Scientists unlock tangled mysteries of DNA

March 6, 2015 by Joann C. Adkins
Each of our cells contains a genetic message encoded in a DNA molecule which is almost 6 feet long. The packing and regulation of the DNA (represented in the figure above using sticks) is possible thanks to its wrapping around chromosomal proteins (represented here by yellow, red, blue and green dots). Credit: Florida International University

Chromosomal proteins hold the key to our DNA and they are changing, according to Jose Eirin-Lopez, marine sciences professor in the Florida International University Department of Biological Sciences.

While today's contains a variety of these proteins, Eirin-Lopez believes they evolved from a single ancestor millions of years ago. This finding, published recently in Molecular Biology and Evolution, is pivotal in unraveling the mysteries of DNA organization and regulation, and could someday lead to innovative biomonitoring strategies and therapies targeting a variety of diseases including cancer.

DNA is the recipe for all living things. Each of our cells has a DNA molecule enclosed within its nucleus, containing the entirety our genetic information. However, like a recipe book, not all that information is required at the same time. Most DNA remains tightly packaged in chromosomes until specific pieces of information are needed to do a job.

It is up to a group of proteins known as chromosomal proteins to unlock the information required to trigger a function in a given cell—to form a bone, determine eye color, metabolize food, fight infections or any other function. While significant information is available about the structure and functions of chromosomal proteins, very little is known about their origin and evolution. The team of researchers is the first to explain the mechanisms responsible for the evolutionary diversification of a specific group of chromosomal proteins known as High Mobility Group Nucleosome-binding (HMG-N) proteins.

"In the early stages of life on earth, cells were rudimentary yet still able to perform their jobs. But evolution, through mutations, drift and natural selection, has led these proteins (along with our cells) to evolve into higher performers," said Eirin-Lopez who co-authored the study with Rodrigo Gonzalez-Romero from FIU and Juan Ausio from the University of Victoria in Canada.

The research unveils the mechanisms responsible for the functional specialization of this group of proteins, from a common ancestor directing a variety of activities to the actual HMG-N lineages working in concert in vertebrate organisms including humans. However, along with a better cell performance, a higher number of chromosomal proteins also provide more potential targets for harmful mutations. If one or more of these proteins are altered or mutated they will target wrong genes in the DNA, giving erroneous instructions to cells. The potential health consequences of such mistakes are massive, often causing cells to grow uncontrollably and resulting in cancer.

"The only way we can alleviate the negative effects of these alterations is by getting an exhaustive knowledge about these proteins and their function, helping us to develop therapies to reinstate the correct communication with DNA and the cell," Eirin-Lopez said. "Nonetheless, our knowledge about chromosomal proteins will never be complete until we determine how they came to be and to fulfill their current roles in the cell. Only evolutionary analyses can answer that question. Understanding this better prepares us to take action in the future."

Explore further: New protein booster may lead to better DNA vaccines and gene therapy

More information: Evolution of High Mobility Group Nucleosome-Binding Proteins and Its Implications for Vertebrate Chromatin Specialization, Molecular Biology and Evolution, mbe.oxfordjournals.org/content/32/1/121.abstract

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JVK
1 / 5 (4) Mar 06, 2015
"...our knowledge about chromosomal proteins will never be complete until we determine how they came to be and to fulfill their current roles in the cell. Only evolutionary analyses can answer that question."

Estrogen receptor α polymorphism in a species with alternative behavioral phenotypes http://www.pnas.o...abstract

Excerpt: "The ZAL2 and ZAL2m alleles code for 597 amino acids, with two fixed differences driving a Val73Ile and Ala552Thr polymorphism in ZAL2m."

Fixation is nutrient-dependent and pheromone-controlled via the same biophysically constrained chemistry of RNA-mediated protein folding in all vertebrates. Conserved molecular mechanisms link RNA-mediated amino acid substitutions to cell type differentiation in species from microbes to man.

Excerpt 2) "...our results illustrate a detailed chain of events linking a chromosomal rearrangement to changes in overt social behavior."

No mutations, no evolution, no drift, just facts.
JVK
1 / 5 (4) Mar 06, 2015
See also: http://www.hawaii...ion.html

"The Genome, positioning, timings. There are major structural differences between the X and Y chromosomes; e.g., centromeric aiphoid repeats sequences and distribution of heterochromatin (Graves, 1995; Wolfe et al., 1985). These structural differences correlate with sexually dimorphic chromosomal positioning within the nucleus..."

