it will simply go away (Tobias, 1998).

    *In her talk earlier the day, Elaine Morgan tried to understand why the idea has been simply denied, instead of scientifically debated. She came to the conclusion that for a large part it may be simply because of her person. She doesn't have an academic degree and at the time she first developed further Alister Hardy's idea, she was a militant feminist. It must be said that at the symposium everyone was impressed by the rational arguments and evidence with which she addressed the different criticisms and how she admitted to have made claims which turned out later to be untenable.

    *humans today are as aquatic as hominids have ever been and thus that if there has even been an aquatic ape, it would have to be ourselves.(langdon)
     
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  3. (Q) Encephaloid Martini Valued Senior Member

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    Spurious

    I find it really strange that the opinions are so polarized on this matter in this forum when there is clearly no definitive evidence for any of these theories. If you think otherwise then please endulge me and point me towards it.

    AAT is based entirely on false "facts." The arguments put forth by the proponents of AAT (Elaine Morgan) are filled with examples of ad hominem, ad hoc, Strawman, Irrelevant Conclusion, Fallacy of Exclusion, and Special Pleading.

    The theory (or more precisely, hypothesis) is internally inconsistent - it is not only contradicted by facts, but by its own claims.

    and no...the theory has not been proven to be false. Some people think it is not true...it is not the same.

    The central idea of evolution is phylogeny, which places the AAT outside of all evolutionary theories to date. One simply has to understand evolution to refute the claims of AAT proponents.

    because adaptations to the 'aquaboreal' lifestyle gave them advantages in the end.... Adaptations that are evolved for one purpose sometimes turn out to be useful for other purposes, or have multipurpose to start with.

    Come now, you can't be serious. You're actually claiming that a group of fat, sweaty, naked aqua apes outcompeted their terrestrially adapted cousins ? Look back and you'll see that the AAT proponents argue that these adaptations (fat,sweaty,naked) make Homosapiens LESS able to compete on land, and that is why they are *proof* that our ancestors are semi-aquatic.

    except that this one was in a peer reviewed journal and I found other articles supporting aqua-arboreal ideas in peer reviewed journals.

    Then you probably also know that the AAT (more precisely AAH) is used in undergraduate courses as a case study.

    I think we settled now the question if ATT is represented in peer review articles or not. It is.

    Citation please.

    AAH is not good science. Whether the proponents of AAH are trying to deceive laymen with their pseudo-babble or they simply have done very bad research - irregardless, the AAH is clearly in the realm of pseudoscience.
     
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  5. spuriousmonkey Banned Banned

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    is ATT scientific or not?

    Q...i'm just going to go through a few essential points and not answer every single point.

    Q..I suspect you are just being malicious here...there have been given several references already...i'm not going to repeat them over and over and you may want to use a scientific search engine yourself if you want more.

    the aquaarboreal theory is not based on false facts, but based on the same facts as the other theories are based on...if you have actually read the article you might have seen that Verhaegen uses the normal evidence that is around, but interprets it differently.

    ++The central idea of evolution is phylogeny.+++

    The central idea of modern evolution is natural selection. There were already evolutionary theories around before Darwin. What Darwin did was to introduce natural selection as a mechanism. And that is what is so attractive about it. See for instance 'the growth of biological thought', Ernst Mayer; Part 2 chapter 8 'Evolution before Darwin.'

    I am under the impression that you might have a view on evolution that is not entirely realistic. There is no reason to assume that adaptations developed for an aqua-arboreal lifestyle could actually turn out to be advantageous in other environments. One of the classic mechanisms of speciation is island-isolation. A certain population of a species is cut of from the parent species (this could be an island, but often the island is merely an analogy). They encounter a different microclimate in this 'island', they evolve into a different species. Later the barrier disappears between parent and modified species, but still the modified species manages to obtain a foodhold in the original terriory of the mother species, or even outcompete them.
    As you can see there is nothing strange about the idea that a hominid species partially adapted to an aqua-arboreal lifestyle could venture out of its original environment and even outcompete your classic terrestial species. it could have been a classic example of island speciation.

