More than just X and Y: A new genetic basis for sex determination

Aug 18, 2014
Cold Spring Harbor Laboratory researchers have found that miRNAs, short RNA molecules, are responsible for sexual differences in fruit flies. Shown here are testes from a male fruit fly where a hormone that controls a key miRNA has been inactivated. The abnormal testes fail to make sperm. They now produce sex determinants (shown in red) that are found in the ovaries of female flies. Credit: D. Fagegaltier/ Cold Spring Harbor Laboratory

Men and women differ in plenty of obvious ways, and scientists have long known that genetic differences buried deep within our DNA underlie these distinctions. In the past, most research has focused on understanding how the genes that encode proteins act as sex determinants. But Cold Spring Harbor Laboratory (CSHL) scientists have found that a subset of very small genes encoding short RNA molecules, called microRNAs (miRNAs), also play a key role in differentiating male and female tissues in the fruit fly.

A miRNA is a short segment of RNA that fine-tunes the activation of one or several protein-coding genes. miRNAs are able to silence the genes they target and, in doing so, orchestrate complex genetic programs that are the basis of development.

In work published in Genetics, a team of CSHL researchers and colleagues describe how miRNAs contribute to sexual differences in . You've probably never noticed, but male and female differ visibly, just like other animals. For example, are 25% larger than males with lighter pigmentation and more abdominal segments.

The team of researchers, including Delphine Fagegaltier, PhD, lead author on the study, and CSHL Professor and Howard Hughes Medical Institute Investigator Greg Hannon, identified distinct miRNA populations in male and female flies. "We found that the differences in miRNAs are important in shaping the structures that distinguish the two sexes," says Fagegaltier. "In fact, miRNAs regulate the very proteins that act as sex determinants during development."

The team found that miRNAs are essential for sex determination even after an animal has grown to adulthood. "They send signals that allow germ cells, i.e., eggs and sperm, to develop, ensuring fertility," Fagegaltier explains. "Removing one miRNA from mature, adult flies causes infertility." More than that, these flies begin to produce both male and female sex-determinants. "In a sense, once they have lost this miRNA, the flies become male and female at the same time," according to Fagegaltier. "It is amazing that the very smallest can have such a big effect on sexual identity."

Some miRNAs examined in the study, such as let-7, have been preserved by evolution because of their utility; humans and many other animals carry versions of them. "This is probably just the tip of the iceberg," says Fagegaltier. "There are likely many more miRNAs regulating sexual identity at the cellular and tissue level, but we still have a lot to learn about these differences in humans, and how they could contribute to developmental defects and disease."

Explore further: Scientists identify a gene that controls the timing of precisely ordered events during maturation

More information: "A Genome-Wide Survey of Sexually Dimorphic Expression of Drosophila miRNAs Identifies the Steroid Hormone-Induced miRNA let-7 as a Regulator of Sexual Identity" appeared online in Genetics on July 31, 2014.

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JVK
1 / 5 (6) Aug 18, 2014
In our 1996 Hormones and Behavior review, we linked small intranuclear proteins, which now appear to be called microRNAs, to alternative splicings of pre-mRNAs, from ecological variation to sex differences in the cell types of yeasts at the advent of pheromone-controlled sexual reproduction in unicellular organisms.

In the context of conserved molecular mechanisms and ecological variation in nutrient-dependent cell type differentiation of all cells in all individuals of all species, we linked the nutrient-dependent pheromone-controlled physiology of reproduction in yeasts to sex differences in cell types in flies and nematodes.

"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...tion.htm
animah
5 / 5 (5) Aug 18, 2014
More spam from James V Kohl, creationist and one-idea man.

pheromone-controlled *anything* in humans is a myth. In our species, the necessary genes have regressed. Genetic sequencing proves this. James V Kohl, you are a fraud.
JVK
1 / 5 (6) Aug 18, 2014
Steroid hormone regulation of miRNA let-7 probably is nutrient-dependent, which makes it likely that regulation of cell type differentiation and sexual identity occurs via the metabolism of nutrients to species-specific pheromones that control the physiology of nutrient-dependent reproduction in species from microbes to man via conserved molecular mechanisms.

The conserved molecular mechanisms are obviously nutrient dependent, which links them from ecological variation to pheromone-controlled ecological adaptations outside the context of mutation-initiated natural selection and outside the context of the evolution of biodiversity.

The claim that the miRNAs examined in the study have been preserved by evolution seems to be based on theory instead of being based on biological facts that link ecological variation to ecological adaptations via conserved molecular mechanisms of protein biosynthesis and degradation in all cell types.

See: http://www.ncbi.n...24693353
JVK
1 / 5 (6) Aug 18, 2014
pheromone-controlled *anything* in humans is a myth. In our species, the necessary genes have regressed.


D'Scent of Man: A Comparative Survey of Primate Chemosignaling in Relation to Sex
http://www.scienc...14001585

"This ever-growing body of evidence points to a critical role of scent in guiding the social behavior and reproductive function throughout the primate order."