"Molecular distance. As measured in centimorgans, human and other species' male and female chromosomes, including the autosomes, tend to have different lengths in various segments. To some extent, this suggests a correlation with physical distance but instead the differing lengths are based upon rates of recombination; although sections of most female chromosomes..."

"Molecular epigenetics. It is now understood that certain genes undergo a process called "genomic or parental imprinting." Early in embryonic development attached methyl groups..."
JVK
1 / 5 (4) Mar 06, 2015
http://www.biomed...64/14/95

"21 otherwise highly conserved genes were identified that each show evidence for positive selection on amino acid changes in the Darwin's finch lineage. Two of these genes (Igf2r and Pou1f1) have been implicated in beak morphology changes in Darwin's finches. Five of 47 genes showing evidence of positive selection in early passerine evolution have cilia related functions, and may be examples of adaptively evolving reproductive proteins."

See also: Nutrient-dependent/pheromone-controlled adaptive evolution: a model.
http://www.ncbi.n...24693353
RealScience
5 / 5 (7) Mar 06, 2015
The biologically uninformed continue to yell: MUTATIONS! (JVK, DEC 18, 2014)


I'll let your own words do the talking, JVK, since you have YET AGAIN introduced that term to a thread.

LMAO!

And your quote from the biomed link is even funnier!

You've already has it explained to you how non-synonymous changes to the sequence of nucleotides in the protein-coding region of a gene cause amino acid changes changes to the resulting protein, and how changes to the sequence of nucleotides are mutations by the standard definition.

So for you to quote

21 otherwise highly conserved genes were identified that each show evidence for positive selection on amino acid changes
is positively hilarious!

ROTFLMAO!
anonymous_9001
5 / 5 (5) Mar 06, 2015
So for you to quote

21 otherwise highly conserved genes were identified that each show evidence for positive selection on amino acid changes

is positively hilarious!


That's irony at its finest.
JVK
1 / 5 (3) Mar 06, 2015
...changes to the sequence of nucleotides are mutations by the standard definition.


Are you claiming they can be placed into this context "...genomic conservation and constraint-breaking mutation is the ultimate source of all biological innovations and the enormous amount of biodiversity in this world." http://www.amazon...99661731

If so, what causes the constraint-breaking mutations? How do they lead to biological innovations. So far as I know, the only thing that mutations do is perturb protein folding, which is stabilized by amino acid substitutions.

The questions arise: How does the standard definition of mutations address the obvious need for nutrient uptake to be linked to increasing organismal complexity? How is increasing organismal complexity manifested differently during life history transitions that lead to epistasis in adults? How do mutations lead to successful reproduction?

What makes science idiots think they know anything?
JVK
1 / 5 (3) Mar 06, 2015
That's irony at its finest.


What are you claiming is ironic? I think it's ironic that you cited the blog site of PZ Myers in your review of my model, and his attack on me for my claims about chromosomal rearrangements linked to biodiversity via the conserved molecular mechanisms of RNA-mediated cell type differentiation we detailed in our 1996 Hormones and Behavior review.

http://freethough...s-place/

"Ecological adaptation occurs via the epigenetic effects of nutrients on alternative splicings of pre-mRNA which result in amino acid substitutions that differentiate all cell types of all individuals of all species. The control of the differences in cell types occurs via the metabolism of the nutrients to chemical signals that control the physiology of reproduction.

These facts do not refute evolution; they simply refute the ridiculous theory of mutation-initiated natural selection..."
RealScience
5 / 5 (5) Mar 07, 2015
So far as I know, the only thing that mutations do is perturb protein folding, which is stabilized by amino acid substitutions.


The biomed article that YOU linked above also shows approximately 15 * 515 = >7500 SYNONYMOUS mutations (see ds rate and error rate) that DO NOT CHANGE the protein folding at all, so if the only thing you know that mutations do is to perturb protein folding, then you don't even understand the articles that you cite.

(But at least this time you acknowledged that it was as far as you knew rather than stating it as a 'fact'...)