    Therefore, theoretically, it is a classic story of evolution, not a story that will not fit with evolution. Although we might personally disagree with this particular theory if you think that the speculation is not warranted and you prefer other speculation

    where you go wrong is that you take the idea too far. When you think of an aquatic ape, you see some kind of dolphin human...what you should be thinking is that humans have evolved a few features that could be explained by a lifestyle that involved spending a large amount of time near/in water. In this envirnoment, these feature could have been beneficial. These features could also have been beneficial in other envirnoments. Humans have never been fully aquatic.


    I have to conclude so far (as a biologist), that ATT is scientific. I also conclude that the evidence for it is flimsy and that gives us reason to doubt it. I also concluded that the evidence for the other theories is equally flimsy...therefore you might doubt them too.
     
    Last edited: Dec 20, 2002
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  7. (Q) Encephaloid Martini Valued Senior Member

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    Spurious

    Q..I suspect you are just being malicious here...

    What reason would I have for being malicious ? Simply because I understand why the AAH is bunk ?

    if you have actually read the article you might have seen that Verhaegen uses the normal evidence that is around, but interprets it differently.

    Interesting you would say that - from your point of view, I would respond that Verhaegen interprets the evidence incorrectly.

    There were already evolutionary theories around before Darwin. What Darwin did was to introduce natural selection as a mechanism

    Then if you understand Darwin's theories, you'll understand why AAH is nonsense.

    I am under the impression that you might have a view on evolution that is not entirely realistic.

    That is your opinion, and of course, I could say the same of you.

    A certain population of a species is cut of from the parent species (this could be an island, but often the island is merely an analogy

    Aside from the AAH, can you cite one single species which would qualify this claim with the understanding that your reasoning is parallel to that of the AAH ?

    As you can see there is nothing strange about the idea that a hominid species partially adapted to an aqua-arboreal lifestyle could venture out of its original environment and even outcompete your classic terrestial species.

    So, by your reasoning, if Homosapien ventured back to the sea and became a Merman/Mermaid, they would outcompete the terrestrial Homosapien upon returning to land ?

    Although we might personally disagree with this particular theory if you think that the speculation is not warranted and you prefer other speculation

    I try not to speculate against hard evidence as anything but what the evidence suggests. One must keep it simple.

    When you think of an aquatic ape, you see some kind of dolphin human..

    I think about aquatic apes exactly the way in which AAH proponents have hypothesized.

    what you should be thinking is that humans have evolved a few features that could be explained by a lifestyle that involved spending a large amount of time near/in water

    Spending time IN water is a lot different than spending time NEAR water.

    I have to conclude so far (as a biologist), that ATT is scientific. I also conclude that the evidence for it is flimsy and that gives us reason to doubt it.

    I don't think that AAT/AAH is good science because there is no evidence to suggest the hypothesis is consistent with accepted theory or even consistent with its own claims.

    I also concluded that the evidence for the other theories is equally flimsy...therefore you might doubt them too.

    Darwin's theories imo, are not flimsy. They are good theories which abound in good evidence. What is it you doubt about them ?
     
  8. Fukushi -meta consciousness- Registered Senior Member

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    Darwin was wrong, in some aspects of his theory's. Not all of it is rubish but the greater part of it is, this is common knowlegde I thought? No?
     
  9. (Q) Encephaloid Martini Valued Senior Member

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    NO!
     
  10. spookz Banned Banned

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    q leans towards the fruitarian evolution theory.

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  11. Fukushi -meta consciousness- Registered Senior Member

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  12. (Q) Encephaloid Martini Valued Senior Member

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  13. Fukushi -meta consciousness- Registered Senior Member

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    Of course Darwin was wrong: his pangenesis theory as a theory of heredity was completely wrong. Because a migration of hereditary material from all parts of the body to the sexual organs and the subsequent inheritance to the offspring, was already refuted during Darwin's lifetime. Darwin was also wrong to believe that acquired characters, for example changes in organs caused by use and disuse, are heritable (Lamarckism) (1, 10).

    How does this affect his theory of evolution? The Common-descent-of-life part of evolution does not depend on a correct theory of heredity. Common descent was quickly accepted in Darwin's time. However the success of natural selection as the main causal factor in evolution depended substantially on a adequate theory of heredity.

