Rare example of Darwinism seen in action (Deluded Darwinists alert)

EurekAlert ^ | July 31, 2007

[GodGunsGuts]

==Sorry but that turns out to not be the case. Lysenko still sat high in the party for nine years after Stalin. From 1930 to 1962 he enforced his view of inheritance with the force of the State. Darwin was not on the wane during that time and Lamarck was quite discredited by Weisman’s (1834-1914) study in mice; at least to those without Communist ideological motivation to deny that selective advantage has its advantages.

True, Lysenko did sit high in the party after Stalin’s death. But Lysenkoism was indeed waived in the 1960s. Lysenko came in at the tail end of what was known as the “eclipse of Darwinism.” This lasted from the 1870s to the 1930s, and it was a time when Lamarck was favored my many evolutionary scientists. Thus, the founders of modern Communism (Marx, Lenin, etc) were Darwinians, then there was a switch to Lamarck/Lysenko under Stalin (at the tail end of while Lamarck was still in vogue), and then a switch back to Darwin in the 1960s.

[GodGunsGuts]

Hello again allmen,

I have been searching and searching, asking questions of my fellow creationists, and otherwise digesting as much as I can on the subject of Vitamin C Synthase and ERVs. I think I have come up with enought to at least venture a few preliminary observations regarding your questions and comments about the same:

==Actually the gene is rendered inoperable by a single point mutation.

Do you have a source for this? While the human version of the LGLO gene has been studied in detail, it would appear that the ape version has not:

“Therefore, as I mentioned in section 4.1, if primates closely related to humans have the SAME crippling mutations in their LGGLO pseudogenes as we see in the human pseudogenes, this finding would support the evolutionary model. As I pointed out, the data on this question are not yet available for the LGGLO pseudogenes”

http://www.talkorigins.org/faqs/molgen/plaisted.html

Furthermore, it also appears that there are many mutations capable of disabling the LGGLO gene both in humans and guinea pigs. This seems to go against your single point mutation assertion:

“As Max goes on to point out, LGGLO pseudogenes have indeed been found in both guinea pigs and humans (Nishikimi et al. J Biol Chem 267: 21967, 1992; Nishikimi et al. J BIol Chem 269:13685, 1994). Not only did both groups retain the LGGLO pseudogene as expected, but in each group the gene had been rendered nonfunctional by different mutations. . . “

http://www.geocities.com/pgspears/he.html

==It’s non functionality is in no way related to the transcriptional control of other genes. Why would we have the gene at all if it cannot fulfill the function it was designed for, the synthesis of Vitamin C?

As one of my creationist friends pointed out, because it has been mutated since it was first created. “The same thing happened to cave fish who have lost their eyes through mutation - - and flightless birds on windy islands, etc.”

==Why would we have pseudogenes at all? It isn’t just the one, there are several.

Again, as my friend pointed out, “losing a functional system because it no longer provides a survival advantage is easy to achieve with random mutation and natural selection. That’s not a problem at all. All creationists believe in that form of ‘evolution’ or ‘change over time’”. Not only that, there are more than just several pseudogenes, there are lots of them. And in so far as I can tell, many pseudogenes serve important functions.

==Why would the pseudogenes, ERV’s and genetic homology all point to common descent in that they are more similar in species that evidence suggests share a recent common ancestor and more divergent in species that evidence suggests have a less recent common ancestor?

If creatures share similar body plans, occupy similar environments, and have similar functional needs, shouldn’t we expect them to have a similar genetic structure for certain types of functional elements like pseudogenes and ERVs?

This will have to do for now. More to follow once I learn more about these subjects—GGG

[GodGunsGuts]

Could you please cite your specific sources from now on...it will definately cut down on my response time!

