Researchers create methylation maps of Neanderthals and Denisovans, compare them to modern humans

Apr 18, 2014 by Bob Yirka report
A Neanderthal skeleton, left, compared with a modern human skeleton. Credit: American Museum of Natural History

(Phys.org) —A team of Israeli, Spanish and German researchers has for the first time created a map of gene expression in Neanderthals and Denisovans and has compared them with modern humans. In their paper published in the journal Science, the team describes how they applied epigentics to the study of our two closest known ancestors and discovered variations that might account for their differences in body shape and susceptibility to some modern neurological diseases.

Scientists know that it's not just our DNA structure that determines how we look and what we're capable of doing, there's another factor involved—the expression of our genes—they can be turned on or off at some point, allowing or preventing certain traits from developing. This process is known as DNA methylation—where methyl group chemicals attach to DNA and prevent them from behaving as they would otherwise. In this new effort, the researchers looked at methylation in Neanderthals and Denisovans to learn more about how they might have been different from us.

Studying methylation in preserved fossils involves noting the way the methyl chemical cytosine decays over long periods of time. Unmethylated cytosines decay to one type of chemical while unmethylated cyctones decay to another. By measuring the amounts of the two resultant chemicals found in fossilized , the researchers were able to create methylation maps of Neanderthals and Denisovans, which they then compared with similar maps for .

The comparisons revealed differences in approximately 2000 different regions, though one in particular stood out—an HoxD cluster that prior research has shown plays an important role in the development of body structure—a finding that could help explain the shorter, stouter limbs (and other features) of our extinct cousins. Interestingly, the team also found that some of the highly methylated regional areas that appear in modern humans do not appear in either Neanderthals or Denisovans, regions that have been associated with neurological disorders such as schizophrenia and autism—a finding that may help shed some light on their source.

Unfortunately, the maps created by the research team are still incomplete, they only had a few bone fragments to work with—they're hoping future studies (and fossil finds) will reveal more. In the meantime, they plan to conduct similar work on other species, such as horses, to help reveal the types of methylation that occurred as they were domesticated.

Explore further: Neanderthal genome shows early human interbreeding, inbreeding

More information: Reconstructing the DNA Methylation Maps of the Neandertal and the Denisovan, Science, DOI: 10.1126/science.1250368

ABSTRACT
Ancient DNA sequencing has recently provided high-coverage archaic human genomes. However, the evolution of epigenetic regulation along the human lineage remains largely unexplored. We reconstructed the full DNA methylation maps of the Neandertal and the Denisovan by harnessing the natural degradation processes of methylated and unmethylated cytosines. Comparing these ancient methylation maps to those of present-day humans, we identified ~2000 differentially methylated regions (DMRs). Particularly, we found substantial methylation changes in the HOXD cluster that may explain anatomical differences between archaic and present-day humans. Additionally, we found that DMRs are significantly more likely to be associated with diseases. This study provides insight into the epigenetic landscape of our closest evolutionary relatives and opens a window to explore the epigenomes of extinct species.

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JVK
1 / 5 (5) Apr 18, 2014
DNA methylation is nutrient-dependent and nutrients metabolize to species-specific pheromones, which control the physiology of reproduction in species from microbes to man.

Thus, this article replaces mutations with methylation and it also replaces evolution with ecological adaptation in the context of ecological variation and the nutrient-dependent pheromone-controlled differentiation of cell types in individuals of all species.

From the Science article: "...the differences in methylation discovered here will help to uncover the epigenetic basis for phenotypic differences between present-day and archaic humans..."

See also: Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems

http://figshare.c...s/994281

Try to dispense with use of terms like mutation in evolution since experimental evidence shows species diversity arises via ecological adaptations.
JVK
1 / 5 (5) Apr 18, 2014
Sunday Book Review: Missing Links: 'Neanderthal Man,' by Svante Paabo
By CARL ZIMMERAPRIL 18, 2014

http://www.nytime...tw-share

"Neither Paabo nor any other scientist can yet clearly link our mutations to our human nature."

That explains why his latest co-authored work links methylation to differences that are clearly nutrient-dependent and pheromone-controlled in every other species on this planet.

http://www.socioa...53/27989

However, the link from the epigenetic landscape to the physical landscape of DNA in organized genomes of all species was never missing. It was simply ignored -- even after our 1996 Hormones and Behavior review article with a section on molecular epigenetics.
http://www.hawaii...ion.html full text "Small intranuclear proteins also participate in generating alternative splicing..."
anonymous_9001
5 / 5 (6) Apr 19, 2014
Thus, this article replaces mutations with methylation


Once again, you prove you can't read.

