Mutant cells that can't copy DNA somehow keep dividing when they shouldn't—with disastrous consequences

August 6, 2015 by Robert Perkins, University of Southern California
Sequential images of abnormal divisions in a mutant cell leading to abnormal nuclei and chromosome rearrangement. Chromosomes are displayed in pink, cell membranes in green. The cell undergoes two aberrant divisions. Credit: Susan Forsburg

Researchers at USC have developed a yeast model to study a gene mutation that disrupts the duplication of DNA, causing massive damage to a cell's chromosomes, while somehow allowing the cell to continue dividing.

The result is a mess: Zombie cells that by all rights shouldn't be able to survive, let alone divide, with their chromosomes shattered and strung out between tiny micronuclei. Sometimes they're connected to each other by ultrafine DNA bridges. (Imagine tearing apart a hot pizza – these DNA bridges are like strings of cheese still draping between the separated pieces.)

Frequently, the micronuclei – which are thought to retain the most damaged portions of the DNA – rejoin the parent nuclei and incorporate mutations into the survivors.

The mutation has been associated with cancer in mice, and micronuclei are often found in human cancer cells. With their new , researchers hope to learn more about each.

"Using a simple yeast system, we have developed a powerful genetic model to investigate a recently identified characteristic of human cancer cells," said Susan Forsburg, senior author of an article about the research that will appear online ahead of print in the journal Molecular Biology of the Cell on August 5. "This will enable us to rapidly identify genes responsible for this abnormal division."

Since the genes that regulate division in human and are the same, this simple organism provides a tool for human cell discovery, Forsburg said.

DNA is vulnerable to damage when it's unzipped into two single strands for replication by a cell's MCM helicase (a cellular component essential to DNA replication). Typically, the single stranded DNA triggers repair of damage by special enzymes, or – in extreme cases – drives the damaged cell to suicide. Either way, mitosis () is halted while the issue is dealt with.

But in , despite the damaged DNA, the cells continue to divide—creating tumors full of genetic mutations. In this study, a mutation in the yeast's MCM helicase triggered responses similar to those in mammals where mutations in this gene are associated with cancer and the formation of micronuclei.

To study the phenomenon, Forsburg and lead author Sarah Sabatinos collected videos of the damaged cells dividing so that they could maintain continuous monitoring of individual cells, and record cell division from beginning to end. They watched what happened in the mutant in real time. Then, they used a super-resolution microscope at USC that generates 3-D images of objects at the nanometer scale, to examine the damage structures in crisp detail.

"The devil's in the division. In , we're able to see that these mutant ignore the damage caused during DNA replication, which results in the creation of unusual structures like micronuclei," said Sabatinos, who conducted the research as a post-doc at USC, and is now an assistant professor at Ryerson University in Toronto.

Their work will inform future studies into how a cancer cell evades biological checkpoints that should halt its division and spread.

Explore further: Some cells don't know when to stop

More information: The article can be found online here: www.molbiolcell.org/content/ea … E15-05-0318.abstract

Related Stories

Some cells don't know when to stop

November 19, 2012

Certain mutated cells keep trying to replicate their DNA—with disastrous results—even after medications rob them of the raw materials to do so, according to new research from USC.

A novel DNA damage alarm

June 25, 2015

How does our body keep its DNA intact? Researchers at Erasmus MC have just found a new piece of this puzzle. They discovered a novel alarm that cells use to signal DNA damage. "We already knew that DNA damage triggers an ...

Dual systems key to keeping chromosomes intact

March 7, 2013

USC scientists have discovered how two different structural apparatuses collaborate to protect repetitive DNA when it is at its most vulnerable – while it is being unzipped for replication.

Recommended for you

Where is the universe hiding its missing mass?

February 15, 2019

Astronomers have spent decades looking for something that sounds like it would be hard to miss: about a third of the "normal" matter in the Universe. New results from NASA's Chandra X-ray Observatory may have helped them ...

What rising seas mean for local economies

February 15, 2019

Impacts from climate change are not always easy to see. But for many local businesses in coastal communities across the United States, the evidence is right outside their doors—or in their parking lots.

Tiny particles can switch back and forth between phases

February 15, 2019

Three years ago, when Richard Robinson, associate professor of materials science and engineering, was on sabbatical at Hebrew University in Israel, he asked a graduate student to send him some nanoparticles of a specific ...

99 comments

Adjust slider to filter visible comments by rank

Display comments: newest first

JVK
1 / 5 (4) Aug 06, 2015
At the advent of sexual reproduction in yeast, their morphological and behavioral phenotypes are nutrient-dependent and pheromone-controlled via the physiology of their reproduction. So far as I know that is how all cell type differentiation is controlled in species from microbes to man.

Nutrient-dependent RNA-mediated gene duplication and RNA-mediated amino acid substitutions appear to link cell type differentiation from the epigenetic landscape to the physical landscape of DNA in all living genera.

Isn't it likely that viruses have caused the damage to the problematic DNA and that the damage is not being repaired as it typically would be via RNA-mediated events linked from ecological variation to ecological speciation via the conserved molecular mechanisms of biophysically constrained protein folding chemistry that is perturbed by viruses?
JVK
1 / 5 (4) Aug 06, 2015
Excerpt: "The devil's in the division. In real time, we're able to see that these mutant cells ignore the damage caused during DNA replication, which results in the creation of unusual structures... "

My comment: I hesitate to invite the trolls by mentioning that this appears to be consistent with a young earth creationist perspective on virus-perturbed cell type differentiation. http://www.icr.or...cle/8661

Excerpt: "In other words, mammalian viruses may not have existed at all before the Curse, but after mankind's sin may have been allowed to develop from DNA sequence already present in the now-fallen people and animals of the earth. Again, cutting-edge genome research confirms the Genesis account of origins."

If the devil's in the perturbed cell type division, what led to the division in the first cell with DNA that replicated sans the pathology?

For fun, let's see what the trolls claim about that.
JVK
1 / 5 (4) Aug 06, 2015
Excerpt: "...they used a super-resolution microscope at USC that generates 3-D images of objects at the nanometer scale, to examine the damage structures in crisp detail."

Is this "word play?" My first impression links it from the CRISPR-Cas9 technology to 3-D protein folding that is perturbed by viruses. The "crisp" details and "3-D" imagery may be the key to understanding the devil is in the details of perturbed RNA-mediated cell type differentiation.

See also: A 3D Map of the Human Genome at Kilobase Resolution Reveals Principles of Chromatin Looping http://www.cell.c...)01497-4
JVK
1 / 5 (4) Aug 06, 2015
I'll try to keep this simple and cite Wikipedia. https://en.wikipe...Helicase

"The common function of helicases accounts for the fact that they display a certain degree of amino acid sequence homology; they all possess sequence motifs located in the interior of their primary structure, involved in ATP binding, ATP hydrolysis and translocation along the nucleic acid substrate. The variable portion of the amino acid sequence is related to the specific features of each helicase.

The presence of these helicase motifs allows putative helicase activity to be attributed to a given protein, but does not necessarily confirm it as an active helicase. Conserved motifs do, however, support an evolutionary homology among enzymes."

If you can link stress from metabolic networks to dysfunctional chromosomal rearrangements via mutations in genetic networks, you can probably link the lack of stress to ecological speciation. If not, there's a model for that!
JVK
1 / 5 (4) Aug 06, 2015
Where are the trolls who support the claims of PZ Myers that include his claim that I am a crank?

"One crank dies, another rises to take his place"
http://freethough...s-place/

Excerpt: "Behold James Vaughn Kohl.

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 that most people here were taught to believe is the theory of evolution.