JVK
1 / 5 (4) Mar 07, 2015
Thanks. What do you know that links the mutations to increasing organismal complexity via what is currently known about the biophysically constrained chemistry of nutrient-dependent RNA-mediated protein folding and amino acid substitutions that stabilize the DNA in the organized genomes of species from microbes to man?

Everyone who is not a science idiot seems to know that mutations accumulate before they are manifested in physiopathology. Indeed, I vaguely recall that someone speculated on the number of amino acid substitutions that might be required to link ecological variation to ecological adaptation for comparison to the ridiculous thoughts of theorists.

Do you known if anyone has claimed that a specific number of mutations leads to the evolution of a new species? Is there a model for that? If not, I think that science idiots have been faced with facts that show how biologically uninformed they really are.

Isn't that embarrassing to you?
RealScience
5 / 5 (5) Mar 07, 2015
...and amino acid substitutions that stabilize the DNA

While there are exceptions, most amino acid substitutions do not stabilize DNA.
Amino acids are part of proteins, and while some proteins do interact with DNA, many others do not.

... mutations accumulate before they are manifested in physiopathology.


SOMETIMES mutations accumulate - Redundancy (including homeostasis) is often advantageous and hence selected for as it allows variety to accumulate.
However SOME mutations show up as a pathology even with just one mutation (especially if in germ-line cells).


... a specific number of mutations leads to the evolution of a new species?

Why would there be a specific number? A few major mutations might render groups incompatible for breeding, yet other groups might be able to interbreed in spite of many thousands of minor mutations.

-continued-
RealScience
5 / 5 (5) Mar 07, 2015
-continued-

I think that science idiots have been faced with facts that show how biologically uninformed they really are.

Isn't that embarrassing to you?


You've already established who is biologically uninformed, JVK.

Even SINCE you stated:
The biologically uninformed continue to yell: MUTATIONS! (JVK, DEC 18, 2014)

you have continued to yell 'mutations' into thread after thread!

Isn't that embarrassing to you?

ROTFLMAO!
JVK
1 / 5 (2) Mar 07, 2015
... most amino acid substitutions do not stabilize DNA.


How is epistasis achieved? Is it by MUTATIONS?

Molecular diversity through RNA editing: a balancing act http://www.ncbi.n...2865426/

Excerpt: "Alteration of amino acid codons, splice patterns, stability or localization of protein-coding transcripts, modulation of regulatory RNA biogenesis and function, as well as crosstalk of RNA editing with RNA processing and silencing pathways provides a rich resource for the generation of molecular diversity and for gene regulation."

Non-Adaptive Amino Acid Convergence Rates Decrease over Time http://mbe.oxford...abstract

Excerpt: "According to this theory, the fitness of an amino acid for any site, and therefore the propensities for the amino acid at that site, is dependent on how well suited it is to the environment formed by the amino acids at neighboring and interacting sites."
JVK
1 / 5 (2) Mar 07, 2015
Why would there be a specific number?


Analysis of 6,515 exomes reveals the recent origin of most human protein-coding variants. Reported as: http://www.nature...-1.11912

"Of 1.15 million single-nucleotide variants found among more than 15,000 protein-encoding genes, 73% in arose the past 5,000 years, the researchers report. 164,688 of the variants — roughly 14% — were potentially harmful, and of those, 86% arose in the past 5,000 years. More broadly, the results suggest that humans are carrying around larger numbers of deleterious mutations than they did a few thousand years ago."

This indicates entropic elasticity has led to epistasis in approximately 5000 genes. How much longer should we wait to see if any mutations can be somehow be linked to epistasis before everyone agrees to start "Combating Evolution to Fight Disease" http://www.scienc...88.short or to die trying?
JVK
1 / 5 (2) Mar 07, 2015
Rather than die or suffer needlessly due to evolutionary theory, intelligent people may want to consider learning the difference between a mutation and an amino acid substitution.

See, for example, "Clinically Actionable Genotypes Among 10,000 Patients With Preemptive Pharmacogenomic Testing" http://www.medsca...24253661

Even Francis Collins, a theistic evolutionist, is supporting the movement towards scientific progress that has been prevented by the NIH's definition of mutations and its use in reports of research that might otherwise be meaningful to serious scientists. As the current director of the NIH, he probably has realized that "The Language of God" (a book he wrote) does not include altered letters that, over time, would make it become unintelligible.

http://publicatio...er1.html "
Over time, mutations supply the raw material from which new life forms evolve."