[allmendream]

Neither pseudogenes or ERV’s have any function, they both are shown to diverge at the rate expected for neutral mutations. If a pseudogene served a genetic function it would not be “pseudo” it would be a gene; and it would show the conservation between species expected of genes. It is, in the case of Vitamin C Synthase in all ape species and humans, incapable of making a protein at all because of an identical frameshift mutation introduced STOP codon terminating the construction of the protein.

And yes, it could very well be an example like a fish in a cave loosing eyesight. Because of our high level of fruit eating in our diet any mutation of the system is not under selection and subject to the neutral mutation rate. But why would it be rendered a pseudogene by neutral mutation in EXACTLY THE SAME WAY in all ape species and man?

Glad you find the subject interesting. God’s glory is indeed manifest in the wonder of his creation; however all evidence suggests he created us through evolution of creatures too small to see (i.e. “dust”); just as the heavens and the earth was created through the convergence of natural law and HIS design. Creating elements through solar nuclear fusion reactions is no less miraculous than willing them into creation de-novo.

[GodGunsGuts]

==Neither pseudogenes or ERV’s have any function, they both are shown to diverge at the rate expected for neutral mutations. If a pseudogene served a genetic function it would not be “pseudo” it would be a gene

Don’t have time for any extended responses at the moment (it is FRIDAY after all!). However, a quick search turned up the following links. Obviously, we are just beginning to scratch the surface of the many *functions* of pseudogenes:

http://www.answersingenesis.org/tj/v17/i1/pseudogene.asp

http://www.answersingenesis.org/tj/v17/i2/pseudogene.asp

http://www.trueorigin.org/pseudogenes01.asp

http://www.scienceblog.com/community/older/2003/A/20036120.html

http://www.nature.com/nature/links/030501/030501-10.html

[AndrewC]

If you really want to know.....

Well, it seems as if it was not blasphemous after all.

I think my answer would be that the union would be fruitless. So far, nature seems to back me up. Now, you say "How is that?" Well, Lev 18:23 was given for a reason. Apparently beastiality occurred then as it evidently does now. Human hybrids do not exist. What are the basics of the prediction as it applies to the hypothetical human/chimp cross?

I strongly hinted at the answer in my post 148 ....

I sincerely doubt that the people who crossed the lion and tiger predicted the outcome. They saw that the Lion father caused a larger offspring and then explained it. That is not prediction to me.

The Liger would be larger. The crosses of the lion and tiger were done in the 19th century so that the outcome was known well before the genetic "prediction" was invented. Plus this site agrees with me about the connected nature of the gene with the sex(which means the sex determining gene) of the parent.

http://www.messybeast.com/genetics/growth-dysplasia.htm

Because of the impossibility of a gene being inherited from only females, there is a competing hypothesis. This hypothesis (allthough not tested) is that the Lion's sperm is damaged somehow during fertilization and that a growth inhibiting gene is typically destroyed. It is impossible for a gene carried on a chromosomes to be passed along only from the mother. The reason for this is there are no chromosomes that only a female can have. Female Tigons and Female Ligers both possess a tiger X chromosme and a lion X chromosome, yet only the female Ligers will grow large, this means something must happen to either alter the genes or that the cause of the growth dysplasia lies at least partially outside of the genes.

[AndrewC]

All the apes listed have pseudogenes, the other species have functioning Vitamin C Synthase genes. As long as your talking about genetic conservation, did you know that pseudogenes and genes have measurably different mutation rates?

You forgot the guinea pig. As to the different mutation rates, I think that conserved vs nonconserved implies a differential rate of mutation, that was not my point. My point was that despite the overall differential rate there was commonality between the different classes. The commonality may be insignificant, but hand waving it away is not the way to address the significance. And the point is not wobble position of codons, it is that some same series of codons are unchanged in those two classes.

As to the rates, assumptions must be made. The first is that the sequences started out from exactly the same sequence because all we have are the ending sequences. Thus we are assuming the relationship that we are using the result to "prove".

[allmendream]

It is called genomic imprinting. You still don't know.

[AndrewC]

It is called genomic imprinting. You still don't know.

