Molecular Evidence 5: Endogenous Retroviruses

All right, this is the fifth podcast in a series of six that I’ve planned on the molecular evidence for evolution. I’ll be using Dr. Douglas Theobald’s resource on Talk.Origins.org pretty heavily, so you can follow along with me there if you like.

The fifth and final piece of evidence is from endogenous retroviruses.

First, I want to get something straight- I know that the plural of virus is virii. But I’ve heard plenty of scientists use the word viruses, so I’m going to use it here. If I was writing a paper, I’d use virii, but this is just a podcast, targeted toward non-science people, so I think viruses is fine. If any of you want to try to talk about this subject with your friends or family, you’ll look a lot less crazy if you don’t insist on calling them virii, at any rate.

I’m sure most of you have experienced some kind of illness from a virus, but what is it, exactly? A virus is about as low as you can go on the complexity scale of life and still have people arguing about whether is actually qualifies as something that’s actually alive. If you remember me talking about transposons from two weeks ago, you remember that a transposon is basically just mobile DNA that has to stay within a cell. Well, a virus is just a little more complex than that- it’s mobile DNA that can leave a cell. Structurally, a virus is a shell made of protein or membrane filled with genetic information. That’s it. A virus can’t reproduce on its own, doesn’t take in energy, doesn’t have a metabolism, doesn’t grow, doesn’t respond to stimuli, and isn’t made out of cells. It violates almost all criteria for life, and yet… it is organized, it is composed of the same macromolecules that all other life forms are composed of, and it can reproduce. It might be a little disconcerting to think that you’ve suffered through an infection by something that isn’t technically alive- at least with a bacterial infection, the little bugs are growing, eating, and reproducing- if they’re alive, they can be killed, and that’s what antibiotics are for. You can’t technically kill a virus, since it’s technically not alive.

Depending on the type of virus, they can be spread in different ways and affect different cells in your body. Some viruses don’t last if they’re exposed to air, some do very well as airborne particles. Some viruses target liver cells, like hepatitis C, and some viruses target immune cells, like HIV. All viruses follow the same basic infection cycle. First, they attach somehow to a host cell. Then, either the viral genome itself or the entire virion moves into the host cell. Once the genome is exposed to the host genetic replication machinery, it begins to transcribe viral genes that code for proteins which are necessary to make more virus particles. The viral genome is also replicated during this time, and these copies are packaged into full virus particles, and this process continues until the cell explodes or until it dies from metabolic drain. At this point, the newly replicated virus particles are free to infect more cells, move around the body, and even venture outside the body where they can come in contact with other potential hosts.

Viruses carry their genome either as DNA or as RNA. For the viruses that use DNA, it’s treated just as the DNA from the host cell. The DNA is transcribed into RNA, which is then translated into protein. Some of the viruses use RNA sequences to store their genetic information, however. These viruses use RNA as their template and make more RNA copies from that template, which are then translated into protein. But there’s another variety of RNA viruses that is a little more complicated. It uses the same proteins that I told you were used by retrotransposons to replicate- reverse transcriptase and integrase. These viruses use reverse transcriptase to reverse transcribe their RNA genome into a DNA sequence, which is then integrated into the host genome. Because of this process, these viruses are called retroviruses. The most well-known retrovirus is human immunodeficiency virus, or HIV, which is the virus that causes AIDS by targeting specific immune cells. Any of you that have cats are probably aware of the Feline Leukemia virus, which is also a retrovirus.

Some of you may be thinking- hey, these retroviruses sound awfully similar to the retrotransposons you talked about before- and they are, certainly. It seems very likely that that retroviruses and retrotransposons share common ancestry way back in the past, but trying to establish which one came first is more than a little difficult at this point.