From the article:

Scientists know that it's not just our DNA structure that determines how we look and what we're capable of doing,


Remember when I told you Shapiro's hypothesis was a SUPPLEMENT to mutation and natural selection? Same thing applies here. Methylation is a SUPPLEMENT. Not a replacement. Contact the authors if you'd like it confirmed.
Egleton
1 / 5 (2) Apr 19, 2014
So. More evidence for the importance of schizophrenia to humans. Schizophrenia is a necessary precondition to creativity.
The culture of all pre-homosap was as boring as bat droppings.
Mad man comes arrives and culture is in an unstoppable state of change. For example we can date pottery shards with accuracy due to their patterns.
Next time you meet a crazed person remember he pays the price for our civilization.
.
And No, Big Pharma, it is NOT a disease that you can make a lot of money out of. It is the essence of our humanity. (Anyone remember the "Wonder Cure" of sub-orbital lobotomy? No? Look it up.)
https://www.youtu...NILW6ILk
Leave us kids alone, you mad bastards.
JVK
1 / 5 (3) Apr 19, 2014
Remember when I told you Shapiro's hypothesis was a SUPPLEMENT to mutation and natural selection?


No, I don't remember that. Did you also tell me HOW mutations and natural selection led to species diversity so that I could place what you now imply is supplemental hypothetical information into the context of biologically-based cause and effect? Or, like other anonymous fools, did you just make the typical pseudoscientific claims refuted by works like this one -- co authored by Paabo?

What do you think this means: "...the differences in methylation discovered here will help to uncover the epigenetic basis for phenotypic differences between present-day and archaic humans..." To me, it clearly states that the differences link the epigenetic landscape to the physical landscape of DNA in species from microbes to man, which is why they are consistently manifested in morphological and behavioral phenotypes (i.e., cell type differentiation and species diversity).
airman000616
not rated yet Apr 19, 2014
What do you think this means: "...the differences in methylation discovered here will help to uncover the epigenetic basis for phenotypic differences between present-day and archaic humans..."


It sounds like the means for a focused study of the changes in species diversity. This links the physical landscape of genetic traits in a single species from man to man.
anonymous_9001
5 / 5 (5) Apr 19, 2014
Did you also tell me HOW mutations and natural selection led to species diversity


This will be the 1,000,001th time I've told you this:
Mutations result in genotypic diversity by shuffling genetic elements or changing their sequence which results in phenotypic diversity.

refuted by works like this one -- co authored by Paabo?


Again, your quote mining is pathetic. How about this one from the Paabo article-

It enables Paabo and his colleagues to draw up a list of mutations that our ancestors acquired after they split from Neanderthals


The part you quoted means they don't yet know what the mutations did, not that they don't believe in mutations resulting in new traits. I urge you to contact Paabo yourself and ask for clarification or do I have to do it myself like I did with Fink and Chelo?
JVK
1 / 5 (4) Apr 19, 2014
Here's another opportunity for idiot minions of biology teachers like PZ Myers and anonymous fools to explain why they believe mutations are involved in evolution when experimental evidence suggests that organisms ecologically adapt. Both of the reports that follow were co-authored by Paabo.

A functional test of Neandertal and modern human mitochondrial targeting sequences
http://www.scienc...10019881

"In spite of recent evolution, and to the contrary of other mutations in targeting peptides, these mutations had no visible effects."

Reconstructing the DNA Methylation Maps of the Neandertal and the Denisovan
http://www.scienc...abstract

"We hope that the differences in methylation discovered here will help to uncover the epigenetic basis for phenotypic differences..."

When a respected researcher like Paabo admits to the truth about the cause of phenotypic differences, what happens to theorists?
anonymous_9001
5 / 5 (5) Apr 19, 2014
What do you think this means:...


Both genetics and epigenetics contribute to phenotype. They're not replacing genetics just because they're investigating epigenetics in more detail.
JVK
1 / 5 (4) Apr 19, 2014
I urge you to contact Paabo yourself and ask for clarification...


I've already clarified the fact that a nutrient-dependent single base pair change and amino acid substitution in mice and in a human population that arose in what is now central China during the past ~30,000 years links nutrient-dependent ecological variation from the epigenetic landscape to the pheromone-controlled physiology of reproduction and physical landscape of our DNA via conserved molecular mechanisms in species from microbes to man.

It would be great if you would contact Paabo to learn if he agrees with my clarification since it is based on experimental evidence that he has included in his published works since at least 2010. He's examined two amino acid substitutions that have no effect. They can be compared to one nutrient-dependent amino acid substitution that effects hair, teeth, sweat and mammary tissue in mammals, which I detailed in:
http://dx.doi.org...i0.20553
JVK
1 / 5 (4) Apr 19, 2014
They're not replacing genetics just because they're investigating epigenetics in more detail.


They are replacing theories of mutations and evolution with experimental evidence of nutrient-dependent methylation and ecological adaptations that result in species diversity, which is what I have done since 1995 in a series of published works and presentations. For a 5.5 minute video summary, see http://youtu.be/DbH_Rj9U524

Paabo and others are still looking for epigenetic effects on networks of genes long after others have linked nutrient-dependent methylation to changes in the pheromone-controlled behavior of the birds...

http://www.pnas.o...abstract

...and the bees...

http://bfg.oxford...050.long

We first detailed the link from molecular epigenetics in a 1996 review, which is why some researchers may be embarrassed to admit that they remained unaware of the biological facts until recently.
JVK
1 / 5 (4) Apr 19, 2014
Paabo, and several others are not as likely as evolutionary theorists are to be embarrassed when biological facts refute theories about mutations and evolution. At some level of expertise, you simply expect theories to be refuted by experimental evidence, and he has achieved that level of expertise.

