So evolution is not random? it works intelligently? So then you agree that all this could not occur by chance? (probability) i.e it must be a defined process in which each cell works by getting instructions from DNA??
Muslim it took me a long time to dismiss creation and form a belief in Evolution. I had the same line of thinking as you. This is an artical from a few years back that influenced my change. I agree with you it takes more than chance or random coding to create evolution. But the Genome can guide itself and direct evolution, this artical gives us some insight into how that happens. So muslim I tottaly agree with your argument, but I offer you evidence to say that your arguement backs up evolution. The artical also contains a basic over view of evolution maybe take your time reading that bit. Genomes don't play dice IT STRUCK me in an examination room. As my colleagues questioned a graduate student about genetics, my mind began to wander between the genetic code and information theory. And that's when it hit, like a strong wind slamming open an unseen door. A single amino acid can be encoded in as many as six different ways. I suddenly realised this means that DNA has the flexibility to carry multiple overlapping messages. Sure, genomes contain more than just genes: they also hold instructions about where in our body and when in our lives to make each protein. But what if our DNA also contained information that made mutation more likely in some parts of the genome and less likely in others? Such a genome would have the potential to influence its own evolution, protecting essential DNA sequences in some places while elsewhere unleashing genetic variations that could explore evolutionary possibilities. There was just one problem. If I was correct, it would mean that not all genetic mutations are random. Such a notion was as heretical two decades ago when I first had this idea as it is today. Nevertheless, in the intervening years, breathtaking advances in genetics have revealed that less than 5 per cent of our genome codes for the amino acids in our proteins, providing even more room for extra information than I imagined. What's more, there is clear evidence from organisms as diverse as humans and bacteria that genomes do indeed contain information that can focus mutations in certain areas and direct it away from others. Yet students are still taught that evolution works through completely random genetic variation acted upon by natural selection, leading to the survival of those organisms with genes best suited to their environment. Surely it is time to rethink the idea that evolution is purely a game of chance: to accept that genomes could have evolved information that allows them to influence genetic change and affect their own chances of survival? Although this may sound like heresy, it does not challenge Darwin's evolutionary theory. Instead it updates it, by recognising that natural selection acts not only on fins and wings, but also on the very mechanisms that copy and repair DNA. It makes perfect sense that these mechanisms would be subject to selection pressures: genomes that managed to steer their mutations, even a little, would have pulled way ahead of others that were throwing darts in the dark. Such genomes would have a better chance of producing fit offspring, so they would tend to become more widespread than genomes that relied completely on random change. Accepting all this has radical implications. It should make us wary of thinking that just because we can translate sequences of DNA bases into amino acids, we understand all the information our genomes contain. The realisation that genomes may contain more information than we imagined should inform our decisions about genetic engineering and medicine. And at a philosophical level, if genomes can learn about the world through natural selection, perhaps we should even consider them to be intelligent. As our ability to examine entire genomes allows us to peer under the hood of evolution, it is increasingly obvious that the long evolutionary journey has not been just a series of random stumbles. Certain types of DNA sequence seem to invite mutation and others seem to repel it. One type of mutation-attracting sequence, found in bacteria as well as us, is "slippery" DNA. Slippery sequences comprise a series of DNA's chemical bases or "letters" repeated over and over again. The repeating unit may be simply a single DNA base - adenine, guanine, cytosine or thymine - or a short string of bases such as CAG. The machinery that makes copies of DNA for the organism's offspring can lose register in such repetitive sequences, copying a unit of the repeat more than once, or skipping over it. TTTT may become TTTTT or CAGCAGCAG become CAGCAG. These deletions and additions generate a great deal of genetic diversity. The mutation rate of slippery DNA can be 1000 times higher than elsewhere in the genome, so in that sense it is not random. But the important question as far as evolution is concerned is whether mutation is random with respect to its effect on survival. Are slippery sequences just wet stones scattered randomly across the landscape, or are they some kind of guidepost? If a slippery sequence occurs in