Is there a model for that?
RealScience
5 / 5 (4) Mar 07, 2015
... most amino acid substitutions do not stabilize DNA.


How is epistasis achieved? Is it by MUTATIONS?

Molecular diversity through RNA editing: a balancing act http://www.ncbi.n...2865426/



There certainly are SOME proteins that interact with DNA, and SOME amino acid substitutions in SOME of those proteins would stabilize DNA. However many proteins do other things entirely - in a eukaryotic cell, for example, MOST proteins are not even in the nucleus of the cell where the DNA is.

When you claim that amino acid substitutions stabilize proteins, at least amino acids are IN proteins so many such substitutions do stabilize proteins (although many others destabilize proteins).

Do you even understand that while amino acids are part of proteins, and that it is nucleic acids, and not amino acids, that are part of DNA and RNA?

RealScience
5 / 5 (4) Mar 07, 2015
"Of 1.15 million single-nucleotide variants found among more than 15,000 protein-encoding genes, 73% in arose the past 5,000 years, the researchers report. 164,688 of the variants — roughly 14% — were potentially harmful, and of those, 86% arose in the past 5,000 years. More broadly, the results suggest that humans are carrying around larger numbers of deleterious mutations than they did a few thousand years ago."


So according to the article that YOU cite, JVK, 840,000 (73% of the 1.15M) variations found in protein-coding genes arose through mutations in the last 5000 years. And 145,000 (88% of the 165,000) potentially harmful ones arose in that time.

That leaves 695,000 mutations accumulated in the last 5000 years that are NOT potentially harmful!
(And that's just in 6500 individuals)

So once again an article that you cite goes AGAINST your point.

LMAO.
RealScience
5 / 5 (3) Mar 07, 2015
Over time, mutations supply the raw material from which new life forms evolve."

Is there a model for that?


You just cited an article that shows that the genomes of just 6500 people have 695,000 mutations that are NOT POTENTIALLY HARMFUL that have ACCUMULATED in just 5000 years, and you still wonder if there is a model for mutations supplying the raw material from which new life forms evolve?

ROTFLMAO!
JVK
1 / 5 (2) Mar 08, 2015
the genomes of just 6500 people have 695,000 mutations that are NOT POTENTIALLY HARMFUL


How does population-wide fixation of the mutations occur that pseudoscientists claim is linked to the evolution of a new species?

See for comparison to whatever ridiculous idea you think makes sense to science idiots: "System-wide Rewiring Underlies Behavioral Differences in Predatory and Bacterial-Feeding Nematodes" http://linkinghub...12015000

Reported as: http://phys.org/n...ing.html

"...each of the 20 neurons in Pristionchus pacificus could be correlated to an exact equivalent in Caenorhabditis elegans.... the evolutionary distance between the two worm species is over 200 million years and they differ markedly in feeding behaviour and in the anatomy of their mouth parts."

I just cited an example of nutrient-dependent pheromone-controlled ecological adaptation in nematodes.
RealScience
5 / 5 (3) Mar 08, 2015
How does population-wide fixation of the mutations occur...


As a general rule it only does for mutations that are significantly beneficial even when two copies are present in a genome. You have even cited a paper on the mathematics of this: http://www.nature...417.html


"...each of the 20 neurons in Pristionchus pacificus could be correlated to an exact equivalent in Caenorhabditis elegans.... the two worm species ... differ markedly in feeding behaviour..."

I just cited an example of nutrient-dependent pheromone-controlled ecological adaptation in nematodes.

You cite the remarkable one-to-one equivalence of their neurons as an example of a nutrient-dependent phenomenon?
Their diets are RADICALLY different - one grazes on tiny single bacterial cell and the other chows down on multicellular creatures roughly its own size!
RealScience
5 / 5 (3) Mar 08, 2015
For example, you would have done much better to claim that the re-wiring was nutrient dependent rather than that the correspondence of cells was nutrient dependent.

But you seem to think that everything is nutrient dependent, so it looks like you weren't being choosy.
JVK
1 / 5 (2) Apr 13, 2015
You just cited an article that shows that the genomes of just 6500 people have 695,000 mutations that are NOT POTENTIALLY HARMFUL that have ACCUMULATED in just 5000 years, and you still wonder if there is a model for mutations supplying the raw material from which new life forms evolve?