However, he might still be ostracized by his peers for publishing experimental evidence of refutations if he came right out and told everyone else that there has never been any such thing as mutation-driven evolution. There are far too many academically irresponsible researcher to contend with, and they tend to make it difficult to continue to provide experimental evidence that refutes popular theories. Elaine Morgan addressed the issue in an entertaining 2009 TED talk:

http://www.ted.co...tic_apes

She would be having the last laugh had she not died before Paabo's works provided overwhelming support for her claims (of ecological adaptations).
anonymous_9001
5 / 5 (5) Apr 19, 2014
nutrient-dependent single base pair change


And yet you still refuse to tell us the enzymatic mechanism by which they occur. I'll rule out one for you: transposons transpose their whole sequence. They don't change single base pairs.

A functional test of Neandertal and modern human mitochondrial targeting sequences
http://www.scienc...10019881

"In spite of recent evolution, and to the contrary of other mutations in targeting peptides, these mutations had no visible effects."


That says the particular mutations they found had no effect, not that mutations in general have no effect. Your lack of reading comprehension strikes again.

It would be great if you would contact Paabo


Sure. I'll do your dirty work. I predict this is going to end with you being contradicted just like my exchanges with Fink and Chelo.
anonymous_9001
5 / 5 (4) Apr 19, 2014
the birds...

http://www.pnas.o...abstract

...and the bees...

http://bfg.oxford...050.long


The first one has nothing to do with methylation. It's talking about different alleles (not epialleles). The second one mentions mutations dozens of times, so it's definitely not refutation of them.
JVK
1 / 5 (4) Apr 19, 2014
The first one has nothing to do with methylation. It's talking about different alleles (not epialleles). The second one mentions mutations dozens of times, so it's definitely not refutation of them.


When someone like Paabo comes forward with experimental evidence that mutations are not the cause of evolution and that nutrient-dependent methylation causes ecological adaptations, it should no longer be required to refute each aspect of the pseudoscientific nonsense from population genetics that has become popular. Simply put, results from experiments have consistently refuted every aspect of what has been taught to generations of students in the context of courses that should have been listed as "Evolution for Dummies."

Paabo's recent works integrate molecular epigenetics and demand that nutrient-dependent methylation be consistently substituted -- in context -- for the term mutation and that ecological adaptations be viewed as the result of pheromone-controlled phenotypes.
JVK
1 / 5 (4) Apr 19, 2014
Here's an example of what happens when people take current works out of their context, and eliminate what makes sense so they can continue to tout their nonsense.

See: Human Remains from the Pleistocene-Holocene Transition of Southwest China Suggest a Complex Evolutionary History for East Asians http://www.ploson....0031918

My comments about their failure to consider ecological variation, methylation, and ecological adaptations in what they think are two plausible explanations for the difference in morphology are available from my blog. See: "Making pseudoscientific nonsense from sense"

Simply put ecological variation, methylation, and ecological adaptations incorporate conserved molecular mechanisms of biophysically-constrained species diversity, which is biologically plausible. Mutation-driven evolution is not biologically plausible because unconstrained adaptations are not likely to occur!
anonymous_9001
5 / 5 (4) Apr 19, 2014
When someone like Paabo comes forward with experimental evidence that mutations are not the cause of evolution


Again, he's supplementing, not replacing.

methylation be consistently substituted -- in context -- for the term mutation


Methylation and mutation are not analogous. Methylation alters expression and mutation alters sequence. Are you still unable to differentiate those? It's an important distinction.
JVK
1 / 5 (3) Apr 19, 2014
Methylation alters expression and mutation alters sequence. Are you still unable to differentiate those?


Arguably, that may be the most simple-minded statement I have ever read. But, yes, I am able to differentiate between the nutrient-dependent Creation of genes and cell type differentiation manifested in individual diversity and in species diversity. Thanks for asking.

You have alerted others to the fact that you think the nutrient-dependent de novo Creation of genes is less important than mutations to genes that somehow then contribute to species diversity -- instead of to diseases and disorders -- via perturbed protein folding.

Please tell someone who taught you such nonsense, so they can anonymously alert others to the plight you have suffered. Only people like you can help others like you to not become more like you, or to simply remain anonymous fools.
anonymous_9001
5 / 5 (4) Apr 19, 2014
Creation of genes


Through a mechanism you have yet to name.
JVK
1 / 5 (3) Apr 19, 2014
Through a mechanism you have yet to name.


Stop being ridiculous! I can't tell you everything about everything in internet discussions. You need to learn, as I have done, from the extant literature or from more than 950 blog posts at Pheromones.com.

Fortunately, you don't need to start 32 years ago as I did, but you need to start somewhere.

If you're not able to grasp what I have detailed, perhaps you can start here: Natural Selection on the Olfactory Receptor Gene Family in Humans and Chimpanzees -- and begin to learn what Paabo has also already detailed during the past decade, which led to replacement of evolutionary theory with ecological variation, methylation, and ecological adaptations in species from microbes to man via conserved molecular mechanisms.

http://linkinghub...07620138
".positive selection acting on intact OR genes. These observations are likely due to differences in lifestyle, between humans and great apes, that ..."
anonymous_9001
5 / 5 (5) Apr 19, 2014
I can't tell you everything about everything


You don't need to tell me everything. You just need to name an enzymatic pathway.