Wrong. I do know what you say it is. I just don't agree.

PS. When you post a link, expect some people to follow the link and read.( your post 71)

[allmendream]

You mean the link entitled “Genomic Imprinting”, where a bunch of Oxford Ph.D’s explain how in reciprocal crosses it makes a differences which species is your father and which is your mother due to genomic imprinting without linking it at all to sex determination? That link? What evidence suggest that you are correct on this subject and the good chaps at Oxford are wrong?

[ElectricStrawberry]

Inheritance of acquired characteristics and Darwin’s ToE (RM+NS) cannot be true at the same time.

BS. They can BOTH be true...as in they're not mutually exclusive. Darwin isn't the end-all be-all of developmental biology....other things ARE involved, you know....just not a Designer or a "design". I love it when ignorant arses tell me, a holder of a degree in Biology and a PhD in an advanced and more specific field of biology...that MY biological knowledge is lacking. DO tell what YOUR expertise is, for it ain't "science" of any kind.

Like I said, I can’t find anything that specifically deals with MDRTB

Then you shouldn't have opened your ignorant brain and typing fingers on the subject of "best evidence" showing ANYTHING about MDRTB. Which is it? "Best evidence" or a "growing body of evidence"? Of course, that "evidence" still remains to be seen, just like I expected.

....and I'll just add a lack of knowledge concerning microbiology to the long list of sciences you have no clue about.

...and I'd bet you don't understand much of the article you just linked. Can't wait for you to bring up horizontal gene transfer among antibiotic resistant bacteria. As in, some of them can pass their antibiotic resistance trait onto other bacteria, even of different species. You DO know that bacteria can pass on bits of their DNA to other bacteria, don't you? Think, that tid-bit refutes evolution too?

Lemme guess: the "best evidence" suggests that was "pre-programmed".

[GodGunsGuts]

For someone who holds an advanced degree in biology you sure are long on hot air and short on specifics. Either make your case or scram.

[GodGunsGuts]

Should I take your silence re: the functionality of pseudogenes to mean you now agree on this point?

[GodGunsGuts]

(This is for you too, OK_Now, as you asked me to start by addressing Allmendream’s questions)

Here’s some more re: functionality of pseudogenes. Before I make my next point, I would like to know if you at least agree that science is increasingly finding (A) functional pseudogenes (B) that said functionality (when extrapolated) may explain why such an abundance pseudogenes are conserved.

At any rate, here’s some more on the functionality of pseudogenes:

“Are pseudogenes themselves merely byproducts of this [evolutionary] process? Or do apparent evolutionary pressures to retain them [natural selection] hint at some hidden biological function? For one particular pseudogene, the latter seems to be true . . . Hirotsune and colleagues report the unprecedented finding that the Makorin1-p1 pseudogene [located on chromosome 5 in mice] performs a specific biological task [it regulates the expression of the Makorin1 gene which is located on a completely different chromosome - chromosome 6 in mice].

The work of Hirotsune et al. is provocative for revealing the first biological function of any pseudogene. It challenges the popular belief that pseudogenes are simply molecular fossils — the evidence of Mother Nature’s experiments gone awry.”

Lee, Jeannie T., Complicitiy of the gene and pseudogene, Nature 423:26-28. 2003

Hirotsun, Shinji et. al., An expressed pseudogene regulates the messenger-RNA stability of its homologous coding gene, Nature 423:91-96. 2003

http://www.detectingdesign.com/pseudogenes.html

“Pseudogenes have been defined as nonfunctional sequences of genomic DNA originally derived from functional genes. It is therefore assumed that all pseudogene mutations are selectively neutral and have equal probability to become fixed in the population. Rather, pseudogenes that have been suitably investigated often exhibit functional roles, such as gene expression, gene regulation, generation of genetic (antibody, antigenic, and other) diversity. Pseudogenes are involved in gene conversion or recombination with functional genes. Pseudogenes exhibit evolutionary conservation of gene sequence, reduced nucleotide variability, excess synonymous over nonsynonymous nucleotide polymorphism, and other features that are expected in genes or DNA sequences that have functional roles. . .