Does anyone who is not an anonymous fool think we are not like other primates or that cell type differentiation in all cells of all our tissues in all our organs and all organ systems involved in our behavior does not occur via nutrient-dependent amino acid substitutions like it does in all other individuals of all other species?

"...the so-called alpha chains of hemoglobin have identical sequences of amino acids in man and the chimpanzee, but they differ in a single amino acid (out of 141) in the gorilla." http://www.jstor..../4444260 Are we mutated gorillas?
anonymous_9001
5 / 5 (10) Aug 18, 2014
we linked small intranuclear proteins, which now appear to be called microRNAs


What on Earth would give you this impression? Proteins and RNAs are ENTIRELY different types of molecules. They didn't rename intranuclear proteins. I'm confused as to how you could even come to that conclusion. It's totally nonsensical.

http://en.wikiped..._protein
RealScience
5 / 5 (11) Aug 18, 2014
small intranuclear proteins, which now appear to be called microRNAs


What? Not even close, JVK.
Proteins are strings of amino acids produced by ribosomes from mRNAs.
miRNAs are strings of nucleic acids transcribed from DNA.

How can you pretend to be an expert when you don't even know the basics?
anonymous_9001
5 / 5 (7) Aug 18, 2014
Claimed that splicing makes changes to the DNA, thought the proteasome and the proteome were the same thing, thought the proteasome mediates protein folding, this gem:

how a beneficial mutation somehow knew it would be beneficial


and now we can include his thinking that proteins and RNAs are the same thing to the long list of Kohl's grand demonstrations of his ignorance of biology 101 concepts.
animah
5 / 5 (5) Aug 18, 2014
Discredited James V Kohl, the man who said:

"There is also an Islamic Creationist who understands biologically-based cause and effect in the context of chemical signaling and olfaction. 'The Miracles Of Smell And Taste'"

Priceless!
JVK
1 / 5 (7) Aug 19, 2014
Excerpt: "It is amazing that the very smallest genes can have such a big effect on sexual identity."

Does that mean the microRNAs are genes?
JVK
1 / 5 (6) Aug 19, 2014
http://books.goog...8Q6AEwAA

"Interestingly, the PABPN1 protein is an essential mRNA polyadenylation factor, and is ... with the formation of RNA-protein intranuclear inclusions, sequestration of factors required for normal alternative pre-mRNA processing and impairment of ..."

Does this mean we did not link small intranuclear proteins, which now appear to be called genes by Fagegaltier, to alternative splicings of pre-mRNAs, from ecological variation to sex differences in the cell types of yeasts at the advent of pheromone-controlled sexual reproduction in unicellular organisms?

Does it mean that non‐coding RNAs are not the bridge between epigenetic mechanisms, lineages and domains of life?
anonymous_9001
5 / 5 (7) Aug 19, 2014
Does that mean the microRNAs are genes?


No. They're referring to the genes that encode for the miRNAs. Like all transcripts, miRNAs originate from coding regions in the DNA.

small intranuclear proteins, which now appear to be called genes by Fagegaltier


What? Nowhere did he refer to intranuclear proteins as genes or vice versa.
JVK
1 / 5 (7) Aug 19, 2014
miRNAs originate from coding regions in the DNA.


Thanks. Do they do this AUTOMAGICALLY?

http://en.wikiped...MicroRNA
MicroRNA: "...a single miRNA may repress the production of hundreds of proteins..."

MicroRNA gene: " ...in some cases a microRNA gene is transcribed together with its host gene; this provides a means for coupled regulation of miRNA and protein-coding gene."

MicroRNA and proteins "... a single miRNA may repress the production of hundreds of proteins."

From our 1996 review:
"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..."

From this news article: "...a subset of very small genes encoding short RNA molecules, called microRNAs (miRNAs), also play a key role in differentiating male and female tissues in the fruit fly."

What is the role of mutations?
shavera
5 / 5 (4) Aug 19, 2014
Can we please just start ignoring JVK? At most just post a warning to other readers that JVK is a known troll of biologically bull-crappery and downvote and move on? You're not going to convince him he's right, you're not going to educate others about why exactly he's wrong.

Let's go back to, you know, discussing articles rather than being side-tracked with JVK's BS in BS.
JVK
1 / 5 (7) Aug 19, 2014
The difference between what we wrote in 1996, and the representation in this 2014 news article may clarify whether or not mutation-initiated natural selection caused the evolution of sex differences in cell types.

We detailed the molecular mechanisms that enable nutrient-dependent pheromone-controlled sex differences to be manifested in cell types, and the conserved molecular mechanisms have since been linked to differences in all cell types in all individuals of all species starting with yeasts.

Do ideas about microRNA genes suggest that they mutate to cause mutation-initiated natural selection and evolution of sex differences in cell types? If so, can evolutionary theorists safely conclude that all cell type differences in all cells of all species are caused by constraint-breaking mutation?

Nei (2013) claims mutations are the ultimate source of biodiversity. I claim biodiversity is nutrient-dependent and pheromone-controlled.

