Human genome was shaped by an evolutionary arms race with itself

September 28, 2014

New findings by scientists at the University of California, Santa Cruz, suggest that an evolutionary arms race between rival elements within the genomes of primates drove the evolution of complex regulatory networks that orchestrate the activity of genes in every cell of our bodies.

The arms race is between mobile DNA sequences known as "retrotransposons" (a.k.a. "jumping genes") and the genes that have evolved to control them. The UC Santa Cruz researchers have, for the first time, identified genes in humans that make repressor proteins to shut down specific jumping genes. The researchers also traced the rapid evolution of the repressor genes in the primate lineage.

Their findings, published September 28 in Nature, show that over evolutionary time, primate genomes have undergone repeated episodes in which mutations in jumping genes allowed them to escape repression, which drove the evolution of new repressor genes, and so on. Furthermore, their findings suggest that repressor genes that originally evolved to shut down jumping genes have since come to play other regulatory roles in the genome.

"We have basically the same 20,000 protein-coding genes as a frog, yet our genome is much more complicated, with more layers of gene regulation. This study helps explain how that came about," said Sofie Salama, a research associate at the UC Santa Cruz Genomics Institute who led the study.

Retrotransposons are thought to be remnants of ancient viruses that infected early animals and inserted their genes into the genome long before humans evolved. Now they can only replicate themselves within the genome. Depending on where a new copy gets inserted into the genome, a jumping event can disrupt normal genes and cause disease. Often the effect is neutral, simply adding to the overall size of the genome. Very rarely the effect might be advantageous, because the added DNA can itself be a source of new regulatory elements that enhance gene expression. But the high probability of deleterious effects means natural selection favors the evolution of mechanisms to prevent jumping events.

Scientists estimate that jumping genes or "transposable elements" account for at least 50 percent of the human genome, and retrotransposons are by far the most common type.

"There have been successive waves of retrotransposon activity in primate evolution, when a transposable element changed to become expressed and replicated itself throughout the genome until something turned it off," Salama said. "We've discovered a major mechanism by which the genome is able to shut down these mobile DNA elements."

The repressors identified in the new study belong to a large family of proteins known as "KRAB proteins." These are DNA-binding proteins that repress gene activity, and they constitute the largest family of gene-regulating proteins in mammals. The human genome has over 400 genes for KRAB zinc finger proteins, and about 170 of them have emerged since primates diverged from other mammals.

According to Salama, her team's findings support the idea that expansion of this family of repressor genes occurred in response to waves of retrotransposon activity. Because repression of a jumping gene also affects genes located near it on the chromosome, the researchers suspect that these repressors have been co-opted for other gene-regulatory functions, and that those other functions have persisted and evolved long after the jumping genes the repressors originally turned off have degraded due to the accumulation of random mutations.

"The way this type of repressor works, part of it binds to a specific DNA sequence and part of it binds other proteins to recruit a whole complex of proteins that creates a repressive landscape in the genome. This affects other nearby genes, so now you have a potential new layer of regulation available for further evolution," Salama said.

KRAB zinc finger proteins are the subject of intensive research as scientists try to sort out their many regulatory roles within the genome. The idea that they are involved in repression of jumping genes is not new—previous studies by other researchers have shown that these proteins silence jumping genes in mouse . But until now, no one had been able to demonstrate that the same thing occurs in human cells.

The UC Santa Cruz team developed a novel assay to test whether a particular KRAB zinc finger protein could shut down certain jumping genes. The first authors of the paper, postdoctoral researcher Frank Jacobs and graduate student David Greenberg, came up with the strategy of testing primate retrotransposons in non-primate cells by using mouse embryonic stem cells that contain a single human chromosome. In the environment of a mouse cell, jumping genes that were repressed in primate cells became active. Greenberg then developed an assay for testing individual zinc finger proteins for their ability to turn off a primate jumping gene in the mouse cell environment.

"We did all our tests in mouse cells because they lack all of the primate zinc finger proteins, so when you put primate retrotransposons into a mouse cell they're all active," Salama explained.

The results demonstrated that two human proteins called ZNF91 and ZNF93 bind and repress two major classes of retrotransposons (known as SVA and L1PA) that are currently or recently active in primates. Assistant research scientist Benedict Paten directed graduate student Ngan Nguyen in a painstaking analysis of primate genomes, including the reconstruction of ancestral genomes, which showed that ZNF91 underwent structural changes 8 to 12 million years ago that enabled it to repress SVA elements.