That theory is far too ridiculous to be anything but a joke..."
jsdarkdestruction
5 / 5 (7) Aug 07, 2015
Rest assured we are here. I think the vast majority of us have grown tired of your games and insults so we don't bother. Also, you do a very thorough job of showing everyone how little you know and your credibility and reading comprehension issues for us. Linking to things that at best don't agree and at worst totally contradict your claims does the work for us.
Vietvet
5 / 5 (7) Aug 07, 2015
jsdarkdestruction.

I've been thinking along the same lines. Thanks for giving voice to what I'm sure are the views of 99.9999999999% of the readers at PO.
anonymous_9001
5 / 5 (6) Aug 07, 2015
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.


How do nutrients enter a cell to affect splicing before they even have a transport protein? In Lenski's, the change that occurred was to the oxic translation of the citrate transporter. How did citrate enter the cell before the promoter shift?

Now, as for splicing- splicing is the process of removing introns from pre-mRNA following transcription. The key word here is REMOVING. Removing is not the same as replacing, aka substituting. AA substitutions stem from codon changes in the DNA, whereas splicing happens to pre-mRNA, not DNA.
JVK
1 / 5 (4) Aug 07, 2015
Chromosomal rearrangements are the obvious link to biodiversity that is nutrient-dependent and pheromone controlled via the RNA-mediated fixation of amino acid substitutions that determine the cell types of all vertebrates and invertebrates.

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

The phylogenetic utility and functional constraint of microRNA flanking sequences
http://rspb.royal...20142983

Role of olfaction in Octopus vulgaris reproduction
http://www.scienc...14004006

If you are not going to accept the most obvious of all biologically-based facts, there is no need to explain anything about nutrient-dependent alternative splicings or how they are perturbed by viral microRNAs that link perturbed protein folding to pathology.

I'm interested in helping the biologically informed.
JVK
1 / 5 (4) Aug 07, 2015
Why aren't the trolls explaining anything about how Lenski's "mutations" could be linked to "evolution" in the context of what is known about virus-perturbed protein-folding and pathology?

Moreover, why don't the trolls ever explain HOW anything that they think supports their ridiculous opinions actually seems to support them?

Why must we wait for someone like Koonin to tell them that their theories failed to include anything known to serious scientists about RNA-mediated cell type differentiation?

http://www.huffin...216.html
Excerpt: "The entire evolution of the microbial world and the virus world, and the interaction between microbes and viruses and other life forms have been left out of the Modern Synthesis..."

Would we not all expect all serious scientists to immediately think about what was missed when they were taught to believe in pseudoscientific nonsense?
anonymous_9001
5 / 5 (5) Aug 07, 2015
If you are not going to accept the most obvious of all biologically-based facts, there is no need to explain anything


That's not how scientific inquiry works. There's no need for more detail yet if your simple explanation doesn't make sense in the first place. These are basic and fundamental questions that are at the very foundation of your model. If you can't explain these, it's ridiculous to expect you to explain even more in depth.

It's like you're asking me to believe you can integrate f(x)=2x^4+x^2+3 but then not being able to demonstrate you can solve a simple algebra equation for x.

How do nutrients enter a cell to affect splicing before they even have a transport protein? In Lenski's, the change that occurred was to the oxic translation of the citrate transporter. How did citrate enter the cell before the promoter shift?
JVK
1 / 5 (3) Aug 07, 2015
I wrote: "If you can link stress from metabolic networks to dysfunctional chromosomal rearrangements via mutations in genetic networks, you can probably link the lack of stress to ecological speciation. If not, there's a model for that!"

Your criticisms of my model show that you know nothing about how cell type differentiation occurs.
http://www.ncbi.n...4049134/

Do not pretend to know how scientific inquiry works. Koonin just told everyone that scientific inquiry had nothing to do with the "Modern Synthesis" and yet you cited PZ Myers's blog posts in your review -- after he attacked me for my accurate representations of biologically-based cause and effect in the context of chromosomal rearrangements.

When facts don't make sense to you, please continue to try to put them into the context of ridiculous theories. Do not ask me to explain anything further to you about physics, chemistry, or conserved molecular mechanisms.

anonymous_9001
5 / 5 (5) Aug 07, 2015
When facts don't make sense to you, please continue to try to put them into the context of ridiculous theories. Do not ask me to explain anything further


That's the complete antithesis of logic and science. If something is unclear, explain it so that proper discussion can be facilitated instead of refusing to clarify your statements and impeding debate.

Accurate representations? Claiming a nutrient can enter a cell before a transport protein is even present is entirely inaccurate. How did the citrate enter the E. coli before the transporter was expressed? That's impossible.

You're aware of the chemical properties of molecules that can penetrate the lipid bilayer, right? You claim expertise in chemistry, so I assume you're aware that citrate is not on that list.
JVK
1 / 5 (3) Aug 07, 2015
Re: If something is unclear, explain it so that proper discussion can be facilitated instead of refusing to clarify your statements and impeding debate.

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

Viruses perturb nutrient dependent RNA-mediated thermodynamic cycles of protein biosynthesis and degradation. Viral microRNAs are linked to all pathology. Amino acid substitutions are linked to cell type differentiation in all living genera.

What's not clear is how neo-Darwinian theory explains RNA-mediated cell type differentiation and speciation linked to biodiversity.

If you can't explain how, please ask Koonin to explain it so that others may understand why he claims he is not abandoning the neo-Darwinian pseudoscientific nonsense.

Claiming a nutrient can enter a cell before a transport protein is even present is entirely inaccurate.


What are you claiming?

Vietvet
5 / 5 (4) Aug 07, 2015


Accurate representations? Claiming a nutrient can enter a cell before a transport protein is even present is entirely inaccurate. How did the citrate enter the E. coli before the transporter was expressed? That's impossible.

You're aware of the chemical properties of molecules that can penetrate the lipid bilayer, right? You claim expertise in chemistry, so I assume you're aware that citrate is not on that list.


@JVK

Instead of answering the the questions, you deflect. That's what stupid young earth creationists do.
anonymous_9001
5 / 5 (6) Aug 07, 2015
What are you claiming?


I'm asking you how citrate got in before its transporter was even expressed. The phospholipid bilayer is selectively permeable to non-polar molecules. Citrate relies on a transport protein to get in.
JVK
1 / 5 (3) Aug 08, 2015
What are you claiming?


How were mutations involved in any aspect of the links from physics to chemistry and biology by what is known about the conserved molecular mechanisms of protein folding?
JVK
1 / 5 (3) Aug 08, 2015
you deflect. That's what stupid young earth creationists do.


No. I tell him he cannot understand any aspect of cell type differentiation because he has been taught to believe in pseudoscientific nonsense.

See A quantum theory for the irreplaceable role of docosahexaenoic acid in neural cell signalling throughout evolution http://www.ars.us...2012.pdf

See also: Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems http://figshare.c...s/994281
anonymous_9001
5 / 5 (6) Aug 08, 2015
How did citrate get in to induce the translocation before its transporter was expressed? This is a basic molecular biology question that you should be able to quickly and easily explain.
JVK
1 / 5 (3) Aug 08, 2015
...a basic molecular biology question...
should be answered by theorists who think we evolved via mutations that changed nutrient-dependent RNA-mediated cell types into the cell types of a different species -- even though no experimental evidence of biologically-based cause and effect suggests that has ever happened since the origins of RNA-mediated cause and effect.

Any theorist who first looks at the question from the perspective of Schrodinger will see that de Vries definition of "mutation" has since led to the end of all ridiculous theories touted by those who have settled into comfortable positions in the evolution industry and big bang cosmology industry where theories need not be supported by anything but more theories-- until someone asks about the role of viruses.