Whose claim is supported by this reported evidence?
Jaeherys
3 / 5 (4) Aug 19, 2014
First off, I research the effects of a specific microRNA and preeclampsia and there is some blasphemous miRNA slamming here! MicroRNAs are bound to the RISC complex, specifically to Argonautes 1-4 in humans, which are < 100 kDa in size. In flies i believe they have Ago1/2 only. This complex exists in the cytosol or in the extracellular environment in exosomes. MicroRNAs have well characterized roles in differentiation and conversely, reprogramming. Furthermore, they can suppress or induce a switch to different cellular programs, this heavily involves splicing changes and chromatin remodeling. They can be found intra or intergenic meaning they are found in the introns of protein coding genes or as their own gene, regulated by their own promoters. Intergenic miRNA are usual in clusters and the pri-miRNA can contain many, ultimately, mature miRNA.

So i have no idea about this intranuclear malarkey as mature miRNA is produced in the cytosol. But its not like i know everything!
JVK
1 / 5 (4) Aug 19, 2014
Thank you, Jaeherys. If sexual differentiation of cell types is nutrient-dependent and pheromone-controlled, ecological variation and nutrient uptake probably cause differences in the microRNA/messenger RNA balance that lead to alternative splicings of pre-mRNA and amino acid substitutions that differentiate all cell types of all individuals of all species (e.g., not just sex differences in cell types). My model: http://www.ncbi.n...24693353

The authors start with steroid hormone-modulated differences in a microRNA, refer to the microRNA as if it were a small gene and appear to conclude that it somehow causes sex differences in cell types, which we showed are nutrient-dependent and pheromone-controlled in all species. (Thus, my regrettable comment about small intranuclear proteins portrayed as microRNAs.)

Do you know anyone who can address the difference in their portrayal of biologically-based cause and effect and the portrayal in our 1996 review and in my model?
JVK
1 / 5 (5) Aug 19, 2014
Can we please just start ignoring JVK?


That's what I would do if I were an evolutionary theorist, and it's typical of what most of them do when confronted with experimental evidence that does not fit within the context of their ridiculous theories.

Let's go back to, you know, discussing articles...


Jaeherys presence and comments here may make that possible -- especially if other serious scientists join the discussion. That might discourage comments from anonymous fools and idiot minions of biology teachers like PZ Myers and limit the amount of added pseudoscientific nonsense.

The representations of sex differences in cell types are already confusing, which is why they need to be discussed. I am able to discuss our representation of molecular epigenetics and how they fit into a model of biophysically-constrained cell type differentiation.

Others may be able to compare experimental evidence that supports or refutes their ideas without insults from ignorance.
anonymous_9001
5 / 5 (8) Aug 19, 2014
What is the role of mutations?


You've had this answered for you dozens of times already.

http://isyeb.mnhn...1997.pdf

http://www.person...-nei.pdf

http://www.pnas.o...40.short

I wish I had the full text of the last one because this is part of the preview Google Scholar gives:

In addition to the well-recognized roles of mutations and recombinations of chromosomal DNA, a nonexhaustive list would include...
JVK
1 / 5 (5) Aug 19, 2014
Thanks. Are you trying to explain with those citations how modern human populations of mutated pygmies evolved?

http://news.natio...science/

They must have learned how to evolve more quickly than the dinosaurs that evolved into birds, if it really took the dinosaurs millions of years to do it. Do you think the dinosaurs were slow learners -- except for the ones that "evolved" into crows, that is?

Do you think the pygmies are slow learners compared to other modern human populations that somehow mutated and evolved? Have you read "A Civic Biology: Presented in Problems," which explains what you are really saying about mutation-initated natural selection and the evolution of different modern human populations in terms that are understood by racists? See pages 193-196, 253-254, 261-263

They (pages -- not the racists) may help you to understand why neo-Darwinism had to be invented and "mutation" defined.
JVK
1 / 5 (5) Aug 19, 2014
"...what allows epigenetic marks to be de novo targeted differently in the male and female germlines..." http://www.mdpi.c.../5/3/635

The question arises in the context of neurogenic niche construction in mice and cell type differentiation in specific cellular niches. In my model, "CHEMICAL ECOLOGY DRIVES ADAPTIVE EVOLUTION VIA: (1) ecological niche construction, (2) social niche construction, (3) neurogenic niche construction, and (4) socio-cognitive niche construction." - via epigenetic effects of olfactory/pheromonal conditioning. Examples link species from microbes to a modern human population in what is now central China. http://www.ncbi.n...24693353

Note, we started with the sexual differentiation of cell types in 1996, and I have extended the section on molecular epigenetics across species in a series of published works since then. Why haven't serious scientists commented on the model to eliminate it or eliminate neo-Darwinism and racism?
zz5555
5 / 5 (7) Aug 19, 2014
What is the role of mutations?


You've had this answered for you dozens of times already.

http://isyeb.mnhn...1997.pdf

I wish I had the full text of the last one because this is part of the preview Google Scholar gives:

In addition to the well-recognized roles of mutations and recombinations of chromosomal DNA, a nonexhaustive list would include...