So, now everyone knows what a retrovirus is, I hope, but what is an endogenous retrovirus? Well, you know that a retrovirus functions by inserting its DNA into the genome of its host cell. Once that happens, the DNA is there for the entire life of the cell. But what if that cell has an exceptionally long life? What if it’s, for lack of a better word, immortal? Germ cells are kind of immortal- the cells that are passed on to descendents during procreation. In males, these would be spermatocytes, and in females, these would be oocytes. Let’s say that a retrovirus infected a germ cell which produced spermatocytes that fertilized and egg and resulted in a new organism. What would happen? Well, since that germ cell has a copy of the viral DNA, and all the cells in the progeny were derived from that germ cell, every single cell in the body of the progeny would also have the viral DNA. At this point, the virus is endogenous- that is, it exists natively in the organisms own’s genome from birth because of an infection that occurred one or more generations previous to it. The virus can still be actively transcribed, and continue to be infectious, but it will continue to be passed on to further progeny. Since the endogenous retrovirus, or ERV, is not necessary for reproduction, there is no selective pressure to keep it free from mutations, and so ERVs will acquire mutations at about the same rate as other non-essential non-coding DNA. Eventually, ERVs are rendered inactive because of these mutations, and they sit quietly in the host genome, a testament to an infection that occurred generations in the past.

The evolutionary hypothesis would posit that for any two given organisms, finding common ERV sequences in their respective genomes would be a confirmation of common heredity between them, since the only mechanism to explain common ERV sequences would be a shared ancestry. There is no conceivable reason, outside of common descent, why any two unrelated organisms would have the same ERV insertions. So let’s look at the evidence.

ERVs make up as much as 8% of the human genome, comprising close to 30,000 separate insertions. There have been seven common insertions characterized so far between humans and chimpanzees, with more expected as the published genomes of both are analyzed more closely. A Russian study looked at the insertions of the Human Endogernous Retrovirus, or HERV-K, and compared insertions of HERV among different primates to see which insertions are held in common by which species of primate. Figure 4.4.1 at the Talk.Origins website that I’ve been referencing comes from this study- I’ve included it also in the mp3 that you’re listening to- if you open it in iTunes, you should be able to see it as attached artwork just after the logo. This figure shows all of the HERV insertions that were found, and a cladogram was constructed to indicate phylogenetic relationships. Individual arrows mark specific insertions, and all branch points to the right of an arrow have that insertion in common. The cladistic relationship predicted by ERV evidence is exactly what is predicted by evolutionary theory- humans and chimpanzees are more closely related, with gorillas as the next most related species, followed by orangutans, gibbons, Old World monkeys, and New World monkeys. This takes into account evidence from 14 separate insertions. Again, there is no reason for insertions to be held in common without common ancestry. The evidence from ERVs is devasating to the null hypothesis, and exceptionally strongly supports evolutionary theory.

Molecular Evidence 4: Redundant Pseudogenes

All right, this is the fourth podcast in a series of six that I’ve planned on the molecular evidence for evolution. I’ll be using Dr. Douglas Theobald’s resource on Talk.Origins.org pretty heavily, so you can follow along with me there if you like.

The fourth piece of evidence is from redundant pseudogenes.

A pseudogene is very similar to a regular gene at the DNA level, but with one crucial difference- it never gets transcribed. You can think of a pseudogene as a vestigial molecular structure- sort of like how the appendix is a vestigial organ in humans. Vestigial means that a structure is in degenerate, or atrophied, or somehow imperfect state. For example, the human appendix is basically a degenerate cecum, which is an essential digestive organ in mammals which eat lots of plant matter. You can get along fine without your appendix, but we still have them as an evolutionary carryover from a more herbivorous ancestor.