At that point, biologically uninformed science idiots like Andrew Jones (aka anonymous_9001) are exposed and begin to ask serious scientists about ecological adaptations.
anonymous_9001
4.8 / 5 (6) Aug 08, 2015
How did citrate get in to induce the translocation before its transporter was expressed?
JVK
1 / 5 (3) Aug 08, 2015
How did citrate get in to induce the translocation before its transporter was expressed?


This is a basic molecular biology question that you should be able to quickly and easily explain.


Please answer what you say is "...a basic molecular biology question..." in the context of what you know about molecular biology.

Something that you thought you knew led you to publish your "Criticisms of the nutrient-dependent pheromone-controlled evolutionary model" http://www.ncbi.n...4049134/

Nothing you have ever claimed indicates you know anything about the conserved molecular mechanisms of RNA-mediated cell type differentiation that we detailed in the molecular epigenetics section of our 1996 Hormones and Behavior review. From Fertilization to Adult Sexual Behavior html http://www.hawaii...ion.html

Did Lenski's "experiments" lead you to challenge our combined expertise?
anonymous_9001
5 / 5 (6) Aug 08, 2015
This cannot be any clearer. Citrate needs a transport protein to enter a cell. How did the citrate in Lenski's experiment enter the E. coli in order to cause the translocation before they expressed the transporter?
JVK
1 / 5 (3) Aug 08, 2015
Lenski's experiments led to the claim he was "The Man Who Bottled Evolution" http://www.scienc...90.short

That claim caused more serious scientists to join those who were already "Combating Evolution to Fight Disease" http://www.scienc...88.short

The result is "Personlized Medicine"

Serious scientists know Lenski exemplified obvious links between ecological variation and ecological adaptation, which are triggered by the innate immune system's response to stress. In the context of nutrient-dependent thermodynamic cycles of protein biosynthesis and degradation stress leads from ecological variation to ecological adaptation via the pheromone-controlled physiology of reproduction in species from microbes to man.

The physiology of reproduction links metabolic networks to genetic networks in all living genera.

That's why I often refer to Andrew Jones (aka anonymous_9001) as a biologically uninformed science idiot.
JVK
1 / 5 (3) Aug 08, 2015
Any three-step process that requires 1) potentiation to make a trait possible, 2) actualization to make the trait manifest, and 3) refinement that makes the trait functional, can now be placed into the context of the "re-evolved" bacterial flagellum (in 4 days), which links the nutrient-dependent pheromone-controlled fixation of RNA-mediated amino acid substitutions and RNA-mediated gene duplication to biodiversity in all genera via the conserved molecular mechanisms of biophysically constrained protein folding chemistry.

Attempts are futile when anyone tries to get me to explain anything that I've already explained in published and unpublished works to biologically uninformed science idiots. They refuse to begin to attempt to understand anything that occurs outside the context of mutations and evolution at a time when serious scientists know that nothing occurs in the context of mutations that doesn't link them to the perturbed protein folding of pathology.
Vietvet
5 / 5 (4) Aug 08, 2015
How did citrate get in to induce the translocation before its transporter was expressed?


JVK wont answer the question because he can't, it's beyond his knowledge and capabilities.
JVK
1 / 5 (3) Aug 08, 2015
I have questions about the knowledge and capabilities of Steven Taylor, who questioned my credibility in a post to Greg Bear's domain. http://www.gregbe...?id=8064

Questions about my knowledge and capabilities can be placed into the context of claims made by Greg Bear in three of his novels, since his claims, like mine, are fact-checked.

Thanks to Greg Bear for trying to explain what could go wrong to evolutionary theorists who have never considered the role that viruses play in causing genomic entropy.

See http://thedailysh...reg-bear
Vietvet
5 / 5 (4) Aug 08, 2015
How did citrate get in to induce the translocation before its transporter was expressed?


JVK wont answer the question because he can't, it's beyond his knowledge and capabilities.


You still haven't answered the question.

You have ZERO credibility.
anonymous_9001
5 / 5 (4) Aug 08, 2015
Attempts are futile when anyone tries to get me to explain anything that I've already explained in published and unpublished works


Oh? You've already explained how citrate got transported into the E. coli without a transporter? Where?

Here's a paper explaining how that system works:

http://jb.asm.org...abstract
JVK
1 / 5 (2) Aug 08, 2015
You have ZERO credibility.


How did you determine that? What about my award-winning reviews, published with others in 2001 and as a monograph/book chapter in 2006/7?
JVK
1 / 5 (3) Aug 08, 2015
Here's a paper explaining how that system works:


It was published 2 years after our Hormones and Behavior review, which linked the molecular epigenetics of cell type differentiation from yeasts to mammals via the biophysically constrained chemistry of nutrient-dependent pheromone-controlled RNA-mediated protein folding.

In 2000 Elekonich and Robinson linked our review to cell type differentiation in insects, and in 2005 Elekonich and Roberts linked it to life history transitions in the honeybee model organism. In 2014, the model was linked to all cell type differentiation in marine invertebrates, which others linked from all crustaceans to all insects via microRNAs.

Stop pretending that you do not know all this. You read my FB group posts at RNA-mediated https://www.faceb...ediated/ and you read my blog posts at http://rna-mediated.com/

Admit that you do not want others to realize how much ignorance you have displayed.
anonymous_9001
5 / 5 (5) Aug 08, 2015
That's fine and dandy, but how did citrate get into the E. coli before a transporter was present?
JVK
1 / 5 (3) Aug 09, 2015
Do not expect me to detail aspects of how the nutrient-dependent de novo creation of G protein-coupled receptors enables the epigenetic landscape to alter the physical landscape of DNA to someone who understands nothing about the thermodynamics of cell type differentiation and thinks that mutations lead to evolution.

You hide under the ridiculous veil of anonymity here, when you could be commenting or asking questions on my FB group and/or blog cite instead of attacking me elsewhere at every chance you get.

You are akin to an internet terrorist who wants only to destroy any effort by others to make scientific progress, which requires co-operation, not your ridiculous antagonism. Tell me again that those who are "Combating Evolution to Fight Disease" http://www.scienc...88.short have not been challenging the ridiculous assertions of neo-Darwinian pseudoscientific nonsense or that you are not fighting on the other side of ignorance.
anonymous_9001
5 / 5 (5) Aug 09, 2015
1. CitT is not a G protein-coupled receptor.
2. Lenski's experiment did not involve creation of a new receptor. It involved oxic expression of a normally anoxic operon due to a promoter translocation.
3. There's no way for citrate to have epigenetically effected that process because it had no way of entering the cell in the first place without CitT present.

Now that those facts have been established, answer the question. You've wasted more than 2 days avoiding it. It should take less than 5 minutes to write up a couple sentences. You're just sticking your fingers in your ears and yelling "LALALA" like a toddler because you're unable to answer me rather than unwilling.
JVK
1 / 5 (4) Aug 09, 2015
Stop pretending you are intelligent enough to understand anything I claim, and stop placing your misinterpretations of what I claim into the ridiculous context of your mutagenesis experiments and Lenski's works. You have not established any facts, and neither did Lenski. Only serious scientists have done that.

See for example: http://www.the-sc...ntities/

I commented there, also MORE THAN A YEAR AGO.

You're just sticking your fingers in your ears and yelling "LALALA" like a toddler because you're unable to answer me rather than unwilling.