It appears the full text can be found at http://arxiv.org/...226.pdf. However, note that the PDF at this link is dated 1 Dec. 2013 and the paper was received for review January 8 2014, so there may be slight differences from the PDF and the final paper.
JVK
1 / 5 (5) Aug 19, 2014
Which sex mutated into the other? When did it happen? Who was the first to notice it led to mutant human males and females who sexually reproduce?

See for comparison to these unanswered questions: Gene duplication as a mechanism of genomic adaptation to a changing environment http://rspb.royal...abstract

"One of the main duplicated gene families are the olfactory receptor proteins [18,117–119] so perhaps their duplication may lead to an increase in sensitivity to a particular odour may be adaptive under certain conditions."

http://www.hawaii...ion.html

"Parenthetically it is interesting to note even the yeast Saccharomyces cerevisiae has a gene-based equivalent of sexual orientation (i.e., a-factor and alpha-factor physiologies). These differences arise from different epigenetic modifications of an otherwise identical MAT locus "
JVK
1.2 / 5 (5) Aug 20, 2014
Non‐coding RNAs as the bridge between epigenetic mechanisms, lineages and domains of life http://jp.physoc....abstract

The bridge does not seem to be limited to species based on the physiology of their sexual or asexual reproduction except after-the-fact. This is clearer in another publication from this lab.

See: Starvation-Induced Transgenerational Inheritance of Small RNAs in C. elegans http://www.cell.c...)00806-X

As is readily apparent to anyone who was not taught to believe in the pseudoscientific nonsense of mutation-initiated natural selection and the evolution of biodiversity, these serious scientists continue to show that ecological variation leads to ecological adaptations in all individuals that eat, because no individual who starves to death becomes part of a species that ecologically adapts.

And, despite what theorists claim, individuals that do not eat do not mutate and become individuals of another species.
anonymous_9001
5 / 5 (6) Aug 20, 2014
And, despite what theorists claim, individuals that do not eat do not mutate and become individuals of another species.


What on Earth are you talking about?
JVK
1 / 5 (4) Aug 20, 2014
What on Earth are you talking about?


Thanks for asking, I'm talking about this. "Mutation-Driven Evolution"

http://www.amazon...99661731
"...genomic conservation and constraint-breaking mutation is the ultimate source of all biological innovations and the enormous amount of biodiversity in this world."

What were you talking about when you asked me if I believed RNA splicing makes new genes?

Feierman's response was: "A simple agree or don't agree is needed to make the interactions in this thread worth posting."

Feierman is the psychiatrist who moderates the International Society for Human Ethology's yahoo group. He banned me from participation because I did not not answer the question posed by the anonymous fool; Andrew Jones (aka anonymous_9001) with a yes or no answer.

What will today's students and their children and grandchildren learn from Medical Doctors like Feierman, and anonymous fools like Andrew Jones, if you don't step in to stop them?
anonymous_9001
5 / 5 (7) Aug 20, 2014
You're getting off topic. You implied "theorists" think organisms that starve to death evolve. Where did you get such a ridiculous idea?

What were you talking about when you asked me if I believed RNA splicing makes new genes?


The only molecular mechanism you mention in your model is RNA splicing. Since new gene variants arise all the time, splicing seems to be the only explanation for it in your model.

He banned me from participation because I did not not answer the question posed by the anonymous fool; Andrew Jones (aka anonymous_9001) with a yes or no answer.


And it clearly taught you nothing about how to properly answer questions asked of you.
JVK
1 / 5 (5) Aug 20, 2014
Feierman wanted "A simple agree or don't agree..." to your question when you asked me if I believed RNA splicing makes new genes.

If you're unable to ask intelligent questions, why would you or anyone else expect others to try and answer them with "A simple agree or don't agree..."?

Note, your comments on my published work include: "Kohl then refers to an allele change that occurred in a population in China 30,000 years ago as 'probably … nutrient-dependent' without making reference to what nutrient caused the change or how. This is followed by the statement 'the effect … is due to an epigenetic effect of nutrients on hormones responsible for the tweaking of immense gene networks'."

Now see: http://phys.org/n...ers.html for the link from ecological variation to ecological adaptations in all mammals without the pseudoscientific nonsense of mutation-initiated natural selection and the evolution of biodiversity.

"...what nutrient caused...
JVK
1 / 5 (5) Aug 20, 2014
"...what nutrient caused..." the de novo Creation of olfactory receptor genes that is clearly the result of ecological variation and is manifested in the morphological and behavioral diversity of species from microbes to man?

That's what you asked, and your question exemplifies the ignorance of biology that is unparallelled except when compared to Feierman's ignorance. Why aren't you engaged in discussions on the human ethology yahoo group? Must I put up with your ignorance in every discussion no matter where I decide to contribute?
anonymous_9001
5 / 5 (4) Aug 20, 2014
Feierman wanted "A simple agree or don't agree..." to your question when you asked me if I believed RNA splicing makes new genes.