If you've detailed it, you know the name of it. If you know the name of it, you can very simply type it and hit "submit". mRNA and transposons don't make DNA base changes, so what does?

And don't merely tell me base changes are nutrient-dependent and pheromone-controlled again. That's like me asking you what I drive down the highway and you answering "it has wheels." Sure, but the answer I'm looking for is "car".

The more you refuse to name it, the more I think you don't know the name of it in the first place.
JVK
1 / 5 (3) Apr 19, 2014
The more you refuse to name it, the more I think you don't know the name of it in the first place.


It should cause you to think about the likelihood that the pathways are far too complex to detail in internet correspondence, which is why I detailed them in published works -- even if the most recent details are only published on-line, and not in peer-reviewed journals like the one whose guest editor invited my most recent review. In any case, the other publications, including two award-winning reviews have been published in peer-reviewed journals and you consistently ignore what I've already detailed.

The fact that you will not provide details on any biologically-based link from the sensory environment to mutations and species diversity in any species tells me you are simply fishing for information you can claim as if it arose from your insight.

Few people will be the wiser, because everywhere else you are merely an anonymous fool.
anonymous_9001
5 / 5 (4) Apr 19, 2014
It should cause you to think about the likelihood that the pathways are far too complex to detail in internet correspondence, which is why I detailed them in published works


Pathways have names and enzymes within them that have names. Names don't require drawn out explanations.

With that in mind, what pathways involving what enzymes make DNA base changes?

There really aren't that many enzymes that interact with DNA, especially those that make sequence changes. However, I don't know of any that make changes to specific bases rather than large sections like reverse transcriptase, which is involved in viral infection and transposons.
anonymous_9001
5 / 5 (3) Apr 19, 2014
The fact that you will not provide details on any biologically-based link from the sensory environment to mutations and species diversity in any species tells me you are simply fishing for information you can claim as if it arose from your insight.


You tried this one before on Yahoo. It's and old, sad excuse.
JVK
1 / 5 (3) Apr 19, 2014
It's not an excuse; the problem is that you obviously know nothing about the Tet family of dioxygenases, and I have absolutely no motivation to tell you about them. You are nothing more than an anonymous fool who believes in mutation-driven evolution and probably always believe in it, no matter how biologically implausible the ridiculous theories are that you have been taught to believe in.

You know nothing about aerobic glycolysis or networks of glycosylation that must enable the nutrient-dependent pheromone-controlled differentiation of cell types via the conserved molecular mechanisms of methylation and amino acid substitutions.

Therefore, even after Paabo and others create methylation maps of Neanderthals and Denisovans for comparison to modern humans, you want to believe in pseudoscientific nonsense.

What's worse is that you want others to believe that I don't know the differences between that nonsense and biological facts supported by experimental evidence.
Whydening Gyre
not rated yet Apr 19, 2014
You don't need to tell me everything. You just need to name an enzymatic pathway.

If you've detailed it, you know the name of it. If you know the name of it, you can very simply type it and hit "submit". mRNA and transposons don't make DNA base changes, so what does?

And don't merely tell me base changes are nutrient-dependent and pheromone-controlled again. That's like me asking you what I drive down the highway and you answering "it has wheels." Sure, but the answer I'm looking for is "car".

The more you refuse to name it, the more I think you don't know the name of it in the first place.

Does DNA "change" it's base pairs? RNA might modify it some. However,
real change occurs in DNA when it ADDs more base pairs, I would think...
JVK
1 / 5 (3) Apr 19, 2014
While they focus on HOXD and variants associated with hand and foot development and some severe deformities, variants in the EDAR gene that influence baldness, the straightness of hair and the amount of terminal hair that people and mice have are also associated with ectodermal dysplasias and effects on the development of nails, skin, teeth, mammary tissue, sweat, and brain development. Of course, funding is limited and no one can look in every direction they are led by their experiments to pursue.

But, while the anonymous fool complains that I won't provide details on pathways and enzymes, the anonymous fool provides no experimental evidence that might support an alternative to nutrient-dependent pheromone-controlled methylation that enables cell type differentiation. If not for efforts to provide an outstanding example of ignorance, I would have given up on the anonymous fool everywhere he (or she) shows up.
JVK
1 / 5 (3) Apr 19, 2014
real change occurs in DNA when it ADDs more base pairs


How do mutations enable the addition of base pairs? That sounds like a very creative thing for mutations to do. Are you a Creationist? Where do the additional base pairs come from -- if not out of thin air?

On the other hand, you may be touting pseudoscientific nonsense. Tell us how DNA adds more base pairs so we can determine what you think -- and if it has anything to do with biologically-based facts.
anonymous_9001
5 / 5 (4) Apr 19, 2014
Thank you. I commend you for cooperating. However, I asked you what makes base substitutions, e.g. A to G, G to T, etc.

http://en.wikiped...genase_1

TET1 catalyzes the conversion of the modified DNA base 5-methylcytosine (5-mC) to 5-hydroxymethylcytosine


Epigenetic markers are not base substitutions or sequence changes.