I can't answer biologically uninformed science idiots in terms that they can understand. See for example your criticisms: http://www.ncbi.n...4049134/

And the response from Dr. Mouras: "...was subjected to standard peer review and the revised version was accepted by me after it had been accepted by both reviewers."
anonymous_9001
5 / 5 (6) Aug 09, 2015
1. CitT is not a G protein-coupled receptor.
2. Lenski's experiment did not involve creation of a new receptor. It involved oxic expression of a normally anoxic operon due to a promoter translocation.
3. There's no way for citrate to have epigenetically effected that process because it had no way of entering the cell in the first place without CitT present.

Answer the question.

I can't answer biologically uninformed science idiots in terms that they can understand.


Stop deflecting. How did citrate get in before CitT was expressed. CitT is REQUIRED for citrate uptake.
JVK
1 / 5 (3) Aug 09, 2015
How did citrate get in before CitT was expressed. CitT is REQUIRED for citrate uptake.


Where shall I start?

http://www.pnas.o...940.full
"The predicted seven-transmembrane α helices of ChR2 are characteristic for G protein-coupled receptors but reflect a different motif for a cation-selective ion channel. Finally, we demonstrate that ChR2 may be used to depolarize small or large cells, simply by illumination."

1. CitT is not a G protein-coupled receptor.


If I start from the light-induced de novo creation creation of amino acids and proceed with nutrient-dependent RNA-mediated protein folding chemistry that biophysically constrains cell type differentiation in all cell types of all individuals of all living genera via the physiology of reproduction, you're just going to ask me about citrate in E. coli again, aren't you?

2. Lenski's experiment did not involve creation of a new receptor.


What changed?
anonymous_9001
5 / 5 (4) Aug 09, 2015
http://www.pnas.o...940.full
"The predicted seven-transmembrane α helices of ChR2 are characteristic for G protein-coupled receptors but reflect a different motif for a cation-selective ion channel. Finally, we demonstrate that ChR2 may be used to depolarize small or large cells, simply by illumination."


CitT is not a channelrhodopsin.

you're just going to ask me about citrate in E. coli again, aren't you?


That depends on how flawed your representation is. Are you under the impression that CitT is a G protein-coupled receptor? If you try to refute Lenski and you don't even understand what the proteins involved are or how they work, I will ask again.

What changed?


I've told you many times and it's described in far more detail in his publications. An oxic promoter translocated to in front of the CitT operon, allowing it to be translated in the presence of oxygen. They began to express an existing channel, not a new receptor.

JVK
1 / 5 (3) Aug 09, 2015
If you try to refute Lenski and you don't even understand what the proteins involved...


There is no need to refute Lenski, since he has never provided experimental evidence of biologically-based cause and effect, which is nutrient-dependent and pheromone-controlled via RNA-mediated events in E. coli. Biophysically constrained RNA-mediated gene duplication and RNA-mediated amino acid substitutions are linked to the organized genomes of all genera.

For comparison, Lenski's claims can be compared to someone saying: "Look, these bacteria mutated and "re-evolved" their flagella "over-the-weekend." Let's report that in Science magazine and see if anyone believes it so we can get some funding that might otherwise have gone to Lenski's group.

Evolutionary resurrection of flagellar motility via rewiring of the nitrogen regulation system http://www.scienc...abstract
JVK
1 / 5 (3) Aug 09, 2015
An oxic promoter translocated to in front of the CitT operon, allowing it to be translated in the presence of oxygen. They began to express...


Where did the energy come from for all this?

Are you under the impression that CitT is a G protein-coupled receptor?


Of course not. I'm under the impression that all cell type functions are energy dependent.
richmadjones
5 / 5 (5) Aug 09, 2015
Answer the question, James.
JVK
1 / 5 (3) Aug 10, 2015
Why are biologically uninformed science idiots so demanding? They have no answers to any questions because they understand nothing about cell type differentiation.

But here, they want me to explain everything about light harvesting to ecological speciation -- as if I hadn't already done it with the help of many other serious scientists.

Even Richard Lenski could probably not imagine how his works would continue to inspire these science idiots during the time everyone else has been linking ecological variation to ecological adaptations in the context of nutrient-dependent RNA-mediated amino acid substitutions and chromosomal rearrangements.
anonymous_9001
5 / 5 (4) Aug 10, 2015
More deflection. Big surprise.
jsdarkdestruction
5 / 5 (3) Aug 10, 2015
Jvk, why do you feel the need to call everyone idiots? You are acting like a child. Did your mother not teach you manners and politeness and how to be a big boy?
JVK
1 / 5 (2) Aug 10, 2015
Thanks for asking. I don't call everyone an idiot.

I use the term biologically uninformed for those who are interested in becoming informed.

Biologically uninformed science idiots are special; they refuse to learn anything more than what they were taught to believe by other biologically uninformed science idiots.

https://en.wikipe...ki/Idiot Excerpt: "An idiot... someone who acts in a self-defeating or significantly counterproductive way."

Example: anonymous_9001 (aka Andrew Jones)

See for comparison http://www.scienc...0.short:

Excerpt: Many microbial opsin genes encode proteins that, upon absorption of a photon, move ions across the cell membrane. The resulting ion flow can activate, inhibit, or modulate cells depending on the type, direction, and quantity of the ion being conducted (1).

The reviewers do not claim that microbes mutate and evolve; they link quantum mechanics to RNA-mediated cell type differentiation.
JVK
1 / 5 (2) Aug 10, 2015
In 1943, Schrodinger may have been the first to intuitively link quantum mechanics to cell type differentiation via the sun's biological energy.

In 1973, Dobzhansky did it with an example of a single amino acid substitution that differentiated the cell types of 3 primate species.

Since 1992, I've linked pheromone-controlled reproductive physiology to ecological adaptations without mention of the fact that adaptations are nutrient-dependent (until 2013) in species from microbes to man.

In 1996, we detailed the required links from RNA-mediated cell type differentiation to differences in the morphological and behavioral phenotypes of species from microbes to mammals. Our model was subsequently extended to insects and the life history transitions of the honeybee model organism before also being extended to marine invertebrates via a link from the substitution of achiral glycine in the GnRH decapeptide.

No one but Andrew Jones has asked about citrate in E. coli
anonymous_9001
5 / 5 (4) Aug 10, 2015
Up to 3 days avoiding what should be an incredibly simple question.

Let's go over this again, shall we? Walk us through it.

You've stated that citrate epigenetically affected the E. coli, causing them to express CitT. Is this correct?
JVK
1 / 5 (2) Aug 10, 2015
No. It is not correct. It is a ridiculous misinterpretation of everything I have clearly stated in a series of published reviews, which link nutrient-dependent amino acid substitutions to cell type differentiation in all living genera via the physiology of reproduction.

I wrote:

No one but Andrew Jones has asked about citrate in E. coli


Why do you think no one else has asked? Could it be that you are the only biologically uninformed science idiot who is left to antagonize me when it has only been 14 months since your criticisms of my 2013 review were published as a subtle joke for delivery to serious scientists who already knew how foolish evolutionary theorists can be?

http://www.ncbi.n...4049134/
JVK
1 / 5 (2) Aug 10, 2015
http://www.amazon...07604664

Forward by Roger Penrose, who wrote: "How often do we still hear that quantum effects can have little relevance in the study of biology, or even that we eat food in order to gain energy?"

My comment: Instead, here we have a biologically uninformed science idiot telling us "An oxic promoter translocated to in front of the CitT operon, allowing it to be translated in the presence of oxygen. They began to express an existing channel, not a new receptor."

And then, he asks:

You've stated that citrate epigenetically affected the E. coli, causing them to express CitT. Is this correct?