Also,
I just cited an example of nutrient-dependent pheromone-controlled ecological adaptation in nematodes.


Now I'll cite this:
Mountain gorillas: Lots of deleterious genetic variation disappeared from population thanks to inbreeding "...were surprised to find that many harmful genetic variations had been removed from the population through inbreeding, and that mountain gorillas are genetically adapting to surviving in small populations." http://www.scienc...3031.htm

Mutations are removed but biologically uniformed science idiots think they are fixed and that they cause new species to evolve.
JVK
1 / 5 (2) Apr 13, 2015
you seem to think that everything is nutrient dependent


Not everything. Every living thing. That fact is consistent with Darwin's "conditions of life." So does the fact that you are a biologically uninformed science idiot. As long as someone feeds you, you will continue to be a biologically uninformed science idiot.
JVK
1 / 5 (2) Apr 13, 2015
"Johnson and her colleagues have now discovered, however, that not only can giant evolutionary leaps happen, but they can do so in a reproducible way."

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

Excerpt: "The results highlight the importance of gene duplication in evolution, said Hughes, and the ability of the resulting diverged proteins to "moonlight" in roles aside from their main function. Indeed, said Jeff Barrick of the University of Texas in Austin who was not involved in the work, such cross-talk gives organisms "greater robustness," allowing them "to restore a function even though they are missing a genetic part."

Gene duplication is nutrient-dependent and fixation of the amino acid substitutions that led to the de novo re-creation of the flagellum exemplifies a pheromone-controlled ecological adaptation.
anonymous_9001
5 / 5 (3) Apr 13, 2015
There is not known to the science even one useful mutation


I've already given you many examples. Stop lying.

Gene duplication is nutrient-dependent and fixation of the amino acid substitutions that led to the de novo re-creation of the flagellum exemplifies a pheromone-controlled ecological adaptation.


What evidence is there of a pheromone change in the rapid flagella evolution paper?
JVK
1 / 5 (2) Apr 13, 2015
What evidence is there of a pheromone change in the rapid flagella evolution paper?


Thanks for asking.

The physiology of reproduction is nutrient-dependent and fixation of the amino acid substitutions is controlled by pheromones. Because every serious scientist knows that, they may have failed to mention it. Most serious scientists do not care what biologically uninformed science idiots believe can be meaningfully interpreted from the meaningless results of mutagenesis experiments.

...which are beneficial mutations that are recognized by the international scientific community?


Andrew Jones was taught at Carthage College to ignore the fact that no beneficial mutations are recognized by the international scientific community. He became so convinced of the pseudoscientific nonsense he was taught that he thinks his examples are recognized by serious scientists.
anonymous_9001
5 / 5 (3) Apr 13, 2015
Remind me please


For starters:

http://www.biomed...48/9/302
http://www.geneti...621.full
http://www.nature...77a.html
http://www.scienc...13.short
http://www.scienc...02008965
http://www.geneti...15.short
http://www.pnas.o...13.short
http://www.scienc...19.short
http://www.nature...925.html
http://www.ncbi.n...3913886/

The last one should be of particular interest to Kohl, because it's the observation of mutations being fixed in something that doesn't even have pheromones.
JVK
1 / 5 (2) Apr 13, 2015
Plants do not produce pheromones and yet ecological variation is linked from their nutrient-dependent physiology of reproduction via the conserved molecular mechanisms that also link the virulence of viruses to ecological adaptations via single amino acid substitutiions.

When serious scientists see a pattern of biologically-based cause and effect that links the de novo creation of light-induced amino acids to substitutions that differentiate cell types in all genera, they stop touting the pseudoscientific nonsense of evolutionary theories.

If serious scientists had not stopped touting that pseudoscientific nonsense during the past two decades there would be nothing known about any aspect of "precision medicine." The links between metabolic networks and genetic networks are clearly nutrient-dependent and pheromone controlled in all animals. See for example, our 1996 review: http://www.hawaii...ion.html
JVK
1 / 5 (2) Apr 13, 2015
http://www.ncbi.n...3913886/
...it's the observation of mutations being fixed in something that doesn't even have pheromones.