You know nothing about aerobic glycolysis or networks of glycosylation that must enable the nutrient-dependent pheromone-controlled differentiation of cell types via the conserved molecular mechanisms of methylation and amino acid substitutions.


I told you back in the Australia thread I don't contest nutrient-dependent/pheromone-controlled cellular differentiation in the sense that our stem cells specialize into distinct cell types (or organism in the case of worker/queen bee) from the same genome, but genomes are not static over generations.
anonymous_9001
5 / 5 (5) Apr 19, 2014
real change occurs in DNA when it ADDs more base pairs


How do mutations enable the addition of base pairs? That sounds like a very creative thing for mutations to do. Are you a Creationist? Where do the additional base pairs come from -- if not out of thin air?

On the other hand, you may be touting pseudoscientific nonsense. Tell us how DNA adds more base pairs so we can determine what you think -- and if it has anything to do with biologically-based facts.


Observation of taq polymerase slipping and inserting extra base pairs during replication:

http://nar.oxford...974.full

Whydening Gyre
5 / 5 (2) Apr 19, 2014
real change occurs in DNA when it ADDs more base pairs

How do mutations enable the addition of base pairs? That sounds like a very creative thing for mutations to do. Are you a Creationist? Where do the additional base pairs come from -- if not out of thin air?
On the other hand, you may be touting pseudoscientific nonsense. Tell us how DNA adds more base pairs so we can determine what you think -- and if it has anything to do with biologically-based facts.

Said nothing of mutations. Added by RNA sequencing, whether biologically directed or not. The addition IS the mutation.
Artist by avocation. Realist and observer, not Creationist, by choice.
Nutrient dependent? Mostly, yes. Pheremone controlled? only one part of a bigger picture.
Quit bringing your "one-side only" schtick to a lay science site.
I'll bet you were an only child... Live outside yourself, man.
JVK
1 / 5 (3) Apr 20, 2014
Thank you. I commend you for cooperating. However, I asked you what makes base substitutions, e.g. A to G, G to T, etc.


You asked
what pathways involving what enzymes make DNA base changes?


... I don't contest nutrient-dependent/pheromone-controlled cellular differentiation in the sense that our stem cells specialize into distinct cell types (or organism in the case of worker/queen bee) from the same genome, but genomes are not static over generations.


Now that you've been told methylation causes morphological changes that differentiate modern and archaic humans, as in the honeybee model of hormone-organized and hormone-activated behavior, which was derived from our 1996 publication in Hormones and Behavior, what do you think is responsible for phenotypic changes in behavior across generations? http://www.ncbi.n.../9047261

You have implied that mutations are responsible for changes in behavior, you anonymous fool.
JVK
1 / 5 (3) Apr 20, 2014
Does everyone who is not an anonymous fool or idiot minion of an atheistic biology teacher realize that nutrient-dependent methylation causes the changes in base pairs and amino acid substitutions that lead to the differentiation of cell types in individuals of all species? If so, my model details the unequivocal fact that the metabolism of nutrients to species-specific pheromones controls nutrient-dependent species diversity. It does not get clearer than that!

Kohl's Laws of Biology and Darwin's 'conditions of life' are nutrient-dependent and pheromone-controlled, and I've included examples from all genera that attest to that fact in:

Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems
http://figshare.c...s/994281

If, after being told that methylation causes differences in morphology, do you still need someone to explain differences in behavior?
anonymous_9001
5 / 5 (4) Apr 20, 2014
Thank you. I commend you for cooperating. However, I asked you what makes base substitutions, e.g. A to G, G to T, etc.


You asked
what pathways involving what enzymes make DNA base changes?


Slight nuances aside, my questions have always been about base sequence changes and considering how long as I've been asking you, there shouldn't be any confusion about what I mean. Methylation can alter expression levels, but when it comes to changes in the SEQUENCE itself, methylation has no effect.
JVK
1 / 5 (3) Apr 20, 2014
when it comes to changes in the SEQUENCE itself, methylation has no effect.


The article concludes:

"We hope that the differences in methylation discovered here will help to uncover the epigenetic basis for phenotypic differences between present-day and archaic humans..."

What's worse is that they conclude this after saying: "Consequently, the fraction of CpG→TpG substitutions (hereinafter, C→T ratio) may serve as a proxy for the levels of methylation in ancient DNA (Figs. 1A, S1)."

The problem becomes one that theorists have never attempted to address. If cause and effect is not driven by nutrients via conserved molecular mechanisms in species from microbes to man, how did mutations lead from natural selection to the evolution of species diversity?

Skip the fact that different 5-hydroxymethylcytosines are associated with differences in cell types that have the same genetic backgrounds.

Q: How are mutations involved in selection?

A: Obviously, they aren't.
JVK
1 / 5 (3) Apr 20, 2014
when it comes to changes in the SEQUENCE itself, methylation has no effect.