If you want to learn anything about how quantum mechanics is linked to quantum biology via quantum smell, and from the de novo creation of nucleic acids to RNA-mediated cell type differentiation in all living genera, see http://rna-mediated.com/ or google "RNA mediated"
anonymous_9001
5 / 5 (3) Aug 11, 2015
No. It is not correct.


Alright, so then what did the citrate do then and what specific changes did it make? Are you denying that CitT was under the influence of an oxic promoter or are you denying that they began expressing CitT? Here's a diagram of the observed sequence changes:

http://www.nature...f2.2.jpg

My comment: Instead, here we have a biologically uninformed science idiot telling us


I'm just relaying the observations that Lenski and his team made:

http://www.nature...514.html
JVK
1 / 5 (2) Aug 11, 2015
I'm just relaying the observations that Lenski and his team made:


"...what potential observational or experimental evidence is there that would persuade you that the theory is wrong and lead you to abandoning it? If there is none, it is not a scientific theory."
http://www.nature...-1.16535

Simply put, now that Eugene Koonin has admitted that neo-Darwinian theory included nothing known to serious scientists about viruses, you have nailed the entirety of the Modern Synthesis to the walls in the halls of academia. Most of the classrooms in the US, which are linked to those halls, teach ridiculous theories. Biologically uninformed science idiots relay the pseudoscientific nonsense in hopes that they can convince others that serious scientists are wrong.

If the serious scientists are wrong, you have nothing to fear.

http://thedailysh...reg-bear Jon Stewart interviews Greg Bear
JVK
1 / 5 (2) Aug 11, 2015
I'm just relaying the observations that Lenski and his team made:


That's like claiming "I was just following orders." Thanks for helping to link your ridiculous perspectives to the war crimes committed by those who followed Hitler.

It ties you to the threat posed by today's terrorists that Greg Bear has helped to detail since his publication of "Blood Music" and "Darwin's Radio" and "Darwin's Children."

As a medical laboratory scientist working in the lab, I am tied to his "fact-checking," Similarly, Eshel Ben-Jacobs' works continue to refute the ridiculous misrepresentation of biologically-based cause and effect that you incorporated into your "Criticisms of the nutrient-dependent pheromone-controlled evolutionary model."
http://www.ncbi.n...4049134/

Did you ever think that your ridiculous review would link you to the actions of terrorists? Have you ever had an intelligent thought about anything?
JVK
1 / 5 (2) Aug 11, 2015
Also, in your "Criticisms..." you linked to the attack on my scientific credibility by PZ Myers.

One crank dies, another rises to take his place
http://freethough...s-place/

Excerpt: "Behold James Vaughn Kohl.

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 that most people here were taught to believe is the theory of evolution."

Do you think PZ Myers might be something more than merely a biologically uninformed atheist blogger/science idiot?
anonymous_9001
5 / 5 (3) Aug 11, 2015
That's like claiming "I was just following orders." Thanks for helping to link your ridiculous perspectives to the war crimes committed by those who followed Hitler.


What a ridiculous hyperbolic comparison. Thanks for confirming Godwin's law once again. The difference here is that those are Lenski's OBSERVATIONS.

If I look out of my window and tell you the sky is blue, you can confirm that, because it's a factual observation. If Lenski et al. observe the utilization of citrate and then sequence the genome and note the change in the CitT operon, you can go back and verify that, because it's a factual observation. They have frozen samples from every 500 generations that they've analyzed.

Did you analyze his E. coli's genome/proteome and observe a novel olfactory receptor?
anonymous_9001
5 / 5 (3) Aug 11, 2015
And again:

Alright, so then what did the citrate do then and what specific changes did it make? Are you denying that CitT was under the influence of an oxic promoter or are you denying that they began expressing CitT?


What happened in this specific scenario? What change did citrate initiate and how?
JVK
1 / 5 (2) Aug 11, 2015
HOW? Not even Feynman could answer your question about citrate.

http://www.scienc...ets-work

Feynman also complained that social scientists are pseudoscientists.

Could the problem be that they accept ridiculous ideas about mutations and evolution without knowing how nutrient-dependent microRNAs prevent the accumulation of viral microRNAs that are linked to all pathology?

Instead, they claim that mutations can sometimes be beneficial, which supposedly explains how all extant biodiversity arose from nothing.

Their claims about evolution can be placed into the context of terrorist threats, but only if dual use of the CRISPR-Cas9 technology is considered, as Feynman would probably consider it, in the context of an atoms to ecosystems knowledge base linked from physics to chemistry and biology via what is known about nutrient-dependent RNA-mediated protein folding.
JVK
1 / 5 (2) Aug 11, 2015
What a ridiculous hyperbolic comparison.


Godwin's Law https://en.wikipe...%27s_law is an Internet adage asserting that "As an online discussion grows longer, the probability of a comparison involving Nazis or Hitler approaches 1"[2][3]—​ that is, if an online discussion (regardless of topic or scope) goes on long enough, sooner or later someone will compare someone or something to Hitler or Nazism.

Godwin's Law makes sense in the context of attempts to explain anything about biologically-based cause and effect to biologically uninformed science idiots. Eventually, all that's left is to attribute their ridiculous belief in pseudoscientific nonsense and/or genocide to the origins of all such beliefs.

The origins of ridiculous beliefs is overwhelming ignorance that cannot be changed by providing accurate representations of cause and effect to those who act like terrorists, or those who are terrorists.
anonymous_9001
5 / 5 (3) Aug 11, 2015
HOW? Not even Feynman could answer your question about citrate.


And yet you claim to know what happened so matter-of-factly.

You said this earlier:

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.


Is that what happened in the E. coli? The citrate modified alternative splicing of pre-mRNA resulting in an AA substitution which created the cit+ strain?
JVK
1 / 5 (3) Aug 11, 2015
And yet you claim to know what happened so matter-of-factly.


No, I claim to have detailed a model of RNA-mediated biologically-based cause and effect that links biophysically constrained cell type differentiation in all living genera.

You claim that my accurate representations of cause and effect have less explanatory power than ridiculous theories about evolution that have never included anything known to serious scientists about viruses and perturbed protein folding, which cannot be linked to the evolution of any species.

Now you ask
Is that what happened in the E. coli?
Why aren't you explaining what you think happened in E. coli?

You wrote: It was a mistake to let such a sloppy review through to be published.-- http://www.ncbi.n...4049134/

I think the biggest mistake ever made by theorists was to invent neo-Darwinism based on assumptions linked to de Vries definition of "mutation." Ask Koonin if he agrees.
JVK
1 / 5 (3) Aug 11, 2015
Does anyone know for sure whether or not Andrew Jones is a terrorist? He seem to be baiting me in attempts to get more information about the role that viruses play in RNA-mediated cell type differentiation, which typically is biophysically constrained.

Does anyone know for sure whether or not PZ Myers is a terrorist? His attack on my model was unprovoked and his idiot minions jumped right in. For all I know, they might all belong to a terrorist group that has not yet been discovered because most of them hide behind the veil of anonymity.

Serious scientists don't hide. Some of them even admit they missed important facts about top-down causation. Rarely does an evolutionary theorist admit there is an anti-entropic force that must be linked from ecological variation to ecological adaptation. How can anyone trust a theorist, even if not one of them is a terrorist?
anonymous_9001
5 / 5 (3) Aug 11, 2015
Why aren't you explaining what you think happened in E. coli?


I already gave you the research from the people that performed that experiment. You claim they're wrong, so I'm asking you what you think actually happened. You've implied citrate caused the duplication shown in this diagram:

http://www.nature...f2.2.jpg

By what means did that occur? What processes were involved?
JVK
1 / 5 (2) Aug 11, 2015
I already gave you the research from the people that performed that experiment.