a place in the genome where it makes no difference to the organism's fitness, natural selection will neither favour nor remove it. If it emerges in a place where any mistake is deadly, organisms with that poorly placed sequence will leave fewer descendants. But if a slippery sequence appears in a spot where it actually provides an advantage, scattering progeny this way and that around dangerous barriers to survival, natural selection will favour it. Generations into the future, a greater proportion of genomes will have slippery DNA at that spot. In a sense, the DNA would have "learned" through natural selection that there is an advantage to having a high mutation rate at that spot. And that is indeed what happens: certain slippery sequences do boost survival. Richard Moxon and his colleagues at the University of Oxford point to the important role of such sequences in DNA that determines bacterial surface proteins (The Journal of Clinical Investigation, vol 107, p 657). Pathogens with "coats" that frequently change thanks to genetic slips have several advantages. Each generation's diverse proteins mean the bacteria can stick to a variety of different tissues within their host, exploring new places to grow. What's more, bacteria that keep changing their coat remain one step ahead of the host's immune system, which is constantly on the alert for the bacteria in its former guise. Many bacteria owe these survival skills to the high mutation rate of slippery DNA. We cannot yet be sure whether the slippery sequences in our own genome are similarly well placed to give us an evolutionary advantage. But we do know that the human genome has several other ways of directing mutation to occur in spots where variation is crucial for survival. Just as the bacteria change their coats to survive, our immune systems need to keep pace with the change to stay on top of such invaders. In the evolutionary arms race between host organisms and their pathogens both parties have to run just to stand still, so human genomes that evolved the ability to increase the mutation rates of antibody genes would have a survival advantage. But there is a catch. Our antibody genes must satisfy two seemingly conflicting requirements. On the one hand, the body's array of antibodies must be as diverse as possible, so that at least one of them will be able to latch onto any given pathogen, even a pathogen the immune system hasn't seen before. On the other, the antibodies must have a reliable, stable, pathogen-disposal plan. If antibody genes achieved diversity through random mutation, mutations would be as likely to destroy the ability to dispose of pathogens as to gain a grip on new ones. Evolution's ingenious solution is that we inherit our antibody genes in pieces. One stretch of our DNA encodes variable regions: a large palette of possible pathogen-binding segments. Another region encodes a few well-conserved pathogen-disposal mechanisms. In each cell destined to become an antibody factory, a piece of DNA encoding one of the wide selection of variable regions is moved into place next to the conserved DNA that tells the antibody how to dispose of pathogens. Once the variable pathogen-binding piece is in place, it is subjected to biochemical mechanisms that focus additional variation in precisely those places in its structure that determine which pathogen it can grab. How this happens is not entirely clear, but Michael Neuberger and his team at the University of Cambridge have suggested that an enzyme attracted to this location cuts off part of the base cytosine. Such damage attracts repair enzymes but, in this case, they don't reverse the damage, and instead leave mutations. However the biochemical mechanisms work, the upshot is that our immune system has evolved the ability to direct mutation to exactly where it is needed, while protecting stretches of DNA that are best conserved. But antibody genes are not the only genes that face the challenge of conflicting requirements of variation and conservation. Might genomes have evolved the ability to focus mutation and cut and paste specific sections of DNA in other genes too? Colour vision is a case in point. To come up with a protein that detects red light, evolution doesn't need to start from scratch. It can make a copy of the pre-existing genes for the protein that detects green, and then tinker. Indeed, many new genes evolve through mutations that modify copies of working genes. Geneticists have assumed that these mutations are completely random, but successful adaptation repeatedly has the same requirement: to vary certain patches of DNA while conserving others. If this kind of tinkering works best, then surely natural selection will favour genomes that tend to steer mutation towards those parts of the genome where it is likely to increase fitness and away from those where genetic change would be damaging. Now that we can compare entire genomes, scientists can study the exploratory cutting and pasting that occurs during the formation of sperm and egg cells, and they have found that it certainly does not look completely random. Last year, Pavel Pevzner and Glenn Tesler from the University of California, San Diego, used a computational comparison of the