Observed biological changes?

The very first sentence is bogus. The claim is that "All observed biological changes involve only conservation or decay of the underlying genetic information". This is wrong, because one class of observed changes is gene duplication and diversification.Which of these two claims is true?Could someone explain to me gene duplication and diversification?

Thread moved here from the Proposed New Topics forum.SlV will not be able to respond for 24 hours but that will give posters time to be clear.This message has been edited by AdminNosy, 06-06-2005 02:00 PM

Hi Siguiendo, and welcome to the forum!For the benefit of other members, I want to clarify what this thread is about. On the Macroevolution thread, Siguiendo referred to some websites covering the evolution/creation debate in order to show that natural selection could not account for macroevolutionary changes. After being told that the websites were "bogus" and could not be used as evidence, he rightly asked for somebody to point out why his references were bogus.I visited the site and responded. The first paragraph of SlV's opening post is copied from my response.So this thread is about whether "all observed biological changes involve only conservation or decay of the underlying genetic information".-----------------------------------------First I want to talk about the conservation, decay and diversification of genetic information. How do we know whether a gene has been conserved, is in the process of decaying, or is diversifying?Let's represent DNA as a string of letters (A,C,G and T). We know that each triplet of letters is used to create a single amino acid, and a bunch of amino acids makes up a protein. So, for example, if our DNA sequence is nine letters long, we get a protein with three amino acids.Under the standard genetic code, we know that the DNA sequence "AAA" codes for the amino acid Lysine. If the DNA sequence suffers a mutation, the amino acid it codes for might or might not change. Here are the possible amino acids that would result from a single nucleotide substitution to the sequence "AAA" (mutations that result in no amino acid change are in bold):we start with AAA: Lysinesingle mutations result in:AAC: Asaragine
AAG: Lysine
AAT: Asparagine
ACA: Threonine
AGA: Arginine
ATA: Isoleucine
CAA: Glutamine
GAA: Glutamic Acid
TAA: STOPSo we know that, if a mutation occurs completely randomly in "AAA", there is a one in nine chance that the translated protein will not change, a seven in nine chance that the protein will change, and a one in nine chance that the mutation will result in a "STOP" codon that will terminate translation but not be expressed as a protein. Mutations that result in the same amino acid (in bold, above) are called silent (or synonymous) mutations, because they don't make any difference to the protein after translation.If a gene is "decaying" randomly (i.e. it is suffering completely random mutations that result in the loss of coding specificity) then we should find, across a long gene, that these mutations are fixed in a population with the specified probability. For example, whenever a mutation occurs in AAA, it should result in a new amino acid with probability 7/9.We can test whether this is the case by comparing genes from different species (or different individuals, or whatever). We take a gene from a monkey, the same gene from a human being, compare them to find out which mutations have occured, and test them against the expected result from our model to see if the mutations are occurring randomly or not.If the observed mutations match our prediction, we can be confident that the genes are "evolving" randomly - i.e. they are decaying. Random mutations are being fixed in the gene pool without reference to the protein for which they code.However we might find that silent mutations are much more common than we expected. Instead of one in nine fixed mutations that occur in "AAA" being silent, and not changing the translated protein, we find that six in nine are silent. This suggests that mutations not changing the protein structure of the gene product are favoured by natural selection. The protein structure is being conserved by natural selection, because mutations that cause the protein to change are weeded out of the population. We might find this kind of pattern in genes that are essential to the function of the organism. Any change results in death, so only silent mutations can be accommodated.We also might find the opposite. We might expect one in nine mutations to be silent, but we find that NO mutations are silent. Every single mutation that is fixed in the population results in a change in the amino acid sequence of the protein. In this case, the protein structure is being diversified by natural selection. Any mutation that does not change the protein sequence is weeded out of the population. We might find this kind of pattern in genes that are harmful, such as cancer-causing genes. If you have a gene that causes you to get childhood leukemia, then only mutations that modify the protein structure and render it less lethal will be passed on.In biology, we calculate a ratio to say how many silent versus non-silent mutations occur in a gene, compared to what we expect under the random hypothesis. This is the dN/dS ratio (the ratio of nonsynonymous to synonymous mutations). If the dN/dS ratio equals one, then the gene is decaying randomly. If the dn/dS ratio is statistically significantly less than one, then the gene is being conserved. And if the dn/dS ratio is statistically more than one, then it is being diversified.Many studies have identified genes with a dN/dS ratio significantly greater than one. As predicted they are frequently found in genes causing disease. Oncogenes, for example, frequently have high dN/dS ratios. The ubiquity of genes with dN/dS ratios greater than one show that natural selection is not only capable of conserving genes, or permitting genes to decay, but also in diversifying genes - favouring genes that code for novel proteins that improve the fitness of their bearers.This is one line of evidence to show that the statement "All observed biological changes involve only conservation or decay of the underlying genetic information" is completely and utterly false.Next post, I will get into gene duplication.CheersMickThis message has been edited by mick, 06-06-2005 03:17 PM