In the same way, pseudogenes are evolutionary carryovers from our ancestors, and we have them for a few different reasons. The first kind of pseudogenes are called “processed” pseudogenes. You’ll remember from last week’s episode that there are important enzymes used by retrotransposons, which allow them to copy and paste themselves throughout the genome. These enzymes, reverse transcriptase, and integrase, function by taking an RNA transcript, which is a copy of the original gene, and copying it back into a DNA form, which is then integrated back into the genome. This process is beneficial to retrotransposons, since it’s the only way that they can proliferate. But the same enzymes that work on retrotransposon RNA transcripts can work on other RNA transcripts as well. Since all genes are transcribed from the genome into RNA transcripts, there is the potential for reverse transcriptase and integrase to take a random RNA transcript, turn it back into DNA, and stick it back in the genome somewhere. Now, you might think, great, extra copies of a gene! That’s got to be a good thing, right? Well, not really. You’ll remember from the Junk DNA episode that I talked about regulatory sequences that exist in the noncoding DNA surrounding a gene. These regulatory sequences are actually quite important, and without them, you don’t get proper expression of a gene. Since integrase is fairly random in the way that it inserts DNA into the genome, what you end up with is a copy of the original gene stuck in a place that is of absolutely no value- it can’t be expressed there, since there aren’t the proper regulatory sequences.

The second way that pseudogenes can form is through gene duplication. This process occurs through improper recombination of chromosomes during the reproductive process called “meiosis,” which is necessary for sexual reproduction. Most organisms are considered “diploid,” which means that they have two copies of each chromosome. For sexual reproduction, the number of chromosomes in a germ cell has to be reduced to one copy for each chromosome, and meiosis accomplishes this through a mechanism that I won’t detail just yet. One of the stages in meiosis involves recombination between both copies of a chromosome before they’re separated, during which each can swap DNA sequences with the other. Picture two identical twin girls, one wearing a blue headband and one wearing a red headband. If they were to exchange headbands, they’d look basically the same, except for that one small change. That’s similar to what happens with chromosomes, in which sister chromatids exchange DNA. But sometimes mistakes can happen, and the exchange isn’t completely equal. Imagine the twin girls again, exchanging headbands, but only one girl is able to make the exchange. What you’d end up with is one girl with no headbands, and the other girl with two. For chromatids, this means that sometimes one can end up with two copies of a gene, which can get passed on to future generations. In addition to chromosomal recombination errors, sometimes whole chromosomes can be doubled, again due to a problem with the meiosis mechanism. This kind of thing rarely happens in animals, and is usually very detrimental. Down Syndrome is also known as Trisomy 21, which means that an extra copy of Chromosome 21 is present and causes developmental problems. Chromosome duplication, also known as polyloidy, is more common in plants. Recently, evidence has been found that long segments of the human genome exist as replications, although the mechanism for this process is unknown. Whatever the case, be it recombination or segmental duplication, these duplicate genes represent a pretty significant portion of the genome- over 15,000 duplicate genes according to a recent review out of the University of Michigan, which is close to 2/5 of all genes.

The final way that a pseudogene can arise is through evolutionary forces. Just like the ancestral cecum shrank down into an appendix because the evolutionary necessity of having a way to digest a large volume of plant matter was no longer present in human evolution, the lack of selective pressure for a particular gene can make it more likely that mutations and other changes can occur without sacrificing evolutionary vigor. To borrow from the cliché, “if you don’t use it, you lose it.” For an essential gene, a mutation that causes it not to work is likely fatal, or at least decreases the ability of that organism to procreate. Either way, mutations in essential genes have a hard time staying in a population. But if a gene isn’t necessary- let’s say, a gene that synthesizes an essential molecule in a population where that same molecule is available in abundance in the common food sources. In that case, mutations that disable that gene aren’t any more likely to occur on an individual basis, but they are more likely to increase in frequency within the population because there’s no selective pressure to maintain a fully-functioning gene. You’ve probably already guessed this, but this is the reason why duplicated genes often become pseudogenes- if you have two copies of an essential gene, there’s no selective pressure to keep both of them free from mutations- you only need the one. This is why many pseudogenes are found in close proximity to fully functional copies of the normal gene- there’s no pressure to keep both copies functional.