Giving an answer initially would have taken mere seconds. Instead, it's been MONTHS since I asked you that and you still sidestep it.

If you're unable to ask intelligent questions, why would you or anyone else expect others to try and answer them with "A simple agree or don't agree..."?


You're unable to explain how it's not an intelligent question. Splicing is the only molecular mechanism you mention by name in your paper. How is anyone supposed to know if your model involves other mechanisms if you don't discuss them? How is anyone supposed to know there's more to your model than splicing if that's all you mention?

Note, your comments on my published work include:


As usual, you quote me and then refuse to refute me or address what I've said.
anonymous_9001
5 / 5 (4) Aug 20, 2014
"...what nutrient caused..." the de novo Creation of olfactory receptor genes ...That's what you asked


That's not what I asked, because it doesn't involve olfactory receptor genes.

The changes in the Chinese population were not of OR genes. The changes in Lenski's bacteria were not of OR genes. The changes in the peppered moths were not of OR genes.

Through what mechanism did citrate cause the promoter shift in Lenski's E. coli? Was it deterministic or random? If it was not random, why didn't it occur in the other 11/12 populations? This is the problem with your model. You try to apply causality to things that are obviously not causal in nature.
JVK
1 / 5 (4) Aug 20, 2014
Jaeherys

Do you know anything about the role of SNPS in microRNAs?

http://www.scienc...1400257X
"In addition to SNP in miRNAs, SNP in target genes of different miRNAs have been identified. For example, the SNP rs10759 (A > C) in the regulator of G protein signaling 4 (RGS4) gene, a downstream target of miR-124, is predicted to increase the risk of schizophrenia (Gong et al., 2013)."

I have no idea on how to follow-up on the SNP rs10759 (A > C) in the regulator of G protein signaling, but suspect the SNP can be linked from the de novo creation of olfactory receptor genes, and other G protein-coupled receptors to the nutrient-dependent pheromone-controlled differentiation of cell types at the advent of sexual reproduction in yeasts.

From there, it is easier to get to epigenetically-effected cell type differentiation in all cells of all individuals of all species via nutrient-dependent changes in protein folding.
Captain Stumpy
4.2 / 5 (5) Aug 20, 2014
Do you know anything about the role of
MORE IMPORTANTLY... do YOU know ANYTHING about the role of MUTATIONS which has been EMPIRICALLY PROVEN and he showed above?

try re-reading the post and comment about THIS
The changes in the Chinese population were not of OR genes. The changes in Lenski's bacteria were not of OR genes. The changes in the peppered moths were not of OR genes.

Through what mechanism did citrate cause the promoter shift in Lenski's E. coli? Was it deterministic or random? If it was not random, why didn't it occur in the other 11/12 populations? This is the problem with your model. You try to apply causality to things that are obviously not causal in nature
this simple response completely undermines your whole stance, world and creationist views
because it is HARD SCIENCE AND EMPIRICAL EVIDENCE PROVING YOU WRONG

go ahead... tell me the REASONS that Lenski's populations didn't ALL mutate!

Captain Stumpy
4.2 / 5 (5) Aug 21, 2014
Do you know anything about the role of SNPS
IN FACT... lets cut all of the BS here and get you to answer directly about Lenski's work

WHAT is the reason only ONE population MUTATED? (using the biological term MUTATION that is defined as: any changes to the nucleotide sequence of the genome of an organism, virus, or extrachromosomal genetic element )

WHY didn't mutation occur in the other 11/12 populations?

Until jvk can answer these questions then I suggest all people simply REPORT jvk's comments as SPAM and TROLLING.

Until jvk can PROVE that Lenski's work is invalid and that he also believes in your grand creationist ideals... then I suggest that EVERYONE simply REPORT jvk for SPAMMING and TROLLING

there is NO ROOM FOR PSEUDOSCIENCE IN SCIENCE
PSEUDOSCIENCE WILL BE REPORTED AS SPAM AND TROLLING

if you continue to post irrelevant and misrepresented posts, especially with regard to your own models and your inability to comprehend your own lexicon, then you'll be reported
Jaeherys
5 / 5 (2) Aug 21, 2014
SNPs in microRNA presumably would have quite an effect given the small length of the seed region. I read a paper about 2 weeks ago (which is at home) about the general binding dynamics of miRNA to target mRNA and bulges were common in the seed region in about 50% of miRNA and increased affinity to their targets. There are multiple papers on pubmed (search: miRNA SNP) but the significance of such mutations are like any other. In any case, if you change the MREs on target mRNA, this acts as a gain-of-function or semi-dominant negative mutation. To place this into context of this nutrient-controlled adaptation is unwarrented, these are classical mutations. SNPs happen at predictable rates but would generally be selected out, even at the cellular level. This has everything to do with cell sensors and repair, and will follow the well characterized roles of neutral molecular evolution. Search pubmed "miRNA heterochromatin" and read up on miRNA transcriptional silencing.
JVK
1 / 5 (4) Aug 21, 2014
In theory, perhaps,
the significance of such mutations are like any other.