Hello again Siguiendo,In my last post I described how we can detect the signature of diversifying selection by comparing genes from different individuals.In this post I will explain how diversifying evolution can result not only in the modification of existing proteins but in the generation of completely novel genes. For a new gene to arise, we need a new chunk of DNA available to natural selection. This DNA often comes from gene duplication.Gene duplication is the result of a mutation during the copying of DNA at cell division. The whole of an existing gene, or part of an existing gene, is copied twice, so that the gametes contain more than one copy of a single gene at different chromosomal locations.This kind of mutation (ipso facto) results in an increase in the amount of genetic information contained within a genome. There isn't any "new" information in the sense that both copies of the gene are identical, but there is "more" information simply because the gene is present more than once. It is not only more information, but useful information, in that the duplicated segment will code for a protein that has useful biological properties.Anti-evolutionists will often claim that this is simply a rare mutation that adds no new information to the genome; the copied gene is not only identical to the original version, but it is often silenced so that it is not expressed and contributes nothing to the living organism. However scientists have attempted to count the number of active duplicate genes in the "average" genome and have come up with some startling figures. According to a recent editorial by Michael Lynch, one of the top molecular evolutionary biologists at work today, the average duplication rate per gene per million years is 1/100. Over hundreds of millions of years, that adds up to a LOT of new genetic material that can be acted upon by diversifying selection.Jianzhi Zhang, from the University of Michigan, has estimated the proportion of genes present in living organisms that have arisen from random duplication events. Here are his resultscommunity-acquired pneumonia bacterium: 44%
peptic ulcer bacterium: 17%
meningitis bacterium: 17%
sulphur metabolizing bacterium: 30%
baker's yeast: 30%
nematode worm: 49%
fruit fly: 41%
mouse-ear cress plant (arabidopsis): 65%
human beings: 38%So, if anybody tells you that gene duplication does not result in new biological information, you can point out that over one third of your coding DNA is in disagreement! The random duplication of genes during cell division and their subsequent diversification is probably THE major source of biological novelty in the world around us.Once a gene has been duplicated, what happens to it? Jianzhi Zhang gives a great overview of the fate of duplicated genes.First, the duplicate gene might decay. It may not be advantageous for an organism to have two copies of a single gene, so mutations to the duplicate copy are not deleterious, and they accumulate until the duplicate is not functional, or is not expressed. In primates you can find many copies of mitochondrial genes which have somehow duplicated themselves and migrated into the cellular nucleus and have become pseudogenes, simply because they have no nuclear function and end up decaying over time. As I recall, the cat has a complete copy of the entire mitochondrial genome inside its nucleus. Obviously the mitochondrial genome can do nothing useful there, so it is in the process of decaying. But it's not only mitochondrial duplications that suffer this fate - there are over 2000 decayed genes ("pseudogenes") in C. elegans, the nematode. That is one eigth of the total number of genes.Second, the duplicate gene might be conserved. It may be useful for an organism to have two copies of a single gene, because that implies that it can get two times as much of the protein product. For example if you life in a very macho environment it might be useful to have two active testosterone genes. This may explain Bruce Willis.Third, the duplicate gene might be subfunctionalized. The idea is that a single gene gets duplicated, then each copy of the gene adapts to a slightly different purpose. The ancestral function of the gene stays the same, but it's partitioned between the two copies. This is probably what happened to major histocompatibility antigens in vertebrates. These are the antigens expressed on the outside of your organs, which are recognized as foreign when you have an organ transplant, and result in the transplanted organ being rejected. There are quite a number of different MHC genes, all very similar to each other, and some of them are expressed only on a certain type of tissue. it's likely that we started off with a small number of MHC antigens that were expressed everywhere, and following gene duplication ended up with tissue-specific varieties.Finally, and this is probably what you're interested in, the duplicate gene might be neofunctionalized. The duplicate gene gets a NEW function, adds a NEW capability to the organism. One good example is the evolution of opsin proteins in primates. Opsins are the light-sensitive proteins that we have in our eyes. New World monkeys have two opsins, one sensitive to short-wave light (i.e. blue) and one sensitive to middle-wave light (i.e. green). Old World primates, on the other hand, have three opsins. The ancestral middle-wave opsin was duplicated and one of the copies has diversified such that it is now sensitive to long-wave light (i.e. red). Old world monkeys can see red by virtue of gene duplication and neofunctionalization; new world monkeys are stuck in a less colorful world. Another example from these species is the ECP gene of old world primates. This arose by gene duplication from EDN (a ribonuclease) around 30 million years ago. ECP underwent a handful of rapid nucleotide changes that resulted in it having an antibacterial capacity (quite different from its original function). New world monkeys lack the antibacterial form.Now, the great thing about all this is that we can use the dN/dS ratio to detect whether duplicate gene copies are undergoing conservation, subfunctionalization, neofunctionalization or random decay. We can empirically test it, and prove it, in the laboratory!Hope this is of interestMick