Experiments with ZNF 93, which shuts down L1PA retrotransposons, provided a striking illustration of the arms race between jumping genes and repressors. The researchers found that, while it is good at shutting down many L1PA elements, there is one subset of a recently evolved lineage of L1PA that has lost a short section of DNA that includes the ZNF93 binding site. Without the binding site, these evade repression by ZNF93. Interestingly, when the researchers put the missing sequence back into one of these and put it in a mouse cell without ZNF93, they found that it was better at jumping. So even though the sequence helps with jumping activity, losing it gives the jumping gene an advantage in primates by allowing it to escape repression by ZNF93.

"That's kind of the icing on the cake for aficionados of molecular evolution, because it demonstrates that this is a never-ending race," Salama said. "KRAB zinc finger proteins are a rare class of proteins that is rapidly expanding and evolving in mammalian genomes, which makes sense because the transposable elements are themselves continually evolving to escape repression."

Corresponding author David Haussler, professor of biomolecular engineering and director of the UC Santa Cruz Genomics Institute, said the study involved close collaboration between his group's "wet lab," directed by Salama, and the "dry lab" where researchers under Paten's direction used the computational tools of genome bioinformatics to reconstruct the evolutionary history of primate genomes. Haussler, a Howard Hughes Medical Institute investigator who has used his background in computer science to do pioneering work in genomics, said he established the wet lab to enable just this kind of collaboration.

"Both parts were integral to this study, and there was a lot of back and forth between them. This paper shows how important it is to integrate computational and experimental approaches to fundamental scientific problems, such as how and why we continuously evolve to be more complex," Haussler said.

Explore further: A multi-function protein is key to stopping genomic parasites from 'jumping'

More information: Nature DOI: 10.1038/nature13760

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29 comments

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verkle
Sep 28, 2014
This comment has been removed by a moderator.
NOM
4.6 / 5 (9) Sep 28, 2014
verkle - go and find a fundie site to post your drivel on. You won't be missed.
OZGuy
4.5 / 5 (8) Sep 28, 2014
@verkle - stop posting drivel
Vietvet
5 / 5 (7) Sep 28, 2014
Another example of @verkle's gross stupidity and dishonesty. He has no shame, the worst kind of hypocrite.
JVK
1 / 5 (7) Sep 28, 2014
Thanks verkle. Others don't seem to think that RNA-directed DNA methylation must precede the RNA-mediated events that link amino acid substitutions to cell type differences via RNA-protein interactions.

As you noticed, they jump forward to DNA binding and the focus becomes on what genes can do.

It's pitiful. We discussed nutrient-dependent pheromone-controlled sex differences in zinc finger proteins in our 1996 Hormones and Behavior review http://www.hawaii...ion.html

"It is generally understood that most genes code for the synthesis of specific proteins. Another example of biological sex differences which are neither gonadal nor hormonal, however, is provided by the homologous but dimorphic zinc finger proteins ZFX and ZFY encoded on the X and Y chromosomes..."

Here we see researchers who think that sex differences somehow evolved so that humans could evolve via mutations to genes and natural selection.
Torbjorn_Larsson_OM
5 / 5 (5) Sep 29, 2014
That this interesting article would attract both the site "wet" anti-science trolls verkle and JVK (the dry ones are crackpots on relativity/electricity) surprise no one. Whatever get their respective rocks off, it becomes all wet and soggy (and without any science) in the end, natch. =D
alfie_null
5 / 5 (4) Sep 29, 2014
Only the most nutty scientists could ever believe and have faith in such evolution nonsense.
This is not science.

Like Linus and his pumpkin patch, we endure this pitiable attempt from Verkle to curry favor with his god. Never any specifics on what's wrong, let alone what would be better. Just this protracted plea "Look at me. I'm pure. I deny all this profane science stuff".

If I were God, I'd certainly view Verkle as one of my more flawed creations. As a proponent of science and the rational understanding of the world, a failure. And all this loathsome, disgusting brown-nosing? Ah well, I suppose God loves all her children regardless.
JVK
1 / 5 (6) Oct 03, 2014
Anti-science???

http://en.wikiped...periment

Apparently, evolutionary theorists still struggle to distinguish between how the Laws of Physics, chemistry, and molecular biology explain biologically-based cause and effect compared to pseudoscientific nonsense that explains nothing about anything.