Thank you. If you examine the details of cell type differentiation via amino acid substitutions, I think you may see the difference between what theorists call mutations and what I detail about the relationship between nutrient-uptake and the microRNA/messenger RNA balance in the context of ecological adaptations.

As you may not have fully considered, no experimental evidence links perturbed protein folding to anything but diseases and disorders, which is why nutrient-dependent SNPs in microRNAs may be the required link from biophysical constraints to nutrient-dependent ecological adaptations via gain of function (not perturbed protein folding).

In the context of cell sensors and nutrient-dependent repair, odors induce the de novo creation of olfactory receptor genes that enable nutrients to enter the cell, which is how nutrient-dependent ecological adaptations are controlled.
JVK
1 / 5 (4) Aug 21, 2014
I need more information from people like "Jaeherys" to move forward. No one need comments from others who do not understand genetics or epigenetics.

Large teams of researchers now publish results of experiments that show the importance of protein folding -- at the same time anonymous fools and idiot minions of biology teachers like PZ Myers continue to tout pseudoscientific nonsense. The response from "Jaeherys" is one of the few intelligent responses I have seen. It is encouraging since it may lead to other intelligent responses in the context of new information like this:

http://dx.doi.org...ure13622

It can be compared in the context of "...mutations likely to cause disease – either because their role was already known or because they disrupted protein function..."
http://medicalxpr...ain.html

Disrupted protein folding did not lead to sex differences in cell types. I need a co-author to present a balanced view.
anonymous_9001
5 / 5 (5) Aug 21, 2014
As you may not have fully considered, no experimental evidence links perturbed protein folding to anything but diseases and disorders


Every paper I've cited over the past few weeks does and so do these:

http://mbe.oxford...04.short

http://jhered.oxf...63.short

http://onlinelibr...ed=false

http://genome.csh...abstract

http://www.hindaw...432/abs/
Captain Stumpy
5 / 5 (3) Aug 21, 2014
No one need comments from others who do not understand genetics or epigenetics.
then WHY DO YOU keep responding?
you can't even comprehend the definitions of your own chosen field to post in... but you still keep coming back and posting here...

and you call US idiot minions?

here is an article you should read. http://phys.org/n...lls.html

you EXEMPLIFY the traits of PSEUDOSCIENCE TROLL with your remarks

you cannot answer the questions without resorting to KNOWN PSEUDOSCIENCE and so you choose to denigrate the poster

just like Myers.
you are a failure... a glorified lab tech who cannot comprehend what Myers and most modern biologists talk about, so you stick to your own PSEUDOSCIENCE and doggedly cling to your faith

sorry jimmy. you are the only idiot minion here
JVK
1 / 5 (4) Aug 21, 2014
"Studies on the functional morphology of insect mandibles have identified their ecological relevance [20], including in Orthoptera more generally, where their chewing ability appears to be under selection [21]. Likewise, genitalia are a good proxy for sexual selection [13]; genitalic characters not only show species-level divergence in Amphiacusta but have also been shown to mediate reproductive success in other taxa [13,14]."
http://dx.doi.org...ure13622

A study of mammalian teeth links cell type differentiation from nutrient-dependent sex differences in pheromone production to controlled development of morphological and behavioral traits associated with ecological adaptation in the jaw and genitals via the insect model. http://phys.org/n...ers.html

Clear similarities link what is known about the conserved molecular mechanisms of cell type differentiation via amino acid substitutions in species from microbes to man.
JVK
1 / 5 (5) Aug 21, 2014
"Accumulated evidence suggests that a considerable fraction of substitutions in the Drosophila genome results from positive selection..." The anonymous fool provided this link and many others and he appears to think it is experimental evidence that somehow links perturbed protein folding / mutations to the evolution of biodiversity.

Someone else may need to tell him the biodiversity manifested in insects is nutrient-dependent and pheromone-controlled, which is what Elekonich and Robinson (2000) detailed in the context of our 1996 model of nutrient-dependent pheromone-controlled cell type differentiation in species from microbes to mammals.

They cited our review, because it is easier for serious scientists to build on works of other serious scientists compared to inventing and adding more pseudoscientific nonsense to the nonsense already touted.

See http://www.ncbi.n...10980296 and the citation to Diamond et al (1996) http://www.ncbi.n.../9047261
JVK
1 / 5 (4) Aug 21, 2014
The anonymous fool also seems to think that an "...inherited gain-of-function mutation in the glycogen synthase (GYS1) gene..." somehow links the de novo creation of an enzyme from the mutation to the evolution of biodiversity and sex differences in males and females that are first manifested in the cell type differentiation of yeasts -- in the context of "Gene duplication as a mechanism of genomic adaptation to a changing environment." http://rspb.royal...abstract

The anonymous fool challenges the fact that "One of the main duplicated gene families are the olfactory receptor proteins [18,117–119] so perhaps their duplication may lead to an increase in sensitivity to a particular odour may be adaptive under certain conditions."