Mick said:
For the benefit of other members, I want to clarify what this thread is about. On the Macroevolution thread, Siguiendo referred to some websites covering the evolution/creation debate in order to show that natural selection could not account for macroevolutionary changes. After being told that the websites were "bogus" and could not be used as evidence, he rightly asked for somebody to point out why his references were bogus.Just so it's clear, I did not post the web sites, I did not link to them. Someobody made the statement that both of the websites are entirely "bogus". I just wanted specifics.This message has been edited by Siguiendo la verdad, 06-08-2005 07:51 PM

Now THIS is "knowlege and understandng through discussion".An explanation, instead of "that's bogus". How radical is that? Thank you mick. I appreciate your taking the time to give an explanation.My only problem is that this whole debate goes a little like this:Evolutionist: "Evolution is common sense everything points to evolution as the explanation of life and humans."Creationist: "This complex world is obviously too perfectly ordered to be an accident, thus Someone had to plan and create it"Evolutionist: "No, that cannot be proven scientifically, evolution can, evolution wins."Creationist: "No, science in its true form supports creation not evolution."Evolutionist: "No, science in its true form supports evolution and here is all the reasons why 1, 2, 3, etc."Creationist: "Here's why those reasons are flowed: 1, 2, 3, AND science is NOT the only way to know all that can be known about reality"Evolutionist: "All you creationists are unscientific, your definitions are wrong and your statements are "bogus"."Creationist: "No, all of your definitions are wrong and your statements are false."Evolutionist; "No your definitions and statements are false"Creationist: "No, yours are false"Evolutionist: "No, yours are"Creationist: "No, yours"Evolutionist" "No, yours"And being a person not well versed on all that is considered science, especially by evolutionists'standards, I am, as I believe the general public is, left to choose which side better reflects the Truth, because we can't all know everything in every field of every area that reveals truth. Thus we are left to our best judgement and, I believe, our life experiences. Short of becoming an expert myself in any one of the many areas of molecular biology, geneticism, DNA and so forth, I choose to focus on the greater impact of any conclusions drawn from any area of knowledge.What I do understand, is that evolution IS contrary to a literal interpretaton of the bible as a whole and Genesis in particular.Thanks again.

I don't want to go too far off-topic on this, but I will say I doubt a single member of this forum will disagree with that.

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Oops! Wrong Planet

I disagree with that.

Ok, so I was wrong.It's happened before

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Oops! Wrong Planet

Well, we might have to start a new topic for this or tag it onto another one already discussing this, but a literal interpretation of Genesis would go a little something like:"God made the earth in six literal 24-hour days and rested on the seventh, with all of the animals fully created, along with humans"While evolutionist would argue that everything may have began a finite time ago, humans weren't there in the beginning and God is not responsible for directly creating humans or even indirectly, if they give Him credit for creating anything at all.These are mutually exclusive points of view, to hold them both as true would be to be in direct contradiction.Something cannot be itself and something else at the same time.