Excerpt:
Reverse genetic techniques allow large-scale manipulations of the genetic code of viruses, such as switching codons whilst leaving the amino acid sequence intact. Codon switching can increase the percentage of mutations that are non-synonymous, thereby decreasing the number of neutral neighbors and reducing the robustness of a virus population (Lauring et al., 2012).


Thanks for the citation.

It may help others realize that only a biologically uniformed science idiot would try to separate the fixation of a mutation from how it supposedly is beneficial to a population of conspecifics with reduced robustness.

Hopefully, if anyone else is foolish enough to share your ridiculous beliefs in a theory, they will recognize their ignorance and begin to learn about top-down causation.
anonymous_9001
5 / 5 (3) Apr 13, 2015
It may help others realize that only a biologically uniformed science idiot would try to separate the fixation of a mutation from how it supposedly is beneficial to a population of conspecifics with reduced robustness.


What do you mean? They observed fixation of two mutations of differing benefit in separate populations.

Whereas this identical mutation fixed in all of the independently evolving robust populations, it was absent in some brittle populations, which instead fixed a less beneficial mutation. We concluded that robust populations adapted faster to the environmental change, and more easily accessed mutations of large benefit.
JVK
1 / 5 (1) Apr 13, 2015
What do you mean? They observed fixation of two mutations of differing benefit in separate populations.


I mean that mutations perturb protein folding and lead to a lack of robustness, not to adaptations. That's why mutations are consistently linked to physiopathology instead of the physiology of nutrient-dependent pheromone-controlled reproduction.

They showed one mutation was not as bad as another and decided to claim that fixation of the less deleterious mutation must be adaptive. That shows how theoretical nonsense begets more theoretical nonsense. No one stops to ask: "Is there a model for that?"

Instead, they would rather believe in the mathematical representations of biologically uninformed population geneticists or other theorists.

anonymous_9001
5 / 5 (3) Apr 13, 2015
Neither were deleterious... They were both beneficial, one being more than the other, but both increased in survivability. Again, reading comprehension would do wonders for you.

The robust populations evolved faster to withstand the disturbance, relative to the less robust (brittle) populations. The robust populations also achieved relatively greater thermotolerance by the end of the experimental evolution. Sequencing revealed that thermotolerance occurred via a key mutation in gene P5 (viral lysis protein), previously shown to be associated with heat shock survival in the virus.


Look at Figure 3 before you embarrass yourself even further.
JVK
1 / 5 (1) Apr 13, 2015
The robust populations evolved faster to withstand the disturbance...


I've had enough of your nonsense. Mutations cannot be linked to the evolution of cell type differentiation and increasing organismal complexity. They perturb protein folding and are linked to physiopathology when they accumulate instead of being eliminated by DNA repair mechanisms.
anonymous_9001
5 / 5 (3) Apr 13, 2015
That's not nonsense, that's direct-as-can-be evidence and observation. For someone that claims so much that people who disagree with him merely say "nuh-uh", you sure are doing a lot of exactly that.
Vietvet
5 / 5 (2) Apr 13, 2015


I've had enough of your nonsense. Mutations cannot be linked to the evolution of cell type differentiation and increasing organismal complexity.


The evidence says otherwise, despite your delusional rantings.
JVK
1 / 5 (1) Apr 14, 2015
What experimental evidence says anything other than this?

...where there were networks of RNA-mediated interactions, natural selection could have led to some RNA molecules responding to changes in conditions in a way that inhibited the activities of other molecules with a similar sequence. They might have modified the structure of these molecules by base-pairing with them, for example. Later in evolutionary history, as the division of labor between nucleic acids (eventually DNA) as information carriers and proteins as the main enzymes and regulatory molecules increased, vestiges of earlier RNA control systems may have remained. These could have become modified to fit the new information system and defend it against foreign RNA and DNA sequences.


Please tell theorists if any experimental evidence of biologically-based cause and effect suggests anything else, They need it to support their ridiculous claims about mutations and evolution.
anonymous_9001
5 / 5 (1) Apr 14, 2015
I gave you direct evidence with that virus paper. It's not my problem that you're just ignoring it because it supports something you claim is impossible.