    And on evidence. Darwin's contemporaries were slow to accept natural selection. For good reasons? Now we have a 'correct' theory of genetics, Lamarckism is rejected, genetics is integrated in evolutionary theory, and natural selection is accepted as an important factor in evolution. The historical question whether Darwin's theories were accepted at the time for good reasons is of course unanswered by the current status of genetics.

    it's still an interesting question. A more interesting and urgent question is: are there good reasons to accept current neo-Darwinism? It's the same question but now applied to the modern Synthetic theory of Evolution. What is true of all criticisms? Do the critics still have some good points? Is current neo-Darwinism well supported by an adequate theory of natural selection and genetics? Do we understand organisms in enough detail to claim that we understand how new species evolved?

    In my opinion it's not merely the species that evolve out of strings of DNA, but it's also the surroundings that transform life itself and heavely influence transformation and evolution.
     
  14. spookz Banned Banned

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    fukushi

    would you have any opinons on epigenetics? science? junk science?
     
  15. (Q) Encephaloid Martini Valued Senior Member

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  16. Fukushi -meta consciousness- Registered Senior Member

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    So Q

    If you take out the effort to search and find this link, you certainly should read this shit, before you proved yourself wrong.

    then you should have thought about this statement (that Darwin's theory has no flaws) a little longer before you spawned it.

    Now, I don't care about copy/pasting normally, but if I do, it means that I agree with something and that I couldn't have put it better. I wasn't trying to make it sound like I wrote this shit, did I? I'm sorry guys

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    but point is:
    (and this is my opinion) That Darwins theory about (especially that one) survival of the fittest, is utterly crap and BS. why? need I to explane why? okay here I go:

    I'm mad at how these theory's are pulled from their original idear and being molded into whatever's applicable. In this way I've seen (for expl) faschist-neo-nazi-skinheads bashing in other people's head,...nice old Darwin provided them the moral and philosophical grounds to inflict their damage onto others.

    How about that example, does it strike some sound, does it?
    I know it's an example out of the extreme, but that's the point.
     
  17. (Q) Encephaloid Martini Valued Senior Member

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    Fukushi

    I wasn't trying to make it sound like I wrote this shit, did I?

    Of course not - besides, your critique was far superior. I particularly like your formal evidence to support your interpretation of "survival of the fittest:"

    Hey... I'm convinced.

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  18. spookz Banned Banned

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  19. spookz Banned Banned

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    in defense of lamarck - jumping genes

    Establishing the Link

    McClintock's early work was more then enough to make her famous. By the 1920s, the idea that genes were located on chromosomes was clearly established, but no one had yet been able to connect a specific chromosome with the groups of genes that geneticists called "linkage groups." McClintock took the 10 linkage groups of maize and gradually connected each one with a specific chromosome. Her microscopic observations of the landmarks on each chromosome were so exact that she was able to observe crossover (recombination events) through the microscope, and then show that they corresponded precisely to genetic recombination events in the next generation of corn.

    This was fundamental work, responsible for establishing one of the great cornerstones of modern genetics, namely, the idea that genes have fixed positions on chromosomes. McClintock continued her research work at several institutions, including the University of Missouri and in 1942 took a position at the Cold Spring Harbor Laboratory on Long Island, New York. In 1944 she was elected to the National Academy of Sciences, and in the same year was elected as President of the Genetics Society of America, the first woman to hold the post. One might have forgiven her if she had decided to rest on her laurels. However, her most remarkable work was yet to come.

    The First Clue:

    It's particularly ironic that McClintock, having helped to establish the location of genes on chromosomes as orthodoxy, was soon to upset the applecart. But it's also characteristic of her style of work.

    In her first two years at Cold Spring Harbor, she noticed some unusual characteristics in a strain of corn. The plants showed streaks and spots of color, an indication that mutations had taken place in the developing body of the plant. These plants, interestingly, contained a broken chromosome #9. McClintock immediately noticed that these patches were arranged in a way suggesting that the rate of mutation was constant for each plant. In a sense, something must be "regulating" the rate of mutation of the pigment genes.

    In a few of these plants, she noticed another interesting sight. Every now and then, small portions of a plant would show greatly increased or greatly decreased rates of mutation. McClintock concluded that these sectors must result from the progeny of a single cell in which the gene regulating the rate of mutations had itself changed. She tentatively concluded that this unusual system must have two elements: first, an element that actually caused the mutations, and second, an additional element that controlled the activity of the first. As usual, she was right on the mark.