For some reason the fool thinks mutations are adaptive under certain conditions and that they lead to sex differences in the cell types of men and women I attribute to the de novo creation of ORGs.
JVK
1 / 5 (4) Aug 21, 2014
Does anyone wonder why the anonymous fool did not cite the works he just provided links to in his criticisms of my published work: http://www.ncbi.n...4959329/

Why would he link to PZ Myers blog cite if he were not one of PZ's idiot minions?

I think part of the problem is that he knows how easily I can refute his ridiculous misrepresentations, which is what I did in my review article -- and it's what I've always done in my published works.

Thus, rather than attempt to refute the experimental evidence I offered, Andrew Jones is here providing links to reviews that he thinks support pseudoscientific nonsense.

He's not even bright enough to realize they support my model of biologically-based cause and effect -- if only by showing how ridiculous theories are used in attempts to make up for the scientific illiteracy of those taught to believe in mutation-initiated natural selection and the evolution of biodiversity.

Anonymous fools may be the biggest of all fools.
anonymous_9001
5 / 5 (4) Aug 21, 2014
The anonymous fool provided this link and many others and he appears to think it is experimental evidence


They're experimental evidence of mutations followed by their selection and you still are unable to refute them. You say they're not evidence, but you cannot explain why.

biodiversity manifested in insects is nutrient-dependent and pheromone-controlled, which is what Elekonich and Robinson (2000) detailed


Your model and the Elekonich and Robinson concern development and behavior, not genotype changes.

For some reason the fool thinks mutations are adaptive under certain conditions


All the papers I post concern identifying mutations, what those mutations do, and why the new variants they produce are more successful. All you can respond with is "you think they're evidence, but they're not" without explaining why they're not.

anonymous_9001
5 / 5 (4) Aug 21, 2014
Thus, rather than attempt to refute the experimental evidence I offered, Andrew Jones is here providing links to reviews that he thinks support pseudoscientific nonsense.


You say mutation and natural selection is false and I provide links that examine mutations and how they're selected in depth. My links are DIRECT refutation of your claims.

He's not even bright enough to realize they support my model


They're direct evidence of mutation and NS, so no they do not. They refute your model.

if only by showing how ridiculous theories are used


How are they ridiculous theories when they're all experimental evidence?

JVK
1 / 5 (4) Aug 21, 2014
I provide links that examine mutations and how they're selected in depth.


I've told you this repeatedly.

Links to papers that report results from works and simply mention the word "mutation" are not experimental evidence of how they are selected. That's why I just refuted two of the misrepresentations.

I have detailed aspects the conserved molecular mechanisms of cell type differentiation via nutrient-dependent amino acid substitutions, and all you have ever done is claim your examples show how cell type differentiation occurs via mutation-initiated natural selection that leads to the evolution of observed biodiversity.

Please stop discouraging others like Jaeherys with your displays of anonymous foolishness. You do nothing more than encourage others to add their ridiculous comments,which makes any attempt at serious discussion impossible. You should be banned from commenting except on PZ Myers blog, where other fools are known to gather.
anonymous_9001
5 / 5 (4) Aug 21, 2014
They are far more than a mere "mention". From the abstract of the last one:

A molecular investigation of the Wrinkly Spreader has provided a mechanistic explanation linking mutation with fitness improvement through the production of a cellulose-based biofilm at the air-liquid interface.


Read through the full text and address the authors if you have any SPECIFIC concerns:

http://www.hindaw.../675432/
JVK
1 / 5 (5) Aug 21, 2014
Excerpt: "The mechanistic explanation of the Wrinkly Spreader success is an exemplar of the modern evolutionary synthesis, linking molecular biology with evolutionary ecology, and provides an insight into the phenomenal ability of bacteria to adapt to novel environments."

Does anyone else but this anonymous fool not understand that the ability of all organisms to adapt is nutrient-dependent? That means the ability is biophysically-constrained. That means you cannot simply invent theories that link molecular biology with evolutionary ecology without providing insight into your phenomenal ignorance of what is biologically plausible and what is a ridiculous assertion.

See for comparison: A quantum theory for the irreplaceable role of docosahexaenoic acid in neural cell signalling throughout evolution http://www.ncbi.n...23206328

The anonymous fool thinks the production of a cellulose-based biofilm at the air-liquid interface arises via mutations.
anonymous_9001
5 / 5 (5) Aug 21, 2014
invent theories that link molecular biology with evolutionary ecology


They didn't invent a theory. They did the research. They investigated what went on at the molecular level. I'll give you a hint as to what they discovered: a mutation resulted in a genetic alteration that allowed Pseudomonas to make a cellulose-based biofilm. The mutation altered the phenotype which made the mutant more successful and it outcompeted the original.
anonymous_9001
5 / 5 (5) Aug 21, 2014
Did you even read the paper past the abstract? If you did, you would be able to point out specifically where they made wrong assumptions, used improper techniques, etc., form a legitimate argument as to why their results are invalid, and pass that along to the authors or to the journal. Instead, you copy and paste the same excerpts from your paper you use as a response to everything and refuse to have a conversation.
JVK
1 / 5 (4) Aug 22, 2014
An emerging role for microRNAs in sexually dimorphic neurobiological systems
http://www.ncbi.n...3654055/