I'll also refer you back to my post from 20 hours ago:

For starters:

http://www.biomed...48/9/302
http://www.geneti...621.full
http://www.nature...77a.html
http://www.scienc...13.short
http://www.cell.c...6-5?cc=y
http://www.geneti...15.short
http://www.pnas.o...13.short
http://www.scienc...19.short
http://www.nature...925.html
http://www.ncbi.n...3913886/
JVK
1 / 5 (1) Apr 14, 2015
Continued attempts to throw more garbage into this discussion or to simply regurgitate the same garbage, rather than discuss how virus-driven cell type differentiation occurs, are futile.

You know nothing about cell type differentiation, and that is a common problem among theorists and biologically uninformed science idiots who know nothing about how to link physics, chemistry, and conserved molecular mechanisms from ecological variation to ecological adaptation.

I'll also refer you back to my post from 20 hours ago


I'll refer you to my two decades of published works and to http://rna-mediated.com/
anonymous_9001
5 / 5 (1) Apr 14, 2015
Irony is you talking about regurgitating garbage and then posting a link to your new site where all you've done is copied and pasted over everything from your old site.
JVK
1 / 5 (1) Apr 14, 2015
The new site is focused on RNA-mediated events.

250 posts include some of the 1200 from the sites that link pheromones to the nutrient-dependent control of RNA-mediated events that link metabolic networks to genetic networks in all genera via the biophysically constrained chemistry of protein folding.

How are metabolic networks and genetic networks linked to increasing organismal complexity in your mutagenesis experiements? Do you realize that evolutionary theorists have missed out on everything known to serious scientists about "Precision Medicine," which links nutritional epigenetics to pharmacogenomics in my published works (e.g., via amino acid substitutions that determine cell types)?

Oppositional COMT Val158Met effects on resting state functional connectivity in adolescents and adults http://dx.doi.org...4-0895-5
anonymous_9001
5 / 5 (1) Apr 14, 2015
Evolutionary Constraint and Adaptation in the Metabolic Network of Drosophila:

http://mbe.oxford...37.short

http://www.ncbi.n...2785887/

We also demonstrate that networks with the same phenotype form large sets that can be traversed through single mutations, and that single mutations of different genotypes with the same phenotype can yield very different novel phenotypes.


http://www.nature...233.html

http://link.sprin...7#page-1

http://genome.csh...05.short
JVK
1 / 5 (1) Apr 14, 2015
Alzheimer's study suggests immune cells chew up an important amino acid.
http://neuroscien...rs-1952/

Pheromones and the luteinizing hormone for inducing proliferation of neural stem cells and neurogenesis http://www.freshp...8009.php

Nutrient-dependent/pheromone-controlled adaptive evolution: a model.
http://www.ncbi.n...24693353

"The honeybee already serves as a model organism for studying human immunity, disease resistance, allergic reaction, circadian rhythms, antibiotic resistance, the development of the brain and behavior, mental health, longevity, diseases of the X chromosome, learning and memory, as well as conditioned responses to sensory stimuli (Kohl, 2012)."

All of the above are linked via RNA-directed DNA methylation and RNA-mediated amino acid substitutions to nutrient-dependent cell type differentiation in all genera. Mutations are linked only to physiopathology.
JVK
1 / 5 (1) Apr 14, 2015
František Baluška: Evolutionary Science 'Stuck' on Wrong Track, Situation 'Out of Control'
http://www.huffin...592.html

Excerpt: "František Baluška: Any theory of evolution must take into consideration the communication between cells, sensory aspects, behavior and cognition. For me the membranes and the energy flows through the membranes are as important, or even more important, than the genetics, DNA. Without membranes there is no life on Earth."

Without receptors in membranes, the anti-entropic epigenetic effects of nutrients could not lead from virus-induced entropic elasticity to nutrient-dependent RNA-directed DNA methylation and RNA-mediated amino acid substitutions that stabilize the organized genomes of all genera via the biophysically constrained chemistry of protein folding.

Behavior is receptor-mediated. It is not mutation-driven. Mutations cause physiopathology, not evolution.
anonymous_9001
5 / 5 (1) Apr 15, 2015
Arginine deficiencies are bad and various chemicals control cell growth? No way! Completely irrelevant to the topic of evolution.

As I've told you before, you misappropriate the honeybee model in attempting to apply it to evolution. Altering expression and development over the course of one lifetime is nowhere near the same thing as genetic changes occurring over subsequent generations.