    McClintock called the element that actually caused the mutations the Ds (dissociator), and the controlling element the Ac (activator). By careful observation she discovered that the Ds element was on the short arm of chromosome #9 (right where the chromosome breaks had occurred) and the Ac was far away, on the long arm of chromosome 9. Those observations, in and of themselves, were interesting, but the most important finding was the fact that these elements sometimes appeared at other locations on the chromosome.

    Transposition:

    By 1951, McClintock had clear evidence that Ac and Ds could change their positions on the chromosome. She coined the term "transposition" to refer to the movement of genetic elements from one position to another, and she had developed convincing evidence that Ac controlled its own mobility within the genetic system. Quite simply, Ac could remove itself from one place on a chromosome and reinsert itself in a different place. It could move.

    For the first time, McClintock had shown that genes did not necessarily occupy fixed positions on chromosomes. The significance of this was not lost on McClintock. Another scientist might have been careless enough to treat the Ac-Ds system as an "exception" to the normal pattern of development, but not McClintock. In fact, her papers indicate that she saw transposition as one of the key events behind development in the growth of large organisms. Some of the differences between individual cells and tissues in the embryo, she thought, might be due to genetic re-arrangements caused by transposition.

    What did this mean for biology? Genetics had just established the central role of genes on chromosomes in passing the determinants of heredity from one generation to another. It had established the rules by which genetic material was sorted, arranged, and recombined, and was beginning to understand how genes were constructed in a chemical sense. There was even hope that the rules by which genes are expressed would soon become clear. To many scientists, it may have seemed that McClintock had clouded this emerging certainty by dropping the wild card of transposition on the table. Just as they were beginning to see genes as genuine entities, here was McClintock telling them that some genes could hop around from one position to another.

    This last point was too much for her fellow geneticists, most of whom simply didn't see the maize results as very important. I should add a personal aside here. I read about McClintock's work as a undergraduate in my first genetics course in the late 1960s. The system of "transposable elements" in maize was presented as a very interesting, but very obscure, exception to the general rule that genes are fixed on chromosomes. McClintock's work was respected, but it did not affect biology as it should have. Not for more than 20 years.

    Transposition Rediscovered:

    Barbara McClintock not only had the insight to see the importance of her work, she also had the good fortune to live long enough to see the rest of the scientific community catch up to her. In 1956 she reported on a second system of transposable elements on maize, known as the suppressor-mutator system. This system involved a series of transposable elements that are often located near pigment genes, suppressing their function, and producing colorless (white) kernels of corn. When the transposable element moves, the pigment gene is reactivated, producing a reddish splotch of cells on the skin of the kernel. Only can look at a spotted kernel and almost "see" the transposable elements moving. Once again, it involved two genes, one of which controlled the movement of the other. The Ds-Ac system was not an isolated exception, at least not in maize.

    If transposition had remained an interesting, obscure, minor exception we might not celebrate McClintock's work today. Little, by little, however, bits and pieces of transposition were spotted in other genetic systems. It became clear in the lacc operon that one gene could control the expression of another. Studies on bacterial viruses (bacteriophage) showed that genetic material could insert itself into a chromosome, and then remove itself. Finally, the elusive genes responsible for resistance to antibiotics in certain bacteria were shown to reside on movable genetic elements. Transposable elements, to use the language that McClintock had developed 20 years earlier. Today the study of transposable elements is a major subfield of genetics and molecular biology.

    Genetic Identity. Are all cells the same?

    What does all of this have to do with us, you might ask? Well, in a way, it reinforces the original point of this essay. Let's think of another one of those things that we learned about biology way back when. For example, the notion that every cell of the human body is genetically identical. This was almost an article of faith when I studied developmental biology. Liver cells, for example, have exactly the same genetic information as, say, muscle cells. The only differences between them are the chances that have been brought about by the processes of development, and these do not involve changes in genetic information. Right?

    Wrong. And that's why McClintock's work is so important.