Find someone who considered the role of viruses in RNA-mediated gene duplication and also considered the role of RNA-mediated amino acid substitutions that stabilize the nutrient-dependent organized genomes of all living genera and tell me how the experimental evidence of biologically-based cause and effect was represented in the design of the experiment and explained in the results.

You've implied citrate caused the duplication shown in this diagram:


Stop putting words into my mouth because your ridiculous theories explain nothing.

I'm asking you what you think actually happened.


I detailed what happened in the context of everything currently known about cell type differentiation in an invited review of nutritional epigenetics. The concise representation takes less than 6 minutes to review: http://youtu.be/DbH_Rj9U524
anonymous_9001
5 / 5 (3) Aug 11, 2015
There's already a well detailed mechanism by which viruses can induce gene duplication. It's called retrotransposition.

Stop putting words into my mouth because your ridiculous theories explain nothing.


Well, that's some progress, I guess. At this point, you've implied a lot of things, but refuse to clarify what you actually think happened. Can we get that list narrowed down a bit? We can compile the following list of what you say didn't happen:

-citrate did not epigenetically effect the duplication, meaning the presence of citrate was not responsible for the duplication
-citrate did not enter the cell before CitT was expressed

Are you saying that retrotransposition was the source of the promoter duplication and the section of DNA labeled B in the picture is more stable than A and that's why it thrived? This seems like a reasonable guess based on what you've said.

http://www.nature...f2.2.jpg
JVK
1 / 5 (2) Aug 12, 2015
There's already a well detailed mechanism by which viruses can induce gene duplication. It's called retrotransposition.


As you know, Greg Bear linked it to the pheromone-controlled physiology of human reproduction via RNA-mediated cell type differentiation in at least three different novels, and Eugene Koonin just admitted that none of what is known to serious scientists and science fiction authors (James Patterson, also) was included in the neo-Darwinian "Modern Synthesis."

http://www.huffin...216.html "The entire evolution of the microbial world and the virus world, and the interaction between microbes and viruses and other life forms have been left out of the Modern Synthesis..."

Why are you still making a "reasonable guess" about what I have detailed in the context of how ecological variation is linked to ecological adaptation by nutrient-dependent microRNAs?
anonymous_9001
5 / 5 (2) Aug 12, 2015
Why are you still making a "reasonable guess" about what I have detailed in the context of how ecological variation is linked to ecological adaptation by nutrient-dependent microRNAs?


Because you refuse to have a polite conversation like a decent human being would. I'm trying to understand you, but it's difficult when you insult rather than clarify. When disseminating information and knowledge, one of the biggest goals is to be concise and clear. Instead, you go out of your way to use words and terms in ways they've never been used before and don't explain anything. The video you posted says nothing different than what you've said here. It didn't explain anything further.
anonymous_9001
5 / 5 (2) Aug 12, 2015
You've been mistaken now about what happened in the E. coli experiment for nearly 2 years. Here's Sean Pitman telling you exactly what I've been telling you back in November 2013:

http://www.andrew...1_28.pdf

There was no new receptor gene, just a duplication putting the existing CitT under an oxic promoter. Do you have evidence from their genome analysis that there was a new receptor gene?

JVK
1 / 5 (2) Aug 12, 2015
...you refuse to have a polite conversation like a decent human being would. I'm trying to understand you...


Everyone else is asking why your criticisms of my detailed review of RNA-mediated amino acid substitutions and cell type differentiation ended with this claim.

It was a mistake to let such a sloppy review through to be published.

http://www.ncbi.n...4049134/

You still can't understand anything and yet you expect me to help -- when you continue your incessant barrage of questions despite knowing that discussion could occur at http://rna-mediated.com/ where more than 400 blog posts add pertinent information from the latest research reports.

Here's Sean Pitman telling you...


Ask Pitman if he realizes neo-Darwinian theory did not included anything known to serious scientists about the role of viruses. What about PZ Myers or any other expert you choose. Koonin exposed the entirety of the evolution industry.
JVK
1 / 5 (2) Aug 12, 2015
Pitman wrote: "I see no evidence for epigenetic factors in play here or thermodynamic instability before or after the changes in function."

See for comparison: "RNA-Mediated Thermoregulation of Iron-Acquisition Genes in Shigella dysenteriae and Pathogenic Escherichia coli" http://dx.doi.org....0063781

How can anyone like Pitman, Lenski, or PZ Myers continue to advise equally biologically uniformed science idiots who do not understand the fact that cell type differentiation is biophysically constrained by the nutrient-dependent chemistry of RNA-mediated protein folding in the context of the physiology of reproduction? Constraint-breaking mutations are the source of pathology, not the evolution of any species.

Why aren't other serious scientists commenting here?
anonymous_9001
5 / 5 (2) Aug 12, 2015
Deflection, pure and simple. You just choose to disguise it as "why explain it when you won't understand" instead of the reality, which is "I won't explain it because I CAN'T explain due to my lack of understanding".

Why aren't other serious scientists commenting here?


Because they're out doing actual research and they're not going to waste their time and effort on your insignificant little "model" that I can debunk in a writeup that took me less than a total of 12 hours to put together. Meanwhile, every researcher I contact has sided against you, including those you've unofficially and officially cited and an unsolicited email from a developmental biologist from Cornell that can see right through your ignorance.
JVK
1 / 5 (2) Aug 12, 2015
From Here to Eternity—The Theory and Practice of a Really Long Experiment
http://journals.p....1002185

The LTEE is a remarkable case study of the interplay of determinism and chance in evolution—and in the conduct of science.


The bad conduct of science is also reported by those who know nothing about how cell type differentiation occurs, but report that the bacterial flagellum "re-evolved" in 4 days.

Evolutionary resurrection of flagellar motility via rewiring of the nitrogen regulation system
http://www.scienc...abstract
"...revealed a single-nucleotide point mutation... causing an amino acid substitution...[Thr97→Pro97 (T97P)] (13). The fast-spreading strain AR2F had acquired an additional point mutation in the σ54-dependent EBP gene ntrC, which alters an amino acid (R442C)..."

Does anyone else need to learn the difference between a mutation and an amino acid substitution?
anonymous_9001
5 / 5 (2) Aug 12, 2015
Does anyone else need to learn the difference between a mutation and an amino acid substitution?


Nobody subscribes to your arbitrary distinction. Methods like error-prone PCR and UV irradiation have been used to produce improved crops and other organisms, yes?
JVK
1 / 5 (2) Aug 12, 2015
every researcher I contact has sided against you


There aren't two sides to the facts. Koonin just admitted to the fact that "The entire evolution of the microbial world and the virus world, and the interaction between microbes and viruses and other life forms have been left out of the Modern Synthesis..." http://www.huffin...216.html

My model links atoms to ecosystems via the conserved molecular mechanisms of biophysically constrained protein folding chemistry that is RNA-mediated in the context of metabolic networks that are epigenetically linked to genetic networks via the physiology of reproduction in all genera.

My model is an accurate representation of everything currently known to serious scientists about personalized medicine. It links nutritional epigenetics to pharmacogenomics via RNA-mediated events. http://www.medsca...24253661
anonymous_9001
5 / 5 (2) Aug 12, 2015
Koonin just admitted to the fact that "The entire evolution of the microbial world and the virus world, and the interaction between microbes and viruses and other life forms have been left out of the Modern Synthesis..."


That doesn't magically nullify the rest of it. Incomplete is not the same thing as completely wrong.
JVK
1 / 5 (2) Aug 12, 2015
Nobody subscribes to your arbitrary distinction.