human and mouse genomes to estimate that in humans there are about 400 of these cut-and-paste "fault zones", representing 5 per cent of the genome. And just a few months later, a team led by Jim Kent and David Haussler from the University of California, Santa Cruz, confirmed that DNA is indeed more likely to be cut and pasted at some spots than at others, and they identified some of these hotspots. It is not yet clear why they are prone to genetic upheaval, but it's possible they are particularly accessible or susceptible to the enzyme SPO11, which initiates recombination of chromosomes when they are being repackaged for the next generation. While slippery genes and genetic cutting and pasting can lead to novelty, in contrast, the human Y chromosome has revealed a way of undoing mutations. Until it was sequenced last year, most researchers had assumed that this partnerless little chromosome was doomed to decline, gradually eroded by the damaging effects of random mutation. With only one copy of the Y in a typical male genome, if repairs need to be made there is less back-up of information than in the other paired chromosomes. But some researchers believe the Y may carry its own back-up copy in the form of information provided by "palindromic" DNA sequences, which are analogous to words that read the same backwards or forwards (Nature, vol 423, p 873). The two long strands that make up each double helix of DNA are held together by pairing between opposing bases on each strand: A pairs with T and G pairs with C. So a strand that begins with, say, AGTTCC and ends in GGAACT can fold back onto itself, creating a little hairpin in which each base is paired with its complement. If a mutation changed the first G to an A, for example, the cell's molecular machinery would notice that the bases no longer matched up in the hairpin, and could restore the A to a G. This clever trick is not confined to humans. The tendency of certain DNA sequences to form self-correcting palindromic hairpins was first identified in the 1980s by Lynn Ripley, now at New Jersey Medical School, in her work with a lunar-lander-shaped virus called T-4 that infects bacteria: a long evolutionary distance from humans. From strategically placed slippery sequences and focused variation in antibody genes to palindromic DNA, the genome does seem to have evolved ways to affect its own fate. Sitting in that examination room, two decades ago, I realised that because almost all amino acids are encoded by more than one sequence of DNA bases, information that focuses mutations could be embedded in the choice of how a protein's amino acid sequence is encoded. One way of encoding a string of amino acids may have a high intrinsic rate of change because it generates slippery sequences, while another way of encoding the same amino acids may form part of a self-correcting palindrome (see Table). For example, the amino acid glycine can be encoded as one of four different triplets, including GGG. And the amino acid pair glycine-glycine can be encoded in 16 different ways, one of which - GGGGGG - looks more slippery than the others. Thus a more stable or more mutation-prone sequence may arise in a certain spot purely by chance. But then natural selection will act, retaining the sequence if it provides a repeated advantage, or culling those genomes where the rate of variation at that spot works against it. Genomes face certain kinds of threats to their survival every time they pass from generation to generation. Through natural selection, they "learn" about the world by exploring and surviving. If natural selection is a teacher, and genomes can learn, should we think of them as intelligent? This question has important implications not only for evolutionary theory, but also for genetic medicine. Until we understand the genome's multiple, interlinked functions, we cannot fix "errors" and assume that we know what effect that will have. At the very least we should consider the possibility that a supposedly faulty gene may in fact have become widespread because it protects people, either by blocking a renegade gene somewhere else in the genome, or by providing its own advantage under certain circumstances - just as sickle cell trait does against malaria. We also know that some genes that look very broken to us have saved people's lives. For example, there is a gene that encodes a protein used by HIV as a doorway to get inside our cells. In some people, this gene is "broken", making them resistant to AIDS. If we had "fixed" those doorways before HIV took hold, our genome would never have shown us the life-saving potential of drugs that could block the opening of this door. Luckily we did not have the ability to purge this gene from our collective genome before HIV struck. The first door-blocking drug has just been approved for treating advanced cases of AIDS. This should make us pause for reflection. We should approach our genome with humility - indeed, with awe - not as engineers and doctors but rather as students, for after billions of years of evolution it surely has much to teach us about survival. And as we look closely, will we come to consider genomes to be in some way intelligent? Perhaps so. After all, what makes us so smart?