So why is this relevant? Well, for one thing, the formation of pseudogenes is controlled by random processes, whether by retropositioning or duplication. So there’s no good reason why two completely different organisms would have the same pseudogenes in the same genomic locations… other than common heredity. But wait, there’s more! Because of the fact that pseudogenes are largely nonfunctional, they pick up mutations at about the same rate as other noncoding DNA. And as you already know, the acquisition of individual mutations is itself a random process, so there would be even less reason for different organisms to have identical pseudogenes in the same locations with the same mutations… other than common heredity. So let’s look at the evidence.

There are, in fact, many shared pseudogenes between humans and primates, including the enolase pseudogene, hemoglobin pseudogene, sulfatase pseudogene, and the steroid 21-hydroxylase pseudogene. In this last pseudogene, an 8-nucleotide deletion has been found in both the human and the chimpanzee versions of the pseudogene, which in both is responsible for deactivating the gene function. Outside of common ancestry, there is no reason why humans and chimpanzees would share the same pseudogenes, and especially no reason why they would share the same inactivating mutations. This evidence strongly supports evolutionary theory.

Molecular Evidence 3: Transposons

All right, this is the third podcast in a series of six that I’ve planned on the molecular evidence for evolution. I’ll be using Dr. Douglas Theobald’s resource on Talk.Origins.org pretty heavily, so you can follow along with me there if you like.

The third piece of evidence is from transposons.

Now, you’ll remember that back in episode 106, we looked at junk DNA, and what it meant. Well, for the past two weeks we’ve been looking at the coding part of the genome, essentially the genes themselves and the products of their transcription, that is, proteins. For the next three weeks we’re going to leave those evidences behind in the coding part of the genome, and we’re going to look at the noncoding part, which some people call “junk.” That’s right- one man’s junk is another man’s treasure, and so-called junk DNA is a treasure of evidence, very powerful evidence in support of evolutionary theory.

Well, what is a transposon? A transposon is a mobile section of DNA. What I mean by saying that it’s “mobile” is that it can literally change its position within the genome. I’m afraid that there really aren’t any good analogies for this, so I’ll just have to resort to some bad ones. You remember that before I said that the genome is kinda like a magazine, where the genes are articles which are separated by pages and pages of advertisements. Well, you know those annoying advertisements that, instead of being printed in the pagestock, are printed on little cards and just kinda stuck in the magazine, near the spine? Or maybe one side of the card is glued to the page with that flimsy, rubbery glue that you have to peel and pull off at the same time? That’s basically what a transposon is. In the same way that those little cards are mobile advertisements, a transposon is mobile DNA.

Let’s say that you’ve got one of those annoying sticky cards in your magazine, and you pull it out. But then you accidentally drop both the card and the magazine, and they both land together. The card is going to be restuck in the magazine, but probably not in the same place. It might be stuck to the front cover. It might be stuck on another advertisement page that had nothing to do with where it came from. Or, it might be stuck on the story that you were reading, obstructing a couple paragraphs and preventing you from finishing the article. Well, that’s also what happens with transposons. A transposon can be cut out of the genome and then reinserted someplace else. The genome is a pretty big sequence, so there’s lots of places a transposon can reinsert. Sometimes a transposon will reinsert at another noncoding region. Actually, this is usually what happens, since there’s so much more noncoding DNA than there is coding DNA. But sometimes a transposon can reinsert in a coding region, and disrupt a gene. Now, in the same way that the stuck card in your magazine prevents you from reading the story, the inserted transposon prevents the gene from being transcribed, effectively turning it off. You might also think of a transposon like a pop-up ad on a website that pops up out of nowhere and obscures the content that you’re trying to see on the page.