    The notion that every cell in the body is genetically identical fails to solve a couple of important genetic problems. One of these is the problem of antibody production. Antibodies, as you know, and proteins produced by the immune system. The immune system is capable of producing an enormous variety of different antibodies when confronted by new antigens, and this is the key to the immune system's ability to fight off disease, even diseases to which it has never been exposed. The number of different antibody proteins which the human immune system can produce is estimated to range from 100,000 to 1,000,000. And there's the problem.

    Antibodies are proteins. Proteins are produced from mRNAs, which are transcribed from genes. Therefore, a human cell must have at least 100,000 antibody genes. But that's impossible. If that were true, virtually the entire human genome would be taken up just with antibody genes, which is most definitely not the case. So what's going on? What's the solution? If genes were fixed on chromosomes, there would be no solution.

    Antibodies -- Shuffling the Deck:

    In 1976, perhaps thinking along the same lines as McClintock, Susumu Tonegawa, a Japanese researcher working at MIT, decided to test the idea that antibody genes occupy fixed positions. He compared the location of different parts of the antibody gene sequence in embryonic cells with the same parts in cells from an adult mouse. To his surprise, the two parts of the gene, which were together in the adult, were separated in the embryo. What was going on?

    The explanation, as Tonegawa showed with a series of elegant experiments, is that the "mature" antibody gene of the adult does not exist in the embryo. Instead, embryonic cells contain hundreds of alternate antibody gene "parts," which must be moved together to assemble the mature, functional gene. And this is what accounts for the ability of the body to make so many different kinds of antibody proteins.

    In each of the millions of cells of the immune system, bits and pieces are moved from place to place on chromosomes to assemble a functional gene. They key is that which bits and pieces are selected is random, so that each cell assembles a slightly different gene. In effect, in each cell the "deck" of antibody parts is "shuffled" in a different way. The result is that the millions of cells of the immune system contain millions of different antibody-producing genes, preparing the body to face virtually any antigen.

    The system that drives this rearrangement does not, strictly speaking, involve transposable elements. However, it does involve the movement of gene sequences from one point on the chromosome to another, reinforcing the generality of McClintock's results on the movement of elements within the genome.


    The Plastic Genome:

    Susumu Tonegawa received the Nobel Prize for his work, which fundamentally altered our understanding of how the immune system develops. As important as his work was, however, the significance of McClintock's studies, which preceded his by 25 years cannot be overestimated. She had clearly broken the ground that enable other researcher, including Tonegawa, to think of genes as elements that could move and rearrange. The genome is plastic.

    In 1983 Barbara McClintock received the Nobel Prize, fortunate as always to have lived long enough to see the importance of her work recognized by others. How important were her discoveries? Barbara McClintock is one of only two women ever to receive an unshared Nobel Prize in science. The other was Marie Curie. Curie's importance to physics is quite comparable to McClintock's importance to biology. When Barbara McClintock died in 1992, one of her obituaries suggested that she might well be ranked as the greatest figure in biology in the 20th century. I think that estimate is about right.



    The Thing About Facts (Barbara McClintock and the Jumping Genes)
     
    Last edited: Dec 23, 2002
  20. spookz Banned Banned

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    in defense of lamarck - baldwinism

    In 1896, Baldwin proposed that the body cells themselves achieve a certain plasticity, allowing them to acclimatize to new conditions, and over time a kind of gradual adaptation takes place throughout the population, which eventually becomes instinct. Baldwinism does not cross the Weissman barrier, and is accepted by neoDarwinism as part of adaptationism. Dennett grudgingly finds it useful to append to his 'cranes' theory, because it does some slight explanatory work, while still conforming to dogma. 'The saving grace for the Baldwin effect' he says 'is that organisms pass on their particular capacity to acquire certain characteristics, rather than any of the characteristics they actually acquire.'

    A New Factor in Evolution By J. Mark Baldwin

    SOCIAL HEREDITY AND ORGANIC EVOLUTION

    The Baldwin Effect: A Bibliography
     
    Last edited: Dec 23, 2002
  21. spookz Banned Banned

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    in defense of lamarck - paramutation

    Facts

    In the 1930's, heritable epigenetic effects due to the interaction of homologous alleles were described and designated paramutation, since Mendel's laws were violated.

    Paramutagenic allele = an allele that will convert a paramutable allele to a paramutant allele.

    Paramutable allele = an allele that can convert to a paramutant state.