I´d say to give up. He´s either a bogus of someone who wants to make other people think that muslims are ignorant and arrogant, or he´s really that ignorant and arrogant, and in this case I don´t have much hope for any acceptation of actual data rather than his own imaginary concepts of evolutionary theory. Gosh, how come mammoths be confused with dinosaurs. One that proposes that declares himself absolutely ignorant of the specifities of bones of different organisms, as if bones could be mistaken that easily. Why don´t he do a favor to all us and to science, go, make a fake fossil of a dinosaur with mammoth bones, and anonymously call to someone to discover it, then reveals that as a fraud, after it was widely accepted as genuine, fooling all the evolutionists-thus-atheists?
Am saying an undiscovered ancient animal. It could be anything, I could discover it an claim its a dinosaurs, its just a fantasy name. For that to work, you have to discover some animal that we don't know of.
A dinsour was an undiscovered ancient animal, then it was discovered, now it is a discovered ancient animal
Well 20 different amino acids, a polypeptide chain of n residues can have any one of 20n possible sequence arrangements. To put what I've said into context, consider the number of tripeptides possible if there were only three different amino acids A, B, and C (tripeptide =3=n;n3=33=27) AAA BBB CCC AAB BBA CCA AAC BBC CCB ABA BAB CBC ACA BCB CAC ABC BAA CBA ACB BCC CAB ABB BAC CBB ACC BCA CAA For a polypeptide chain of 100 residues in length, a rather modest size, the number of possible sequence is 20100, or because 20 = 101.3, 10130 unique possibilities. Let me tell you these numbers are more than astronomical. The reason for this being that an average protein molecules of 100 residues would have a mass of 13,800 Daltons (average molecule mass of an amino acid residue = 138), 10130 such molecules would have a mass mass of 1.38 x 10134 Daltons. Now let me bring to your attention the mass of the observable universe is estimated to be 1080 proton masses and that is about 1080 Daltons. Thus, the universe lacks enough material to make just one molecule of each possible polypeptide sequence for a protein only 100 residues in. So your whole argument based on amino acids is shattered!
Do you know that there is a difference between "non-random" and "intelligent"? Your PC is "not random" in its workings - but it is also not intelligent. Evolution is not random. It is not intelligent. It is merely a process. If you pour some dirt onto a seive, and shake, the larger stones don't fall through. One method of evolution is the "shaking" of the environment - and those unable to adapt, or not suited to survive, do not fall through to the next era - and die out.
Not at all, in fact you are backing up my point that the sequence cannot be random because the possibilitys are too huge. Therefore, the Genome itself has evolved to make it transitions more guided. The figuers you are giving are for a random mutation we both agree that random mutations do not make sense. Are you sure your not an evolutionist, you make better points for evolution than me?
What... the.. hell are you on about? Surely you mean 20^n?! That's 1.26x10^130 combinations. Yes, 100 admino acides is a rather modest length. 1000 might be closer. But what are you getting at? Why is it necessary to have have one of each? this has nothing to do with the argument.
I refer you to a previous post of mine that demonstrates how utterly ridiculous your use of probability is:
Alex, are you talking about active evolution? I.e. deliberate mutations in responce to something? Or are you just talking about some regions of DNA being more protected than others? I don't think active evoltion occurs. (except when we GM stuff, of course).
Here are a few pictures if you merge all of these images together in your mind you will see how Muslim's distant relatives would have looked like. http://www.visual-evolution.com/images/content/newtail.jpg http://www.five.tv/programmes/hiddenlives/wolfboy/ http://img.dailymail.co.uk/i/pix/2006/03/timewarpfamilyBBC070306_450x298.jpg
I am talking about Evolution at work within the Genome. Therefore the Genome itself has mutated to code for certain areas of mutation that by the Evolutionary process has proven successful by its very survival. It's still in some sense a random process because it’s not a stimulus/response sequence. So I agree with you that it is not an active process by your terms. To me this makes a lot of sense if you believe in evolution than it is a logical step to believe that the process of evolution evolves itself. This is common sense as a negative mutation will lead to destruction therefore, the evolution process must evolve, but it is still only directed by chance, but a much more controlled chance than a random mutation.