Please seek competent advice from someone who is not an anonymous fool before ever commenting again on any topic that involved biologically-based cause and effect. Alteratively, seek help from a psychiatrist who might cure you of your delusions about evolution.
anonymous_9001
5 / 5 (3) Apr 20, 2014
Methylation is not entirely causal in inducing C to T mutations (which occur through spontaneous deamination following methylation) because apparently, the vast majority of CpG cytosines are already methylated in mammals.

http://en.wikiped...CpG_site

On top of that, all other substitutions besides C to T remain unexplained by epigenetic means.

anonymous_9001
5 / 5 (4) Apr 20, 2014
This is the same causation issue we run into when you claim the presence of citrate caused the promoter shift in Lenski's E. coli. If it only occurred in 1 out of 12 populations (or however many), it obviously wasn't causal.
JVK
1 / 5 (3) Apr 20, 2014
all other substitutions besides C to T remain unexplained by epigenetic means.


No. All other substitutions that contribute to increased organismal complexity are obviously nutrient-dependent and pseudoscientific claims unsupported by experimental evidence are the only claims that suggest mutations might lead either to the creation of anything beneficial or to its fixation in the organized genome of any organism.

Those who cannot grasp the meaning of Lenski's experiments are under-informed theorists who know too little about what is currently known about biological facts, which is why Noble wrote: "If you learnt evolutionary biology and genetics a decade or more ago you need to be aware that those debates have moved on very considerably, as has the experimental and field work on which they are based." (p 1014) http://jp.physoc....abstract Arguing with the president of the International Union of Physiological Sciences exemplifies only ignorance.
anonymous_9001
5 / 5 (4) Apr 20, 2014
Deamination is spontaneous and is not mediated by an enzyme, so there's no way to control it. It is, by definition, random, and is classified as a mutation.

Here's one thing I don't understand- you claim to have detailed these pathways in your papers, but it took this much pressing from me for you to finally bring up methyltransferases. There's nothing even remotely related in your papers.

Those who cannot grasp the meaning of Lenski's experiments...


Which apparently you know better than Lenski. Tell me- how was the promoter shift non-random when it only happened in one of his populations?

JVK
1 / 5 (3) Apr 20, 2014
...it took this much pressing from me for you to finally bring up methyltransferases.


That's because you dismissed what I told you about glucose dehydrogenase, which made it clear you would dismiss everything else and continue to tout ridiculous pseudoscientific theory no matter how much experimental evidence refutes the nonsense. That's what you have done.

Now, we're back to Lenski's experiments -- after this report that methylation causes morphological differences in Neanderthals and modern humans. The authors are not claiming that mutations cause the differences, but even after I provided you with information on methyltransferases, you want others to believe that mutations are somehow involved -- or to persuade them to consider methylation in the context of mutations.

There's nothing even remotely related in your papers.


You can't comprehend the physics or chemistry of constrained ecological adaptations, which means you can't recognize what's in my papers.
JVK
1 / 5 (3) Apr 20, 2014
Others may not know that I have expertise in microbiology, which I developed during the last few years of my medical laboratory scientist career while working, almost exclusively, in a hospital laboratory microbiology department.

When an anonymous fool or idiot minion of a atheistic biology teacher challenges my perspective on Lenski's experiments without detailing how mutations might have resulted in species diversity, it may seem that I am dealing too harshly with their comments.

If, instead, you were aware of the deaths that occur via evolutionary theory -- because antibiotic resistance has been reported to develop due to mutations -- you might better understand why I want the pseudoscientific nonsense about mutation-driven evolution to end.

Identification of pathogens always involves differences in what they eat, and their reproduction is pheromone-controlled. They never mutate into another species; they ecologically adapt or die before the patient does.
anonymous_9001
5 / 5 (4) Apr 20, 2014
you dismissed what I told you about glucose dehydrogenase


Because glucose dehydrogenase is simply responsible for dehydrogenating glucose, as I've told you multiple times. It's as useless as saying nutrient-dependent. While technically correct, it's so far removed from the processes being discussed, it means nothing. An analogy I've used before, but is still relevant: It'd be like me asking you how your car's power steering works and you telling me it's gasoline-dependent. Well, duh... but that's useless information.

Methylation is not a guarantee of base substitution:

In mammals, 70% to 80% of CpG cytosines are methylated


http://en.wikiped...CpG_site

If methylation directly led to deamination, you would have a point, but that's not the case.

anonymous_9001
5 / 5 (4) Apr 20, 2014
You can't comprehend the physics or chemistry of constrained ecological adaptations, which means you can't recognize what's in my papers.


There's nothing direct or indirect relating to methyltransferases in your papers. Not a mention or even an implication. Nobody would ever read your papers and say "oh yeah, he's talking about methyltransferases in this passage!" None of your citations concern them.
JVK
1 / 5 (3) Apr 20, 2014
My comment was not posted to Science but it was posted to the Scientist on 3/25/14

http://www.the-sc...ost98263

I suspect the reason it was not posted to Science was because the editors knew this article about methylation was soon to be published. There is little doubt that they also understand the involvement of 5hmcs in the complex systems biology that links epigenetic cause and effect. See for example: http://www.scienc...abstract

The fact that anonymous fools and idiot minions of atheistic biology teachers understand little to nothing about biologically-based cause and effect is the problem. If they did, they would know what information is included in reviews even when everything ever written about a specific aspect is not cited.