The human genome and all organized genomes were shaped by RNA-mediated events that link amino acid substitutions to cell types.
Captain Stumpy
5 / 5 (4) Oct 04, 2014
They should thank God that their ignorance cannot be placed on trial... locally
Actually, YOU should be thanking your god for this, as well as praying that you don't get lynched for being a lying hypocrite who is libelous and trying to denigrate a PhD who has a far better standing as a scientist AS WELL AS a far batter understanding of science and biology/Genetics than you ever will.

for more info on how jk was SPANKED by a PhD from Harvard, read this thread: http://phys.org/n...firstCmt

And for those who are wanting to know: I not only forwarded VERBATIM copies of jk quotes on PO, BUT I also left links to PO as well as to his perfume crap site so that she could verify what stupidity jk was spouting.

the result?

I was right! jk is wrong in his belief and he is also wrong in his statements (and LIE) about her studies supporting his creationist PSEUDOSCIENCE stand on-line
JVK
1 / 5 (6) Oct 04, 2014
http://www.scienc...4349.htm

"...an RCas9 tethered to a protein translation initiation factor and targeted to a specific mRNA could essentially act as a designer translation factor to "up-" or "down-" regulate protein synthesis from that mRNA."

That would mimic the effect of nutrient uptake on the microRNA/mRNA balance, which is the basis of RNA-directed effects of DNA methylation that link the epigenetic landscape to the physical landscape of DNA in organized genomes via amino acid substitutions that differentiate all cell types of all individuals of all species via conserved molecular mechanisms.

Now that others realize how protein biosynthesis is regulated they can include the Laws of Physics, which link chemistry to molecular biology, instead of simply attributing evolution to vague processes of protein biosynthesis that somehow enable mutations to lead to the RNA-mediated biodiversity manifested in morphological and behavioral phenotypes.
JVK
1 / 5 (6) Oct 04, 2014
see also: http://www.scienc....2.short

"RNA can both store information in its linear sequence and take on critical structural and catalytic roles in the cell, such as during the translation of messenger RNA into proteins. These latter functions depend on the complex higher-order structures RNA is able to form. Homan et al. now report a method to probe these intricate conformational states. They chemically modified exposed segments of three complex RNA structures. They then sequenced the RNA to map the locations of the multiple modifications in each individual linear RNA molecule. This allowed the researchers to deduce interactions in three-dimensional space, and to uncover new and previously hidden conformations, providing valuable information on the folding and function of RNAs."

Biodiversity manifested in increasing organismal complexity has always been RNA-mediated. It cannot arise via mutations and evolution. That's pseudoscientific nonsense!
Captain Stumpy
5 / 5 (3) Oct 05, 2014
Biodiversity manifested in increasing organismal complexity has always been RNA-mediated. It cannot arise via mutations and evolution. That's pseudoscientific nonsense!
You are saying here that YOUR OWN MODEL cannot create biodiversity

your model causes mutations: we've already PROVEN that... and you've already admitted that, remember.. I asked
DOES your model make any changes to the nucleotide sequence of the genome of an organism, virus, or extrachromosomal genetic element?
This is a yes or no answer
(this is the DEFINITION of mutation) to which you answered
YES!
--Thanks for asking
so we can conclude that if you are posting the above to say that mutations are not beneficial (against the overwhelming evidence to the contrary) then you are also saying that your own model cannot be beneficial OR promote biodiversity

your own words, little jimmy
you are saying YOUR OWN MODEL IS BULLCRAP PSEUDOSCIENCE

(mensa? HA!)
JVK
1 / 5 (5) Oct 05, 2014
See also: http://books.goog...;f=false

What 'SSgt Stumpy' wants others to believe is that he somehow has determined that nutrient-dependent RNA-directed DNA methylation involves metabolism by enzymes like those in the link above via random events (e.g., evolutionary events).

Although no biologically-based evolutionary events have ever been described, he is certain that they occur because he believes Lenski's E. coli exemplify mutation-driven natural selection and the evolution of biodiversity.