Oppositional COMT Val158Met effects on resting state functional connectivity in adolescents and adults http://link.sprin...4-0895-5 The A or Met allele is associated with lower enzymatic activity (due to thermoinstability), and with exploratory behaviour.

The link to the honeybee model organism of life history transitions is the single amino acid substitution (not a mutation).

In my review, I wrote: 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). http://www.ncbi.n...3960065/

... your arbitrary distinction.


It is not an arbitrary distinction.
JVK
1 / 5 (2) Aug 12, 2015
Incomplete is not the same thing as completely wrong.


Of course it is, and nothing can make it right. You cannot simply ignore the facts in microbes and proceed to explain what you think might be happening in other organisms because you can see that they also have differentiated cell types.

Evolutionary theorists have delayed what otherwise might have been significant progress towards ending all virus-driven pathology -- if only by learning how cell type differentiation occurs. Instead, we now have dual use technology for gene repair and the creation of GMOs by using viruses.

Greg Bear has warned us about that.

Still pseudoscientists won't admit that they have been misleading generations of biologically uniformed science idiots. They are too embarrassed to admit they were wrong, even at a time when all serious scientists know that.

See for example: http://www.huffin...450.html
anonymous_9001
5 / 5 (3) Aug 12, 2015
It is not an arbitrary distinction.


Yes it is. Nobody but you exclusively refers to negative base substitutions as mutations and beneficial base substitutions as AA substitutions. What do you call synonymous base substitutions? They don't make AA substitutions, yet they're not deleterious.

Functional Compensation of a Detrimental Amino Acid Substitution in a Cytotoxic-T-Lymphocyte Epitope of Influenza A Viruses by Comutations

http://www.ncbi.n...C479054/

Of course it is


If I write a dictionary and leave out the word "ampersand" it doesn't mean the rest of it is wrong.
JVK
1 / 5 (2) Aug 12, 2015
Sex differences in cell types and somatic differences in cell types are nutrient-dependent and RNA-mediated via gene duplications and amino acid substitutions.

In the current Journal of Neuroscience the cell type differences are linked from yeasts to humans via the nutrient-dependent pheromone-controlled physiology of reproduction in octopuses and the conserved molecular mechanisms of biophysically constrained protein folding chemistry linked to the stability of all organized vertebrate genomes by substitution of the achiral amino acid glycine in the decapeptide gonadotropin releasing hormone (GnRH).

http://www.scienc...14004006

See also:
https://www.googl...mediated

https://www.googl...mediated+dna+methylation

https://www.googl...mediated+thermoregulation

http://www.rnasociety.org/

http://rna-mediated.com/

https://www.faceb...ediated/
Vietvet
5 / 5 (2) Aug 12, 2015
"Prof. Bukau explains that damaged proteins do not only clump during the ageing process. Protein aggregates can also occur through changes in the protein structure due to mutation or chemical or environmental stresses."

Read more at: http://phys.org/n...html#jCp

@JVK

Are: Nadinath B. Nillegoda, Janine Kirstein, Anna Szlachcic, Mykhaylo Berynskyy, Antonia Stank, Florian Stengel, Kristin Arnsburg, Xuechao Gao, Annika Scior, Ruedi Aebersold, D. Lys Guilbride, Rebecca C. Wade, Richard I. Morimoto, Matthias P. Mayer & Bernd Bukau science idiots?
anonymous_9001
5 / 5 (3) Aug 12, 2015
somatic differences in cell types are nutrient-dependent and RNA-mediated via gene duplications and amino acid substitutions


Stem cells are differentiated through a variety of signals, not just nutrients. Growth factors seem to be the main players, but nutrient gradients are also involved. These modulate when and which genes are expressed in the stem cells, but they do not cause duplications during development. Besides those like RBCs, which get rid of their nuclei, all of your cells have the same genes.

https://en.wikipe...h_factor
http://genesdev.c...129.long
http://www.garlan...inal.pdf
http://www.biolog...ent.html
http://www.ncbi.n...18006108
JVK
1 / 5 (2) Aug 12, 2015
Stem cells are differentiated through a variety of signals...


Ecological variation in nutrient availability links RNA-mediated gene duplication and RNA-mediated amino acid substitutions to the differentiation of all cell types in all vertebrates via the physiology of reproduction and chromosomal rearrangements.

The chromosomal rearrangements link the RNA-mediated amino acid substitutions to the stability of organized genomes.

Viruses perturb that stability, which is why the accumulation of viral microRNAs must be prevented by nutrient-dependent microRNAs. The nutrient-dependent microRNAs prevent entropic elasticity from becoming genomic entropy via accumulated mutations.

For example of genomic stability without ecological speciation see: Estrogen receptor α polymorphism in a species with alternative behavioral phenotypes http://www.pnas.o...abstract

Please provide an example of mutation-driven speciation and stability.
JVK
1 / 5 (2) Aug 12, 2015
Are: Nadinath B. Nillegoda et al., ....science idiots?


Why do you ask? Have they failed to link mutations to pathology? Have they not linked unperturbed nutrient-dependent thermodynamic cycles of protein biosynthesis and degradation to healthy longevity?

Is there any aspect of their work that falls outside the context of my atoms to ecosystems model of ecological adaptation?

Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems http://figshare.c...s/994281
Vietvet
4.5 / 5 (2) Aug 12, 2015
Are: Nadinath B. Nillegoda et al., ....science idiots?


Why do you ask? Have they failed to link mutations to pathology? Have they not linked unperturbed nutrient-dependent thermodynamic cycles of protein biosynthesis and degradation to healthy longevity?

They never mentioned viruses.
anonymous_9001
5 / 5 (3) Aug 12, 2015
For starters, there was no variation in nutrient availability in Lenski's experiment. All 12 populations were in identical media.

Rearrangements do not necessarily lead to genome stability. In fact, they've been known to cause instability:

http://www.ncbi.n.../9729329

As I've also said before, they're also heavily involved in cancer formation.

the accumulation of viral microRNAs must be prevented by nutrient-dependent microRNAs


In what way do nutrient-dependent miRNAs counter viral miRNAs? miRNAs bind to mRNAs and mediate translation. I'm not aware of any examples of host miRNAs inactivating viral miRNAs. Could you link some examples of that?
JVK
1 / 5 (2) Aug 12, 2015
They never mentioned viruses.


Neither did I in my 2013 review. But if I had mentioned viruses, I would not have linked them to beneficial mutations, since there is no such thing as a beneficial mutation and viruses perturb protein folding, which is why they are linked to pathology.
JVK
1 / 5 (2) Aug 12, 2015
I'm not aware of any examples of host miRNAs inactivating viral miRNAs.


You are not vaguely aware of anything that might lead to cell type differentiation via the conserved molecular mechanisms of epigenetically-effected RNA-mediated protein folding. You are at least two decades behind the explanatory power of my model, and refuse to move forward by admitting there is no other model that links the biophysically constrained chemistry of nutrient-dependent protein folding chemistry to cell type differentiation in all living genera.

However, now that the octopus genome has been sequenced, you and others like you can link marine invertebrates from crustaceans to insect and mammals, including humans, via what I have already detailed in a series of published works that link the microRNA/messenger RNA balance to cell type differentiation.

That's what Anna Di Cosmo's group did last year: http://www.scienc...14004006
Vietvet
5 / 5 (2) Aug 12, 2015
They never mentioned viruses.


there is no such thing as a beneficial mutation---

Research says otherwise.

https://scholar.g...as_sdtp=

Vietvet
5 / 5 (2) Aug 12, 2015


viruses perturb protein folding, which is why they are linked to pathology.


Viruses aren't the only thing that perturb protein folding.