An extensive and fast-increasing literature does not justify a sharp division between genes and pseudogenes that would place pseudogenes in the class of genomic “junk” DNA that lacks function and is not subject to natural selection. Pseudogenes are often extremely conserved and transcriptionally active. . .

There seems to be the case that some functionality has been discovered in all cases, or nearly, whenever this possibility has been pursued with suitable investigations. One may well conclude that most pseudogenes retain or acquire some functionality and, thus, that it may not be appropriate to define pseudogenes as nonfunctional sequences of genomic DNA originally derived from functional genes, or as “genes that are no longer expressed but bear sequence similarity to active genes”. Rather, pseudogenes might be defined as DNA sequences derived by duplication or retroposition from functional genes that are often subject to natural selection and therefore retain much of the original sequence and structure because they have acquired new regulatory or other functions, or may serve as reservoirs of genetic variability.”

http://arjournals.annualreviews.org/doi/abs/10.1146%2Fannurev.genet.37.040103.103949

[AndrewC]

it makes a differences which species is your father and which is your mother due to genomic imprinting without linking it at all to sex determination

Why are you so blind that you cannot see that the difference between father and mother is their sex?

[allmendream]

Yes, some pseudogenes that do not conform to the neutral mutation rate, and are therefore conserved based upon the concept of common ancestry, THESE psuedogenes have been found to play a function (confirming once again the predictive power of the theory). Many others are not conserved, change between related lineages is at the expected neutral mutation rate. This data point tends to confirm the link between function and conservation between lineages. Why is there conservation between lineages if not for common descent?

[GodGunsGuts]

==THESE psuedogenes have been found to play a function (confirming once again the predictive power of the theory).

Ah, but you contradict yourself. In your previous post you unequivocally stated that “Neither pseudogenes or ERV’s have any function, they both are shown to diverge at the rate expected for neutral mutations. If a pseudogene served a genetic function it would not be “pseudo” it would be a gene”

You can’t have it both ways. Both can’t be true at the same time. So which is it?

[allmendream]

I was not at all trying to have it both ways. But great example!

A pseudogene is not conserved, changes at the neutral mutation rate (same as ERV’s), and doesn’t usually make a functional transcript (if it makes one at all) and certainly doesn’t make a functional protein- and any mutation or outright deletion of the sequence will have no ill effect. This is what a pseudogene is; and in talking about Vitamin C Synthase one needed get further into the subject because Vitamin C Synthase fits all these criteria to a T.

However there is an exception, in that the transcript that some pseudogenes make does serve a function in translation. These ‘pseudo-pseudogenes’ do not make a protein, but do serve a function and cannot be mutated or deleted without harm.

Until Hirotsune’s discovery they thought NO pseudogene had any function. After his discovery they thought a few transcribed pseudogenes might have a function.

In making transgenic mice they discovered that makorin1-p1 was important in development. Nobody knew the makorin1-p1 was anything other than a pseudogene of makorin1 until the Hirotsune group’s mice indicated that it has a role in the proper expression of makorin1. This is due to its transcript stabalizing the transcript of makorin1. Most pseudogenes do not undergo transcription at all(or arrested transcription in the case of human Vitamin C Synthase) and so cannot fulfill this function.

Both non-functioning pseudogenes and ERV’s are not conserved, but change at the neutral mutation rate; and unlike makorin1-p1 an insertion or deletion in the middle will have no effect at all. A better word for makorin1-p1 would be “non-translated gene” or “Transcriptionally functional pseudogene”; but they are too rare to bother naming.

BUT THE AMAZING THING IS as the theory predicts....... Makorin1-p1 is shown to be conserved and not mutate at the neutral mutation rate. MOST pseudogenes DO change at the neutral mutation rate.