Reviews are supposed to move others forward. You remain stuck in the distant past with ridiculous assumptions about Lenski's work and works by others.
anonymous_9001
5 / 5 (4) Apr 20, 2014
they would know what information is included in reviews even when everything ever written about a specific aspect is not cited.


The (presumably) main mechanism of your model is not merely a specific aspect! If it's as important to your model as you make it seem now, it should have been elucidated earlier.

JVK
1 / 5 (3) Apr 20, 2014
What mechanism of mutation-driven evolution was elucidated? The epigenetic effects of olfactory/pheromonal input on mammalian GnRH has been the basis of my model since the early 1990s. The fact that more details to support the model have come from experimental evidence -- including evidence for the role of 5hmcs in cell type differentiation -- is meaningless to those who cannot think about anything except mutations. You have shown that.

Now, you tell me what I should have elucidated and when. Others should see this for comparison: Nutrient-dependent / Pheromone-controlled adaptive evolution: (a mammalian model of thermodynamics and organism-level thermoregulation)
http://youtu.be/DbH_Rj9U524

In 5.5 minutes I refute theory with a model of epigenetic cause and effect that links the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man. But you tout Lenski's experiments and tell me what I should have elucidated. Jerk!
anonymous_9001
5 / 5 (4) Apr 21, 2014
What mechanism of mutation-driven evolution was elucidated?


Observation of taq polymerase slipping and inserting extra base pairs during replication:

http://nar.oxford...974.full

Now, you tell me what I should have elucidated and when.


It's hard to convince anyone of the validity of your model if all you do is offer extremely vague overviews without any detail. It's harder still when you refuse to offer those details when asked.

evidence for the role of 5hmcs in cell type differentiation -- is meaningless to those who cannot think about anything except mutations.


Again, I'm not denying the role these epigenetic mechanisms play in intraorganismal and caste differentiation.
Captain Stumpy
3.7 / 5 (3) Apr 21, 2014
It's hard to convince anyone of the validity of your model if all you do is offer extremely vague overviews without any detail. It's harder still when you refuse to offer those details when asked.
@anonymous_9001
and even harder still when the person makes up definitions or ignores the fact that his definition does not match the given definition used by the professionals in the field.

or worse yet, uses terms or words incorrectly and without regard to the prescribed use per the lexicon of the field which is there to facilitate communication.

redundant, redundant, redundant, redundant REEEEdundant....
JVK
1 / 5 (3) Apr 21, 2014
It's hard to convince anyone of the validity of your model if all you do is offer extremely vague overviews without any detail.


The validity of the model is self-evident since examples from model organisms are included. The experimental evidence that established use of these model organisms in explanations of biologically based cause and effect can be compared to the theory that constraint-breaking mutations cause species diversity. "...constraint-breaking mutation is the ultimate source of all biological innovations and the enormous amount of biodiversity in this world." http://www.amazon...99661731

I'm not denying the role these epigenetic mechanisms play in intraorganismal and caste differentiation.


Great! But you're not providing any alternative explanation for species diversity, which means you're sneaking in the back door via use of the honeybee model organism that links species from microbes to man (e.g., in my model).
JVK
1 / 5 (3) Apr 21, 2014
kleptogamy: A behavior pattern in which males from outside a group, or lacking in status within the group, attempt to mate with females from the group, often by means of some deceptive behavior. http://www.encycl...eptogamy

The common term for this is "sneaky ..cker" but "anonymous fool" or "idiot minion" or "PZ Myers" could be substituted in the context of what happens when overwhelming experimental evidence causes the paradigm shift that leads nearly everyone to dismiss pseudoscientific nonsense.

At that point, those who practice kleptogamy come out of the wood-work like roaches trying to digest that last piece of garbage available before other roaches eat it up and regurgitate it in contexts that make it appear they have known all along about the biophysical constraints on DNA methylation that link the epigenetic landscape to the physical landscape of DNA in the organized genomes of all species.
anonymous_9001
5 / 5 (2) Apr 21, 2014

Great! But you're not providing any alternative explanation for species diversity


Don't play dumb.

Observation of taq polymerase slipping and inserting extra base pairs during replication:

http://nar.oxford...974.full


http://www.nature...ated-331

This one is particularly good-

http://www.jbc.or...87.short
JVK
1 / 5 (3) Apr 21, 2014
This one is particularly good-


It's from 1985, you idiot!

My comment on Reconstructing the DNA Methylation Maps of the Neandertal and
the Denisovan has been approved and is now live at:
http://www.scienc...abstract
anonymous_9001
5 / 5 (3) Apr 21, 2014
This one is particularly good-


It's from 1985, you idiot!


Irrelevant. Did you even read it? What specifically is wrong about it?
JVK
1 / 5 (3) Apr 21, 2014
What specifically is wrong about it?


Nothing that hasn't already been addressed during the past nearly 30 years of research results reported in the context of experimental evidence. For example, the book I published with co-author: the late Robert T. Francoeur, was published in 1996 with an update in 2002.