Now, one of the obvious questions at this point is: why in the world do transposons exist? They seem pretty annoying, from a strictly genetic perspective, and they also seem dangerous, since by inserting into a gene a transposon could cause a debilitating mutation or disease. And indeed, this is the case- transposons are mutagenic, and are associated with a number of diseases, including hemophilia, severe immunodeficiency, and cancer. So why do transposons exist in genomes at all? Well, you can think of a transposon as existing as a separate selective entity to its host genome- almost like a DNA parasite. Now, admittedly, this is a hard concept to grasp, since we’re talking about a chunk of DNA and not something typically associated the word “parasite,” like a mosquito or a tick. But remember that even though it’s easier for us to think of concepts in black and white terms, science isn’t quite so discrete. Transposons come in two basic types: class I transposons, which are also called “retrotransposons,” and class II, which are simply DNA transposons. Retrotransposons function by allowing their sequence to be transcribed into RNA. It’s at this point that a retrotransposon does something odd- it reverse-transcribes the RNA sequence back into DNA, and this DNA copy of the original retrotransposon sequence is then integrated back into the original genome, but at a different location. Both of these functions are carried out by enzymes whose genes are encoded for within the retrotransposon sequence itself- pretty clever. In fact, this is the same way that retroviruses like HIV work- except that a retrotransposon never leaves the cell in a virus particle. You can almost think of a retrotransposon as a virus that made itself comfortable within an organism and decided never to leave. DNA transposons use a different enzyme called transposase, which actually cuts out the genomic transposon sequence and puts it back into the genome in a different location. This skips the whole process of reverse transcription of RNA that retrotransposons use, but you get the same basic effect.

Retrotransposons themselves come in two basic types- long and short. The longer ones are called “long interspersed elements,” or “LINEs.” The shorter ones are called “short interspersed elements,” or “SINEs.” LINEs contain the two enzymes necessary for the reverse transcription and integration that I already mentioned- called, predictably, “reverse transcriptase” and “integrase.” SINEs, on the other hand, don’t carry these genes, and so are dependent on LINEs for their propagation. You can think of the enzymes used by the retrotransposons as a “copy and paste” function, just like in a word processor. The transposase used by the DNA transposons is more like the “cut and paste” function, however. And I’m sure you know that if you cut and paste words in a document, you may screw up the meaning of the text, but you’re not going to significantly add or subtract to the length of the text. If you copy and paste, though, you’ll find that not only have you screwed up the meaning of the text, but you’ve also added overall length to it, and depending on how many times you paste, you may have added a lot of length to it. And that’s what we see with retrotransposons- both LINEs and SINEs are found all throughout the human genome, for example, and are responsible for nearly 30% of the total size of the genome. 30%! That’s a lot of space wasted on DNA parasites.

But it’s not all for naught. Because so much of the genome is made up of these predictable sequences, and because these sequences occur randomly in different places in the genome, transposons offer an excellent way to identify individuals genetically. I’m sure you’ve heard of technology like “DNA fingerprinting,” or something similar, that is used to establish paternity using a genetic test. These tests take advantage of the fact that two different individuals in a population having the transposon sequences in the exact same location is extremely rare, so much so that you can conclude genetic relation based on similar patterns of genomic transposons. Well, I’m sure you’re all astute enough to realize that if transposons can be used to establish a hereditary relationship between a father and his offspring, it can also be used to establish a hereditary relationship between two organisms from different species! Remember, the only observed mechanism for two organisms to have similar genomic sequence is through heredity, and so if two different species can be shown to have similar genomic sequences, then we can conclude that they share a common ancestry. So we hypothesize that if evolutionary theory is correct, and different species share common ancestry, then closely related species will share common transposon insertions. So let’s look at the evidence.

We’ll look at one of the common SINE retrotransposons, called the Alu element. This is a sequence only about 300 nucleotides long, and it found in all mammal species, and particularly in humans, where it composes close to 10% of the entire genome. In alpha-globin gene cluster, 7 separate Alu elements are known to exist, and all seven are found in the exact same location in the corresponding chimpanzee gene. According to our hypothesis, corresponding transposon sequences imply shared ancestry, and thus this evidence supports evolutionary theory.