Don’t you find it interesting that once again the ‘functionality’/’evolutionary conservation between species’ paradigm is once again validated? Why would we have non-functioning pseudoges and ERV’s at all if they can be mutated or deleted without effect?

Here is a source for my assertion that ERV’s and pseudogenes change at the neutral mutation rate (and can be mutated without ill effect); while makorin1-p1 is conserved (and cannot be mutated without serious harm).

http://mbe.oxfordjournals.org/cgi/content/full/21/12/2202

Pseudogenes are nonfunctional relics of formerly functional genes and are thought to evolve neutrally. In some pseudogenes, however, the molecular evolutionary patterns are atypical of neutrally evolving sequences, exhibiting sequence conservation, codon-usage bias, and other features associated with functional genes. Makorin1-p1 is a transcribed pseudogene first identified in the mouse Mus musculus. The transcript of Makorin1-p1 can regulate the stability of the transcript of its paralogous functional gene Makorin1. Specifically, the half-life of Makorin1 mRNA increases significantly in the presence of Makorin1-p1 transcript, and targeted deletion of Makorin1-p1 is lethal in mice. Here, we show that Makorin1-p1 originated after the separation of Mus and Rattus but before the divergence of M. musculus and M. pahari. The transcribed region of Makorin1-p1 exhibits rates of point and indel substitutions that are two to four times lower than those in the untranscribed region, suggesting that the transcribed region is under functional constraint and is not evolving neutrally. Although the transcript of Makorin1-p1 likely functions by its sequence similarity to Makorin1, we find no evidence of gene conversion between them, indicating that functional conservation alone is sufficient to maintain their coordinated evolution. A duplication-degeneration model is proposed to explain how Makorin1-p1 was co-opted into the regulatory system of Makorin1. There are over 10,000 pseudogenes in a typical mammalian genome, and it is plausible that many functional but untranslatable pseudogenes exist. Our results illustrate the potential of using evolutionary analysis to identify such pseudogenes from genome sequences.

[GodGunsGuts]

(Andrew, I pingin you too as I thought you might be interested in this discussion—GGG)

==I was not at all trying to have it both ways. But great example!

You do understand that your new position re: pseudogenes is a far cry from your original position (”Neither pseudogenes or ERV’s have ANY function”), right?

==A pseudogene is not conserved, changes at the neutral mutation rate (same as ERV’s), and doesn’t usually make a functional transcript (if it makes one at all) and certainly doesn’t make a functional protein- and any mutation or outright deletion of the sequence will have no ill effect. This is what a pseudogene is...

Everything you just said is directly contradicted by the scientific literature. As posted before, Balakirev and Ayala (in PSEUDOGENES: Are They “Junk” or Functional DNA?­) state the following:

“Pseudogenes have been defined as nonfunctional sequences of genomic DNA originally derived from functional genes. It is therefore assumed that all pseudogene mutations are selectively neutral and have equal probability to become fixed in the population. Rather, pseudogenes that have been suitably investigated often exhibit functional roles, such as gene expression, gene regulation, generation of genetic (antibody, antigenic, and other) diversity. Pseudogenes are involved in gene conversion or recombination with functional genes. Pseudogenes exhibit evolutionary conservation of gene sequence, reduced nucleotide variability, excess synonymous over nonsynonymous nucleotide polymorphism, and other features that are expected in genes or DNA sequences that have functional roles. . .

An extensive and fast-increasing literature does not justify a sharp division between genes and pseudogenes that would place pseudogenes in the class of genomic “junk” DNA that lacks function and is not subject to natural selection. Pseudogenes are often extremely conserved and transcriptionally active. . .