Among others, he is living in a world of assumptions and invented theories that have led to deaths and suffering that could have been avoided by medical practitioners who continue to live in the 'dark ages' of evolutionary theory. Thank God some do not!
Captain Stumpy
5 / 5 (3) Oct 05, 2014
What 'SSgt Stumpy' wants others to believe is
what I want others to KNOW is that you are a liar, and that is proven by the above comment as well as by experimental data supported by various Dr's etc
I can clarify that although our work does, we hope, provide an example of how nutrition/ecology could affect the evolution of potentially adaptive traits, you [Cpt Stumpy] are right that we in no way claim that mutations in the heritable genome play no role in evolution. Indeed, as you correctly state, just because we provide evidence that nutritional conditions play a role, this does not negate a role for mutations. Indeed, in that very same paper, we provide evidence that heritable differences in the genome sequences between Drosophila species, in other words, mutations, ALSO play a role in the evolution of the trait we are studying.

So Kohl is mistaken if he is claiming that my study (or Rich Lenski's work) provide evidence AGAINST the role of mutations in evolution.
[sic]
Captain Stumpy
5 / 5 (3) Oct 05, 2014
he is certain that they occur because he believes Lenski's E. coli exemplify mutation-driven natural selection and the evolution of biodiversity
I am "certain" because feedback from authors tells me that I interpret their work correctly and that you are interpreting the work INCORRECTLY... see last post for quote supporting this assertion
he is living in a world of assumptions and invented theories that have led to deaths and suffering that could have been avoided by medical practitioners who continue to live in the 'dark ages' of evolutionary theory
I am not the one who cannot comprehend the experimental evidence, little jimmy
you are
therefore YOU are the one living in a delusional fantasy because you refuse to accept the empirical evidence in favor of protecting your fallacious religion

Your scales are thick, but science is reality
Eventually you will be lost to history, possibly a footnote as the crackpot who trolled the world with perfume and lies... that is it
Captain Stumpy
5 / 5 (3) Oct 05, 2014
Although no biologically-based evolutionary events have ever been described
had to address this last:
you are saying that your model does not describe "biologically-based evolutionary events" either, then
you are also forgetting that Dr. Extavour as well as Lenski HAVE described exactly that... and as you can see in my post above, explain it contrary to your delusional beliefs in perfume and ignorant anti-mutation rants

they also point out that you (specifically) are wrong in your assessment that mutations are not beneficial

YOU YOURSELF point out that you cannot comprehend your own model and that it makes mutations (see above for more details)

PLUS
you yourself, using your own words, say that YOUR OWN MODEL IS BULLCRAP PSEUDOSCIENCE above
Biodiversity manifested in increasing organismal complexity has always been RNA-mediated. It cannot arise via mutations and evolution. That's pseudoscientific nonsense!
YOUR WORDS jimmy, not mine
you call YOURSELF a crackpot
JVK
1 / 5 (5) Oct 05, 2014
"...substitution of the F-G loop in CYP2C9 to that of CYP2C19 enhances tolbutamide p-methyhydroxylase and diclofenac 4'-hydroxylase activities and confers partial (S)-mephenytoin 4'-hydroxylase and omeprazole 5-hydroxylase activities, which are attributed to CYP2C19." http://www.ncbi.n...18511451

The quantum leap from nutrient-induced Tet-dependent DNA demethylation and cell type differentiation in ES cells was made and linked to the de novo creation of olfactory receptor genes and 5-hydroxymethylcytosine patterning in olfactory neurons after I published last year on nutrient-dependent pheromone-controlled ecological adaptations.

Everyone who understands molecular biology realizes that mutations do not link ecological variation to ecological adaptations because nutrient uptake is the link. They may not know that ecological adaptations are pheromone-controlled because they believe in ridiculous theories, not the pheromone-controlled physiology of reproduction.
Captain Stumpy
5 / 5 (3) Oct 05, 2014
Everyone who understands molecular biology realizes that mutations do not link ecological variation to ecological adaptations because nutrient uptake is the link. They may not know that ecological adaptations are pheromone-controlled because they believe in ridiculous theories, not the pheromone-controlled physiology of reproduction.
1- YOU do not understand molecular biology then
2- IF "mutations do not link ecological variation to ecological adaptations"
THEN your own model is PSEUDOSCIENCE
THEREFORE per your own words YOUR MODEL IS PSEUDOSCIENCE
you yourself, using your own words, say that YOUR OWN MODEL IS BULLCRAP PSEUDOSCIENCE above
Biodiversity manifested in increasing organismal complexity has always been RNA-mediated. It cannot arise via mutations and evolution. That's pseudoscientific nonsense!
YOUR WORDS jimmy, not mine
you call YOURSELF a PSEUDOSCIENCE CRACKPOT

you would think that by now you would have learned SOMETHING
other than to blatantly LIE
Captain Stumpy
5 / 5 (3) Oct 05, 2014
Everyone who understands molecular biology
HERE is a thought:
I have seen you denigrate all the worlds scientists because they do not believe in YOUR way of thinking... which is a BIG red flag for a pseudoscience crackpot ( http://sci-ence.o...-flags2/