So, to review, transposons are mobile DNA sequences that create distinct insertion patterns that allow us to distinguish hereditary links between individuals of the same species, as well as to establish common ancestry between organisms of different species. Once again, the evidence of common transposon insertions in humans and chimpanzees strongly supports the evolutionary hypothesis. Next week, we’ll look at pseudogenes, and how these broken genes also support evolutionary theory. Take care!

Molecular Evidence 2: DNA Functional Redundancy

All right, this is the second podcast in a series of six that I’ve planned on the molecular evidence for evolution. I’ll be using Dr. Douglas Theobald’s resource on Talk.Origins.org pretty heavily, so you can follow along with me there if you like.

The second piece of evidence is DNA functional redundancy.

The basic concept behind this piece of evidence is very similar to that which I discussed last week, which should be pretty obvious since they both have very similar names. They’re so similar that I’ll go ahead and review the basic argument behind last week’s evidence, since it has relevance here. All organisms share a number of proteins which are universally necessary for basic life processes; these proteins are called “ubiquitous proteins.” Because of the functional redundancy implicit in the structure/function relationship of amino acid sequences, there are a vast number of potential sequences for any given ubiquitous protein. Since the only mechanism for sequence similarity between organisms is common ancestry, similar amino acid sequences imply a phylogenetic relationship. As a specific example, I pointed out the ubiquitous protein cytochrome C, which has the exact same amino acid sequence in humans and chimpanzees, which strongly indicates common ancestry between the two species. The sequence similarity of cytochrome C between humans and just about every other species is higher than would be predicted if evolution is not a valid hypothesis. Thus, protein functional redundancy is strong evidence supporting evolutionary theory.

DNA functional redundancy is basically the same phenomenon, but instead of comparing amino acid sequences of protein, the underlying DNA sequences are compared. Now, you’ll remember from the Molecular Biology Primer two weeks ago that the amino acid sequence of a protein is determined by the nucleic acid (that is, DNA) sequence found in the corresponding gene. The nucleotide sequence of a gene is transcribed into an RNA message, which is then translated into an amino acid sequence, forming a functional protein. All right, and I’m sure you also remember that the genetic code which translates nucleotides to amino acids also reads the nucleotide sequence in groups of three, called codons. Since there is a 1:1 relationship between codons and amino acids, that means that there’s a 3:1 relationship between nucleotides and amino acids. If you haven’t already guessed it by now, the short answer to the question of DNA functional redundancy is that you take the strength of the evidence for protein functional redundancy and raise it to the power of 3.

I’ll try to explain a few of the details of this before getting into specific examples again. You’ll remember from the Molecular Biology Primer that I said that there are 64 different codons. You get this by raising the number of different nucleotides, 4, to the power of 3, which is the number of individual nucleotides in a codon. You’ll also remember that I said that there were only 20 different amino acids that are used to make proteins. Obviously, this means that you have 44 more codons than you actually need, if you were trying to be as efficient as possible. Theoretically, codons could be assigned completely at random, and the genetic code could be different for different organisms. If it were true, it would be an excellent refutation of evolutionary theory, but this is not what we observe. Interestingly, we find that for any three-nucleotide codon, the identity of the third nucleotide is less important for determining the corresponding amino acid than the first two. This phenomenon is referred to as codon degeneracy. Degeneracy means that for just about any codon, the third nucleotide can be changed to something different without affecting the corresponding amino acid that will result from translation. For example, the amino acid alanine has a four-fold degenerate codon, since any codon starting with guanine and cytosine will result in the translation of alanine. That is, you can find GCT, GCC, GCA, or GCG in the sequence of a gene, and all four will be eventually translated as an alanine. Other amino acids are less degenerate-tyrosine, for example, is only translated by codons beginning with thymine and adenine and ending with thymine or cytosine. The other two degenerate codons, the ones ending in adenine or guanine, are reserved as signals telling the transcription machinery to stop- they’re basically called “stop codons.”