There seems to be the case that some functionality has been discovered in all cases, or nearly, whenever this possibility has been pursued with suitable investigations. One may well conclude that most pseudogenes retain or acquire some functionality and, thus, that it may not be appropriate to define pseudogenes as nonfunctional sequences of genomic DNA originally derived from functional genes, or as “genes that are no longer expressed but bear sequence similarity to active genes”. Rather, pseudogenes might be defined as DNA sequences derived by duplication or retroposition from functional genes that are often subject to natural selection and therefore retain much of the original sequence and structure because they have acquired new regulatory or other functions, or may serve as reservoirs of genetic variability.”

http://arjournals.annualreviews.org/doi/abs/10.1146%2Fannurev.genet.37.040103.103949

In addition, your assertion that “any mutation or outright deletion of the (ERV) sequence will have no ill effect” also seems to be incorrect. For instance, scientists have identified some mutations or deletions of ERVs that can result in serious health problems or even death. ERVWE1 provides a case in point. This ERV was recently acquired, and its env gene was coopted in both humans and primates to serve in a crucial role in placental development. In their PNAS paper, Mallet et al note the following about this startling discovery:

“The definitive demonstration of a role for a recently acquired gene is a difficult task, requiring exhaustive genetic investigations and functional analysis. The situation is indeed much more complicated when facing multicopy gene families, because most or portions of the gene are conserved among the hundred copies of the family. This is the case for the ERVWE1 locus of the human endogenous retrovirus W family (HERV-W), which encodes an envelope glycoprotein (syncytin) likely involved in trophoblast differentiation. Here we describe, in 155 individuals, the positional conservation of this locus and the preservation of the envelope ORF. Sequencing of the critical elements of the ERVWE1 provirus showed a striking conservation among the 48 alleles of 24 individuals, including the LTR elements involved in the transcriptional machinery, the splice sites involved in the maturation of subgenomic Env mRNA, and the Env ORF. The functionality and tissue specificity of the 5’ LTR were demonstrated, as well as the fusogenic activity of the envelope polymorphic variants. Such functions were also shown to be preserved in the orthologous loci isolated from chimpanzee, gorilla, orangutan, and gibbon. This functional preservation among humans and during evolution strongly argued for the involvement of this recently acquired retroviral envelope glycoprotein in hominoid placental physiology.”

http://www.pnas.org/cgi/reprint/101/6/1731

So much for ERVs having no function. This particular ERV was elevated to the status of a bonifide gene! I forgot to note whether the ENV was inserted into a common “hot spot.” But it’s way too late for me to go back and figure that out now. Perhaps one of you two (Allmendream or Andrew C.) could take a look at the paper and let me know. I would go back and do it myself, but as it stands now, I have no idea how I’m going to manage to drag myself out of bed in the morning (in the morning!...it’s already morning!). Why do I keep doing this to myself...aaarrrggghhh! So with that I bid you both good night, good morning, etc. etc.—GGG

[allmendream]

The point was about Vitamin C Synthase being a pseudogene and pseudogenes not having a function and changing at the neutral mutation rate. The fact that out of over 10,000 pseudogenes in the typical mammalian genome, there are some transcriptinally active ‘pseudogenes’ that do have a function and do not change at the neutral mutation rate tends to reinforce the theory that it is functionality that leads to conservation. An exception that reinforces the rule doesn't contradict my point.

Why is the Vitamin C Synthase pseudogene (should I say “TRUE pseudogene” from now on?) present at all if not as a relic of evolution? It has been shown to have no function, and it changes at the neutral mutation rate. Yet despite this higher mutation rate it shows the SAME disabling frameshift mutation at exactly the same position in primates; yet a different disabling mutation in guinea pigs. Why would we have it at all? Why would we have the same disabling mutation present in related lineages but a different disabling mutation in unrelated lineages?

Another good example with ERVWE1; but it is another contrary example that reinforces the point. It shows conservation and function. No function= no conservation. The vast majority of ERV’s show no conservation and no function. What explains that? Why is the most common recognizable sequence in the human genome Reverse Transcriptase which is useful only to an RNA virus?