Myers described you perfectly, and you are angry at being called out and shown your stupidity world wide (on-line)... but you can't do anything about it because it is TRUE

so WHY are you arguing on a pop-sci site about your failed religious beliefs?
You can't get REAL scientists to hear you out?
so far, your Science Mag posts are IGNORED for the garbage that they are

keep proving that you are pushing pseudoscience
I don't mind
i will simply point it out to others
Thanks
JVK
1 / 5 (5) Oct 05, 2014
we in no way claim that mutations in the heritable genome play no role in evolution.


The fact that mutations cannot lead to increased organismal complexity means nothing. No one can prove that what doesn't happen never happens. Others at Harvard have incorporated mutations and natural selection into their reports on evolution for several decades without ever reporting how an evolutionary event might be linked via changes in protein structure to biological function.

That Harvard reseachers would ever claim that mutations in the heritable genome play no role in evolution is far-fetched. Unless they continue to claim what others before them have claimed and avoid the truth, the entirety of the pseudoscientific nonsense they have touted will be revealed, which is exactly what's been happening for several years.

See: http://news.scien...s-weekly
JVK
1 / 5 (5) Oct 05, 2014
You can't get REAL scientists to hear you out?


The series of my publications include one that won a social science publication award, and one that one an award for integrating neuroendocrinology and ethology.

What makes you think any other scientists have not heard me out?

http://www.ncbi.n...24693353 (2013) viewed more than 8100 times this year

Human pheromones: integrating neuroendocrinology and ethology (2001) cited only 80 times, because serious scientists are only now realizing they were taught to believe in pseudoscientific nonsense.

They have begun to look at published works with explanatory power that is based on what is currently known about how the epigenetic landscape is linked to the physical landscape of DNA in the organized genomes of species from microbes to man.

http://comments.s....1255023 Not ignored; accepted as a factual representation that scares the pseudoscientists that tout their nonsense.
JVK
1 / 5 (5) Oct 05, 2014
"In addition, residues 212-222 in the F-G loop form helices F' and G', which was not observed in rabbit CYP2C5 and bacterial CYPs. In the 1OG2 and 1OG5 structures, the heme is stabilized by hydrogen bonds between the propionates and the side chains of W120, R124, H368 and R433."

Ecological variation cannot lead to ecological adaptations without RNA-directed DNA methylation and other RNA-mediated events that link amino acid substitutions to cell type differentiation in rabbits and bacteria via the stability of biophysically-constrained protein folding / hydrogen bonds. Continuing to refer to ecological adaptations in morphological and behavioral phenotypes in terms of mutations and evolution is left-over from the invention of neo-Darwinism by population geneticists due to the propagation of ridiculous theories by those who cannot understand the simple fact that biodiversity is nutrient-dependent and pheromone-controlled by the physiology of nutrient-dependent reproduction.
Captain Stumpy
5 / 5 (3) Oct 05, 2014
The fact that mutations cannot lead to increased organismal complexity means nothing. No one can prove that what doesn't happen never happens. Others at Harvard have incorporated mutations and natural selection into their reports on evolution for several decades without ever reporting how an evolutionary event might be linked via changes in protein structure to biological function
so you are illiterate and you cherry pick data to support what you believe... still makes you WRONG
also- the only thing you are doing on science magazine is saying that "your mutations are better than their mutations"

this ALSO makes you WRONG

there is only SCIENCE, and you've been proven WRONG, by your own words, actions as well as by the scientific community
MUTATIONS CAN BE beneficial! You've said so yourself

all you are doing above is LYING
and trying to distract from the blatant lies you are making by muddying the water with irrelevant posts

isn't that considered WRONG in your religion?
Captain Stumpy
5 / 5 (3) Oct 05, 2014
... RNA-directed DNA methylation and other RNA-mediated events that link amino acid substitutions to cell type differentiation in rabbits and bacteria via the stability of biophysically-constrained protein folding / hydrogen bonds...reproduction
convoluted word salads are not proving YOUR point, but mine
call a mutation a mutation! it describes a particular set of things so that you can portray a series of events, things etc quickly and rapidly by using a word or symbol that communicates the idea or intent clearly.