The Scent of Eros: Mysteries of Odor in Human Sexuality http://www.amazon...exuality

My first presentation to American Mensa was in 1992 and I presented the latest research to them in 2010: video excerpts here: https://www.youtu...youtu.be

That an anonymous fool would first tell me what I should have elucidated and then ask why I didn't bother with a link to a 1985 paper reminds me of the ridiculous comment
PZ Myers made in the context of discussion on biophysically-constrained adaptations....
JVK
1 / 5 (3) Apr 21, 2014
... see: A Challenge to the Supremacy of DNA as the Genetic Material
http://blogs.plos...aterial/

"Perhaps you need to go back and read what biologists were saying in the 1950s and 1960s. Your version of the central dogma is idiosyncratic and wrong."

Note to others. The attacks of the idiot minion Captain Stumpy parallel those that came from discussion after PZ Myers attacked my scientific credibility in his typical fashion. See: http://freethough...s-place/

As others can quickly see by scanning the lengthy discussion thread, there is no experimental evidence that will be considered by Myers' followers. But, the followers of others who were taught by biology teachers who cannot understand biological facts and teach theory instead, are represented everywhere discussion arises that pits theory against the facts. Theorists prefer theory and despise facts!
JVK
1 / 5 (3) Apr 21, 2014
Correction, the book I co-authored was published first in 1995. The review article that explained what was known about molecular epigenetics and methylation in species from yeasts to other mammals was published in 1996 in Hormones and Behavior. http://www.ncbi.n.../9047261

Excerpt: "Genomic-imprinting is also manifest in specific parts of the X-inactivation region's related XIST gene. Here male- and female-specific methyl-group patterns participate in X-inactivation in females and also in the preferential inactivation of the paternal X in human placentae of female concepti (Harrison, 1989; Monk, 1995). This process indicates that tissues of the early conceptus can sense and react differentially to epigenetic sexual dimorphisms on the female conceptus' own two X chromosomes. Furthermore, variations of X-inactivation patterns often account for traits discordance in monozygotic twin females..."
anonymous_9001
5 / 5 (3) Apr 21, 2014
What specifically is wrong about it?


Nothing that hasn't already been addressed during the past nearly 30 years of research results reported in the context of experimental evidence.


If you can't concisely sum it up, chances are you didn't read it or don't understand it. What, specifically, refutes that paper?
anonymous_9001
5 / 5 (3) Apr 21, 2014
http://www.jbc.or...87.short

The frequency and specificity of mutations produced in vitro by eucaryotic DNA polymerase-beta have been determined in a forward mutation assay


I sure would love to see you try to refute this. It's plain as day. Nothing you could possibly say changes what they found in this study. This enzyme produces A, B, and C mutations at X, Y, and Z rates. It's in vitro, so you can't say nutrients or pheromones (somehow) produced the mutations rather than replication error.
JVK
1 / 5 (3) Apr 21, 2014
This enzyme produces A, B, and C mutations at X, Y, and Z rates. It's in vitro, so you can't say nutrients or pheromones (somehow) produced the mutations rather than replication error.


Is anyone else, besides the idiot minion Captain Stumpy, not aware of the difference between a mutation and the proposal that one or more accumulated mutations are involved in species diversity, which occurs in the context of ecological variation and nutrient-dependent pheromone-controlled ecological adaptations in species from microbes to man?

If so, there may be more ignorance here than what any group of researchers, including one with a researcher like Svante Paabo, can address by providing experimental evidence of biological facts that replaces mutations with methylation and replaces evolution with ecological adaptation.
anonymous_9001
5 / 5 (3) Apr 21, 2014
replaces mutations with methylation


Considering methylation and deamination results in mutation... you know, that whole "spontaneous" thing?

http://en.wikiped...mination

Spontaneous deamination is the hydrolysis reaction of cytosine into uracil, releasing ammonia in the process.


Spontaneous deamination of 5-methylcytosine results in thymine and ammonia. This is the most common single nucleotide mutation.


Deamination of guanine results in the formation of xanthine...This results in a post-replicative transition mutation ... G-C base pair transforms into an A-T base pair. Correction ... involves the use of alkyladenine glycosylase (Aag) during base excision repair.


Deamination of adenine results in the formation of hypoxanthine. Hypoxanthine ... selectively base pairs with cytosine instead of thymine. This results in a post-replicative transition mutation
JVK
1 / 5 (3) Apr 21, 2014
Deamination links nutrient uptake to the pheromone-controlled physiology of reproduction in the mouse to human model I used as an example of how DNA methylation links invertebrates to vertebrates.

Nutrient-dependent/pheromone-controlled adaptive evolution: a model
http://www.socioa...53/27989

If you are claiming that mutations link nutrient uptake to the physiology of reproduction and species diversity, please support your claims with details and experimental evidence that links one mutated primate species or any other mutated species to archaic and modern humans via the conserved molecular mechanisms touted in Gokhman et al (2014) who wrote: "We hope that the differences in methylation discovered here will help to uncover the epigenetic basis for phenotypic differences between present-day and archaic humans..."

They did not write: We hope to learn more about HOW mutations are involved, but maybe you can tell us HOW.
anonymous_9001
5 / 5 (2) Apr 21, 2014
Deamination isn't controlled, so that alone ruins your link. Methylation may be controlled, but as I've been pointing out this entire time, deamination is spontaneous, i.e. a mutation.

And just because Gokhman et al. focus on epigenetics doesn't mean they deny mutation.