    Paramutant allele = an allele of lower function caused by paramutation, inherited somatically and germinally.

    Paramutant alleles do not require the continued presence of the paramutagenic allele to maintain their state. They do, however, revert to the paramutable state with some frequency.

    For the Rlocus of maize, the paramutant state is correlated with increased methylation of Rlocus DNA.

    Transgenes will sometimes become silenced. Often, the silencing correlates with increased methylation of the transgenes.

    Silencing by methylation resembles RIP'ing.

    Not all gene silencing occurs by methylation coupled mechanisms. Some may be triggered by heterochromatization of the repeated gene. Others (Co-suppression) appear due to post-transcriptional events.

    Interpretations

    Induced changes in methylation status are metastably heritable and can affect gene expression.

    Paramutation may be a manifestation of an important as yet undiscovered regulatory mechanism.


    Paramutation

    greek!
     
    Last edited: Dec 23, 2002
  22. spookz Banned Banned

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    in defense of lamarck - genomic imprinting

    Genomic imprinting is a genetic mechanism which determines the expression or repression of genes according to parental origin. This modification of genetic material is reversible between generations i.e. epigenetic suggesting that the inactivation event is not a mutation.The phenomenon has been well studied in mice.

    Evidence from human disease

    Evidence supporting the existence of imprinting in humans has been obtained from the study of human chromosome deletion studies such as Prader-Willi and Angelman syndromes.

    Myotonic muscular dystrophy (MMD) and Fragile X syndrome exhibit genetic anticipation, whereby the phenotype of the disorder becomes progressively more severe with each generation. Although the genes for these disorders contain unstable triplet repeats these diseases still fulfill the definition of genomic imprinting because each disease locus is affected differently upon passage through female versus male gametogenesis. Expansion of the triplet repeats leading to disease only occurs through female transmission.

    In 10% of families with MMD, the disorder is more severe when maternally inherited.
    Fragile X linked mental retardation is more common in later generations of an affected family.
    Juvenile-onset Huntingtons disease is more common in offspring of affected fathers.

    Other diseases affected by genomic imprinting includere congenital heart disease, neural tube defects and cerebellar ataxia

    Cancer and genomic imprinting

    In certain cancers i.e. Wilms' tumor, osteosarcoma, bilateral retinoblastoma and embryonal rhabdomyosarcoma, the origin of the tumor-suppressor gene remaining in the tumour appears to be invariably paternal. In the two-hit hypothesis of cancer, the first inactivation of a tumour-suppressor allele would occur through imprinting rather than mutation. Because the inactivation is not dependent on the tumour-suppressor allele but rather the genes responsible for the generation of the imprint, the inheritance of the tumour phenotype will not be linked to the tumour-suppressor locus. This is confirmed by studies of large families with Wilms' tumours and less convincingly with rhabdomyosarcoma.

    Uniparental disomy

    UPD is caused by meiotic non-disjunction followed by trisomy or monosomy rescue and is associated with advanced maternal age. Studies of the phenotypes associated with UPD have been used to determine an imprinting map.

    UPD has been reported for 25 out of the 47 possibilities for entire chromosomes.
    Assessment of whether the phenotypic consequences are due to imprinting is complicated by the affect of trisomy on the placenta or foetus or autosomal recessive disease due to homozygosity. If a consistent abnormal phenotype is present in different documented cases of UPD autosomal recessive disease can be excluded . Conversely, if a single case of UPD is associated with a normal phenotype this provides strong evidence of a lack of an imprinting effect for a particular chromosome.

    Chromosomes associated with imprinting

    15 maternal 20-25% PWS
    15 paternal <5%AS
    11 pat 20-25% BWS
    7 mat short stature 4/30 patients with Russell-Silver syndrome
    14 mat distinct phenotype

    Other chromosomes which have shown possible genomic imprinting effects include 16mat,14pat,6pat,2mat,20pat and XXpat but interpretation has been complicated by the presence of trisomy. 13mat and 22mat are unlikely to show imprinting effects


    Evidence for genomic imprinting

    more greek
     
    Last edited: Dec 23, 2002
  23. spuriousmonkey Banned Banned

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    i was not talking about evolution..but about the savanah theory etc....
     
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