" Protein aggregates can also occur through changes in the protein structure due to mutation or chemical or environmental stresses."

Read more at: http://phys.org/n...html#jCp
anonymous_9001
5 / 5 (2) Aug 12, 2015
I said:

I'm not aware of any examples of host miRNAs inactivating viral miRNAs. Could you link some examples of that?


The important part being the second sentence. miRNAs modulate the activity of mRNAs, not other miRNAs. Have you discovered an example of host miRNAs deactivating viral miRNAs? Where has that research been reported?
JVK
1 / 5 (1) Aug 13, 2015
I can't recall the question anonymous_9001 asked about the link from RNA to DNA on the ISHE human ethology group, but I couldn't answer it in less than a thesis length response -- and as always, biologically uninformed science idiots like Andrew Jones (aka anonymous_9001) want simple answers. The question got me banned from the group, because I couldn't answer it.

Banning me prevents others from being held accountable for preventing progress that has been made in understanding RNA-mediated cause and effect via fixation of amino acid substitutions. They can always claim that I didn't explain myself so that they could understand anything more about cell type differentiation than the fact that it must automagically occur in the context of mutations and evolution.

Alert to biologists: Ribosomes can translate the 'untranslated region' of messenger RNA
http://phys.org/n...ger.html
JVK
1 / 5 (1) Aug 13, 2015
see Jones thesis at
http://www.scribd...s#scribd

"Despite their challenges, ribozymes have made an interesting niche for themselves in the field of abiogenesis. The evolution of a successful RNA polymerase ribozyme is a lofty goal. While its discovery would not be the be-all and end-all of abiogenesis research, it would represent an important stepping stone between prebiotic chemistry and life. The encapsulation of such a ribozyme is also an important step, as it would enable a system of heredity and evolution through natural selection. Based on progress in current research, it is only a matter of time before that ribozyme is discovered."

Andrew Jones: Have you seen any scientific progress that details how the encapsulation of the automagically evolved ribozyme links abiogeneis to cell type differentiation? If not, when will you retract this: http://www.ncbi.n...4959329/
JVK
1 / 5 (1) Aug 13, 2015
See also: Nuclear Fractionation Reveals Thousands of Chromatin-Tethered Noncoding RNAs Adjacent to Active Genes http://www.cell.c...900793-7

Do not keep asking me the same questions about RNA-mediated amino acids and cell type differentiation if you are not willing to learn anything about how nutrient-dependent biophysically constrained cell type differentiation occurs in all living genera.

anonymous_9001
5 / 5 (1) Aug 13, 2015
I can't recall the question anonymous_9001 asked about the link from RNA to DNA on the ISHE human ethology group


I asked if you believed splicing made sequence changes to DNA. That does not necessitate a 20 page paper as an answer.
JVK
1 / 5 (1) Aug 15, 2015
"...the macroclimate and the geology are the same on both slopes of the canyon, and yet, if you look into the African slope, the south facing slope, which gets up to 800% more solar radiation than the European north facing slope -- you see dramatic differences in the biodiversity between the savannoid African and forested European slopes. . . . This represents a cradle of sympatric speciation, i.e., the origination of new biological species within freely inbreeding populations of abutting slopes. . . . "
http://www.huffin...764.html

Schrodinger (1943) "What is Life" linked the sun's biological energy from quantum mechanics to sympatric speciation in the context of what Eibi Nevo portrayed in a ridiculous misrepresentation of biologically-based cause and effect that was automagically placed into the context of ridiculous theories. What kind of biologically uninformed evolutionary biologist ignores quantum biology?
JVK
1 / 5 (1) Aug 15, 2015
I asked if you believed splicing made sequence changes to DNA.


Please frame your question in the context of "Alternative RNA Splicing in Evolution" http://jonlieffmd...volution

Excerpt: "It now appears that alternative splicing is, perhaps, the most critical evolutionary factor determining the differences between human beings and other creatures."

How does what I believe about splicing and sequence changes to DNA make any difference in the context of what is known to serious scientists about biologically-based cause and effect?

In our 1996 Hormones and Behavior review we wrote: "Small intranuclear proteins also participate in generating alternative splicing techniques of pre-mRNA and, by this mechanism, contribute to sexual differentiation in at least two species, Drosophila melanogaster and Caenorhabditis elegans..." http://www.hawaii...ion.html
JVK
1 / 5 (1) Aug 15, 2015
Re: "....generating alternative splicing techniques of pre-mRNA and, by this mechanism..."

I asked if you believed splicing made sequence changes to DNA.


In our section on molecular epigenetics we included everything known about sex differences in cell type differentiation, which has since been extended to cell type differentiation in all cell types of all individuals of all genera via the sequencing of the octopus genome.

See also: "Role of olfaction in Octopus vulgaris reproduction" http://www.scienc...14004006 Excerpt: "The OL acting as control centre may be target organ for metabolic hormones such as leptin like and insulin like peptides, and olfactory organ could exert regulatory action on the OL via epigenetic effects of nutrients and pheromones on gene expression (Kohl, 2013; Elekonich and Robinson, 2000)."

Do you remember what you said about Kohl (2013)? http://www.ncbi.n...24693353
JVK
1 / 5 (1) Aug 15, 2015
Re: "...epigenetic effects of nutrients and pheromones on gene expression (Kohl, 2013; Elekonich and Robinson, 2000)."

Eleckonich and Roberts (2005) extended our model epigenetically-effected hormone-organized and hormone-activated behaviors to life history transitions in the honeybee model organism.

In Kohl (2013), I wrote: "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)."

Andrew Jones (aka anonymous_9001) wrote: It was a mistake to let such a sloppy review through to be published. http://www.ncbi.n...4049134/

What else can be said to someone who thinks the only model of cell type differentiation in all genera was presented in a sloppy review?
anonymous_9001
5 / 5 (1) Aug 15, 2015
Please frame your question in the context of "Alternative RNA Splicing in Evolution"


How would one go about doing that? It's a straightforward question as is.

What else can be said to someone who thinks the only model of cell type differentiation in all genera was presented in a sloppy review?


Volvox is a model organism for cellular differentiation. These are models:

http://www.ncbi.n.../1843415
http://www.fasebj...full.pdf
http://javeriana....itro.pdf
http://arxiv.org/abs/1303.7319
http://genesdev.c...129.long

Your paper is a review that covers a few model organisms, but in and of itself, is not A model and brings no new information to the table because you don't perform primary research. You merely reviewed others' and added in a few personal thoughts and faulty conclusions.
JVK
1 / 5 (1) Aug 15, 2015
I provided examples that link the molecular mechanisms of RNA-mediated biodiversity to all living genera via their biophysically constrained chemistry of nutrient-dependent protein folding and fixation of amino acid substitutions in the context of the physiology of reproduction, with the primary example being the honeybee.

http://www.ncbi.n...24693353
Excerpt: "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)."

You merely reviewed others' and added in a few personal thoughts and faulty conclusions.


What were the faulty conclusions? "Feedback Loops Link Odor and Pheromone Signaling with Reproduction" http://dx.doi.org...5.09.027
JVK
1 / 5 (1) Sep 04, 2015
You merely reviewed others' and added in a few personal thoughts and faulty conclusions.


I exemplified the ignorance of biologically uninformed science idiots.

Excerpt: "The conclusions stated above are subject to the limitations of statistical inference, but correlations of this magnitude with all 190 amino acid pairs cannot be due to chance." http://www.scienc...abstract

Please sign in to add a comment. Registration is free, and takes less than a minute. Read more

Click here to reset your password.
Sign in to get notified via email when new comments are made.