So what does all this coding redundancy imply? Well, when all is said and done, it basically means that there are an astronomical number of ways that one could encode just about any given gene, without changing a single amino acid of the final protein sequence. Thus, there is no reason to assume, a priori, that any two organisms would have the same nucleotide sequence for any particular gene, even if they had the exact same amino acid sequence. Let me stress that again. Two different species with the exact same amino acid sequence for a protein have no biological reason, outside of common ancestry, to have high similarity between their corresponding nucleotide sequences. There isn’t even a name (I think) for the number of different possible nucleotide sequences. You just have to use exponents and powers of 10.

Well, let’s go back to the same example I used last week- cytochrome C. This, again, is a ubiquitous gene- it’s found in all living organisms. For this gene, the number of possible nucleotide sequences for any given amino acid sequence is higher than 10^49. That’s quite a lot. And remember, the human and chimpanzee cytochrome C sequences are exactly the same. So, there’s 10^49 different nucleotide sequences that could exist for the human and chimpanzee genes. Now, what happens when we compare the human and chimp sequences? We find they’re only different by 4 nucleotides. That’s only 1.2% different between them. The chance of this happening without common ancestry is infinitesimally small. And this evidence supports the existing fossil evidence. Most fossil evidence estimates that humans and chimpanzees separated from a common lineage somewhere around 10 million years ago, maybe sooner. We can measure the background mutation rate in humans (and other mammals), and we’ve shown it to be about 1-5 every 100 million nucleotides per generation. Since the average primate generation is 20 years, the predicted difference between a chimpanzee gene and a human gene is less than 3%. For cytochrome C, this prediction is undoubtedly fulfilled. And this is true for most other genes too- every gene that I’ve looked at, no less. In fact, I’d like to challenge anyone who’d like to disprove this evidence to find a gene that shows more than 3% difference- I’ll even do the work for you, even thought it’s easy to do by yourself.

Fortunately, the good people at the American National Center for Biotechnology Information (which can be found at the difficult to remember address of “ncbi.nlm.nih.gov”- I’d recommend just typing in “NCBI” to your Google search) have done everyone the service of publishing the entire human genome and the entire chimpanzee genome online. You can, if you like, download the entire human genome right to your computer. Burn it on a CD. Upload it to your iPod. Whatever. But the great thing is that you can use tools that they provide on their site to directly compare the sequences for yourself. You don’t need to take my word for it. But there’s not enough time now for me to tell you exactly how to use the website, so you can either spend some time fooling around with it on your own, or you can see what I’ve done with it. There’s a new resource website that I’ve started that has some gene comparisons including cytochrome C that you can look at for yourself. Just go to: http://www.drzach.net/evolution101/. I know, I know- another website to remember. I’ve tried to keep links reasonably redundant between the Freethought Media site, the blog, and this resource site- you can decide which one you want to bookmark. I’ll be updating the resource page with more information eventually, including a tutorial on how to use NCBI’s tools to analyze sequence similarity on your own. I’ve also tried to compare genes between as many organisms as are available, including orangutan, gorilla, cow, pig, dog, zebrafish, mouse, rat, etc. Comparing all these different organisms allows me to construct a genetic cladogram, and the predictions based on genetic similarity reinforce the phylogenetic relationships predicted by anatomy.

So, to review, DNA functional redundancy shows that the extra layer of redundancy implicit in the coding of DNA reinforces the evidence from protein functional redundancy, and makes it even less likely that organisms share similar DNA sequences for any reason other than common ancestry. This one-two punch of protein and DNA evidence has hopefully been convincing- next week we’re going to leave the strong evidence within the coding part of the genome and look at some equally strong, if not stronger evidence within the noncoding part of the genome.