Another Huffington Post opinion article about somebody downplaying DNA's importance? All he's saying is that when and how often genes are expressed is just as important as the genes themselves. Everybody is well aware of this. It doesn't disprove Darwinism, it just adds another level of selection. Regulation of a gene is just as important to the resulting phenotype as the sequence of the gene.

virus-induced entropic elasticity


What does this mean? Entropic elasticity is merely a polymer's tendency to resist stretch.

http://en.wikiped...al_chain
anonymous_9001
5 / 5 (1) Apr 15, 2015
Mutations cause physiopathology, not evolution


Unfortunately for you, all 15 links I've posted so far directly refute that.
JVK
1 / 5 (1) Apr 15, 2015
How do mutations cause evolution?

Why do you think serious scientists are "Combating Evolution to Fight Disease" http://www.scienc...88.short

Beyond Genetic Evolution. A Conversation With Eva Jablonka
https://evolution...ablonka/

"...a good opportunity to move to the second dimension of evolution, epigenetics."

The epigenetic landscape is linked to the physical landscape of DNA by the biophysically constrained chemistry of nutrient-dependent RNA-directed DNA methylation and RNA-mediated amino acid substitutions that alter protein folding. The substitutions are fixed in organized genomes via the physiology of their reproduction.

Epigenetic top-down causation is not a "second dimension of evolution." Epigenetic effects on cell type differentiation link physics, chemistry, and conserved molecular mechanisms from ecological variation to ecological adaptations.
JVK
1 / 5 (1) Apr 15, 2015
mTORC1 controls protein synthesis
Re: amino acids (AAs)
AAs reportedly activate mTORC1 through the lysosome-associated machinery for AA sensing involving Rag GTP-binding proteins (Sancak et al., 2008), the scaffolding complex Ragulator (Bar-Peled et al., 2012; Sancak et al., 2010; Zoncu et al., 2011a), and vacuolar H+-adenosine triphosphatase (v-ATPase) (Zoncu et al., 2011b). The first essential step in AA-induced mTORC1 activation is its recruitment to lysosomes by Rag proteins, providing an activation platform on which mTORC1 colocalizes with GTP-bound Rheb (Sancak et al., 2008). Rheb is therefore necessary but insufficient for mTORC1 activation.
http://www.cell.c...)00112-4
They identified a protein that is a molecular link connecting Rheb-GTP to mTORC1 activation at lysosomes in AA responses. Depletion of the protein links a chain of interactions to mTORC1 inactivation.
JVK
1 / 5 (1) Apr 15, 2015
I reiterate: mTORC1 controls protein synthesis.

They claim:
The first essential step in AA-induced mTORC1 activation...


They are addressing the biophysically constrained chemistry of RNA-directed DNA methylation and RNA-mediated protein folding. The chemistry of RNA-mediated protein folding links ecological variation to ecological adaptation via amino acid sensing.

If their findings were placed into the context of my model of nutrient-dependent pheromone-controlled ecological adaptations, their links from AA sensing and metabolic networks to genetic networks would fit perfectly and differentiate between mutations that cause physiopathology and amino acid substitutions linked to the increasing organismal complexity of biodiversity.

Theorists can now attempt to explain (and fail to explain) how the evolution of High Mobility Group Nucleosome-Binding Proteins and vertebrate chromatin specialization links mutations to the evolution of biodiversity.
JVK
1 / 5 (1) Apr 15, 2015
Re:
how the evolution of ... Nucleosome-Binding Proteins and vertebrate chromatin specialization links mutations to... biodiversity.


"MCRS1 was initially described as a nucleolar protein p120 interactor (Ren et al., 1998), associated with transcription regulation (Andersen et al., 2010; Ivanova et al., 2005; Lin and Shih, 2002; Wu et al., 2009). However, it participates in other processes, including cellular senescence (Hsu et al., 2012), cell division, and survival by interacting with the centrosomal protein Nde1 (Hirohashi et al., 2006) and is reportedly an essential RanGTP-regulated factor for bipolar spindle assembly protecting them from depolymerization (Meunier and Vernos,
2011) MCRS1 regulates mTORC1 independently of microtubule networks and its nuclear function argues that cells may contain several MCRS1 pools with different functions, without excluding a general role of MCRS1 in scaffolding small GTPase proteins."

What argues for the role of mutations?

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