writing a BS word salad that argues mutations are bad while using mutations as a replacement is plain STUPID
it's like saying "a member of the paraphyletic group of organisms that consist of all gill-bearing aquatic craniate animals that lack limbs with digits being utilised for battery in cultural art that generally involves movement of the body, often rhythmic and to music" instead of saying Fish Slapping Dance
https://www.youtu...Qp-q1Y1s
JVK
1 / 5 (5) Oct 05, 2014
"...a mutation... describes a particular set of things so that you can portray a series of events, things etc quickly and rapidly by using a word or symbol that communicates the idea or intent clearly."


Attempts to link mutations to natural selection or any other means to get to the evolution of biodiversity have failed because no biologically-based evolutionary event has been described that links the evolution of one species to another.

Instead, you take the typical idiot minion's approach and claim that mutations do something they cannot. They cannot lead to increasing organismal complexity because they perturb protein folding.

The structural alterations lead to non-functional or dysfunctional proteins, not biological functional proteins.

Your inability to understand the terms I use to detail cause and effect, does not make my terms "word salad."

Amino acid substitutions are not mutations; they stabilize protein folding; they do not perturb it.
Captain Stumpy
5 / 5 (3) Oct 06, 2014
Attempts to link mutations to natural selection or any other means to get to the evolution of biodiversity have failed
You are saying here that your own model is a failure
you take the typical idiot minion's approach and claim that mutations do something they cannot
well, YOU are saying that your model supports biodiversity & "increasing organismal complexity" and in doing so, that means MUTATIONS support biodiversity & "increasing organismal complexity", and thus evolution
They cannot lead to increasing organismal complexity because they perturb protein folding
but YOUR OWN MODEL causes mutations, and therefore you are now saying here that YOUR OWN MODEL PERTURBS PROTEIN FOLDING...
that is what you cannot get through your thick skull!
any time you denounce MUTATIONS you are denouncing your own model, moron
so your arguments above are also against your own model because, per your own admission, your model causes mutations

Captain Stumpy
5 / 5 (2) Oct 06, 2014
Amino acid substitutions are not mutations; they stabilize protein folding; they do not perturb it.
Hmmmm....
lets see...
what is the DEFINITION of mutation used by GENETICISTS and BIOLOGISTS per the lexicon of the field?
In genetics, a mutation is a change of the nucleotide sequence of the genome of an organism, virus, or extrachromosomal genetic element. Mutations result from unrepaired damage to DNA or to RNA genomes (typically caused by radiation or chemical mutagens), errors in the process of replication, or from the insertion or deletion of segments of DNA by mobile genetic elements.[1][2][3] Mutations may or may not produce discernible changes in the observable characteristics (phenotype) of an organism. Mutations play a part in both normal and abnormal biological processes including: evolution, cancer, and the development of the immune system
[sic]
https://en.wikipe...Mutation

Captain Stumpy
5 / 5 (2) Oct 06, 2014
Your inability to understand the terms I use to detail cause and effect, does not make my terms "word salad."
I guess you ARE illiterate... or you cannot comprehend basic english... i said
writing a BS word salad that argues mutations are bad while using mutations as a replacement is plain STUPID
let me explain it in small words so you can understand
just because you can make something SOUND complicated does not make you intelligent NOR does it make the issue complicated
YOU are simply trying to make it SOUND complicated so that you don't look stupid... but you look even MORE stupid because you are WRONG (and it is PROVEN)

and YOU said that your model causes mutations
remember.. I asked
DOES your model make any changes to the nucleotide sequence of the genome of an organism, virus, or extrachromosomal genetic element?
This is a yes or no answer
(this is the DEFINITION of mutation) to which you answered
YES!
--Thanks for asking
remember?
JVK
1 / 5 (2) Oct 06, 2014
http://newswire.r...icrobes/

My comments at http://ow.ly/2OE5l3

Re:
DOES your model make any changes to the nucleotide sequence...


The changes are epigenetically effected, which is what I exemplified in my model. Claims that I said my model causes mutations are the ramblings of a fool.

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