Muslim: Correct. No. Merely because something is a non-random process, does not mean that intelligence is involved. Highly complex snow flakes will always form from simple water droplets under certain conditions. This does not indicate that intelligent processes guide snow flake formation. Correct. The synthesis and evolution of DNA does not occur due to random processes. DNA synthesis follows certain chemical laws, and DNA evolution is 'guided' by the phenomenom of natural selection.
LMAO I believe, gentlemen, I have solved the mystery of muslim's sudden seemingly coherent post. To begin: the "1080 proton masses" thing really threw me off. I'm no physicist, nor chemist, nor astronomer but I couldn't follow why the universe would possess little more than a thousand proton masses! It made no sense. I decided to check up on muslim's link. First I tried "how many proton masses does the universe contain" on Ask.com - no dice, a jumble of sites, nothing important. Variations of the above produced variations on the original theme in the hits. Then I decided to hit the "1080 Daltons" issue specifically. Surely, if this were some well-known fact, the issue should just merely "pop up", no? It seemed reasonable. Well, this is what I found: http://www.web.virginia.edu/Heidi/chapter5/chp5.htm "A Deeper Look Given 20 different amino acids, a polypeptide chain of n residues can have any one of 20n possible sequence arrangements. To portray this, consider the number of tripeptides possible if there were only three different amino acids, A, B, and C (tripeptide = 3 = n; n3 = 33 = 27): AAA BBB CCC AAB BBA CCA AAC BBC CCB ABA BAB CBC ACA BCB CAC ABC BAA CBA ACB BCC CAB ABB BAC CBB ACC BCA CAA For a polypeptide chain of 100 residues in length, a rather modest size, the number of possible sequences is 20100, or because 20 = 101.3, 10130 unique possibilities. These numbers are more than astronomical! Because an average protein molecule of 100 residues would have a mass of 13,800 daltons (average molecular mass of an amino acid residue = 138), 10130 such molecules would have a mass of 1.38 x 10134 daltons. The mass of the observable universe is estimated to be 1080 proton masses (about 1080 daltons). Thus, the universe lacks enough material to make just one molecule of each possible polypeptide sequence for a protein only 100 residues in length." The first thing you'll all note is that the text in the box "A deeper look" matches almost exactly what muslim posted. Ergo, another plagiaristic cut-and-paste, and a pretty desperate one by the look of it. My first Scooby-clue was the number "1080 Daltons". That's just too damn small. There's probably more Daltons in a Scooby-snack. You'll all note immediately that "20100", "101.3", "10130", and especially "1080" are actually meant to be written "20^100", "10^1.3", "10^130" and "10^80" in the source ref, that is: ^ being "to the exponent of". Thus the "1080 Dalton" mystery has been solved. And frankly 10^80 still sounds low to me, I mean, seriously - the mass of the entire universe compressed into a mere number to the 80?? Come on. My arse probably has more material than that. "Gasp! Old man Withers!" "And I would have got away with it too, if it weren't for you meddling evolutionists!" A more direct answer to muslim's out-of-context plagiarised quote would have been: why exactly would we need a copy of every such molecule? What possible function would they provide? What evidence is there that anything beyond a comparitively quite limited set is required for life on earth? Geoff
This is what I said to him, but he said that "it's just the name is was dubbed, it doesn't mean anything". He posted the pic on another forum after I said I didn't understand what "a sneak with feet" meant. Apprently this immediately rebutts evolutionary theory completely, instead of supporting it by showing that snakes ('sneaks' lol, those stealthy critters) indeed have the coding for an ancestral form.
http://www.whozoo.org/herps/herpphylogeny.html Please Register or Log in to view the hidden image! A skink is not a snake.