"In this review we cite studies detailing the contribution of miRNAs to neuronal development, cellular maintenance, and the etiology neurological diseases. Importantly, sex steroid hormones play an essential role in maintaining a fine balance between homeostatic and pathological outcomes for all of these processes. From sexual differentiation in the developing brain to the presentation of sex disparities in mental health and AD, it is clear that both hormones and miRNAs are central regulators of these processes, and the overlap between the regulatory processes governing each is vastly understudied."

I reiterate: "...both hormones and miRNAs are central regulators of these processes..." Attributing the preservation of miRNAs to evolution in the context of sex differences is pseudoscientific nonsense.
animah
5 / 5 (3) Aug 24, 2014
Elekonich and Robinson are evolutionary biologists so no JVK, their work DOES NOT support your conclusions.
gtsimpedes
not rated yet Aug 24, 2014
So if the author is correct we can be looking at a process that controls cravings, desires, addictions, mental illness as well as our ability to control our temptations. In such a case it can be referred to as the devil made me do it mechanism. Well I might be getting a bit delusional here but it seems like good science nonetheless.
JVK
1 / 5 (3) Aug 24, 2014
Genomes in turmoil: Quantification of genome dynamics in prokaryote supergenomes
http://www.biomed...abstract

"The rates of 4 types of elementary evolutionary events (hereinafter Genome Dynamics Events or GDE)..."

GDE replaces the pseudoscientific nonsense of mutations, natural selection, and the evolution of biodiversity. Not with "the devil made me do it," but with examination of how ecological factors determine adaptations via the conserved molecular mechanisms of nutrient-dependent amino acid substitutions in species from microbes to man.

Excerpt from Elekonich and Robinson: "The development of species-typical and sex-specific adult behaviors in vertebrate animals is influenced by gonadal steroid hormones, non-gonadal hormones, and non-hormonal factors working on the underlying neural circuitry (reviewed in Diamond et al., 1996...). That's Diamond, Binstock and Kohl (JVK). They linked our model to theirs and did not try to support ridiculous theories.
anonymous_9001
5 / 5 (4) Aug 24, 2014
GDE replaces the pseudoscientific nonsense of mutations, natural selection, and the evolution of biodiversity.


Considering they talk about selection... no.

Contact the authors next time before you make false assumptions.
JVK
1 / 5 (4) Aug 24, 2014
You appear to think that anyone who mentions mutations, natural selection, or any other pseudoscientific nonsense linked to the evolution of biodiversity supports your ridiculous opinions.

Asking me to contact authors who change terms used from "evolution" to GDE in the context of ecological variation and ecological adaptations is more proof of your ignorance.

Why don't you contact an author who can tell us HOW nutrient-dependent pheromone-controlled sex differences in cell types "evolved?"

What kind of anonymous fool (e.g., Andrew Jones) criticizes my refutation of evolutionary theory with his opinions: http://www.socioa...67/34076

But wait... now Andrew Jones wants me to question authors who replace "evolutionary events" with accurate representations of the link between ecology, GDE, and adaptations manifested in all cell types of all species. Should I ask Eugene Koonin if he agrees that Andrew Jones is a fool?

JVK
1 / 5 (4) Aug 24, 2014
Andrew Jones wrote: "In addition, Kohl demonstrates a blatant disregard for established nomenclature. For example, he routinely attempts to redefine 'natural selection'."
http://www.socioa...67/34076

More than a year later, Koonin's group demonstrates his blatant disregard for the term "evolutionary events." See also his 2005 co-authored work: A universal trend of amino acid gain and loss in protein evolution http://dx.doi.org...ure03306

All of his co-authors probably agree by now that the link between ecology and evolution is nutrient-dependent amino acid substitutions. Even if they cannot fully comprehend how amino acid substitutions differentiate all cell types in all individuals of all species, they appear to know that proteins do not "evolve." That means biodiversity does not "evolve." Biodiversity arises via epigenetically effected GDE (Genome Dynamics Events) that lead to controlled ecological adaptations.
JVK
1 / 5 (3) Aug 24, 2014
"...what allows epigenetic marks to be de novo targeted differently in the male and female germlines..." http://www.mdpi.c.../5/3/635

I reiterate: Koonin's group demonstrates his blatant disregard for the term "evolutionary events." The fact that Andrew Jones continues to exemplify ignorance here -- in the context of what could have been intelligent discussion (e.g., about microRNAs) -- attests to the ignorance of all theorists who have not yet accepted the concept, which Koonin's group labels "Genome Dynamics Events."

No matter what you call these events, which are manifested in cell type differentiation via amino acid substitutions, only those who continue to call them "evolutionary events" will be called on to explain why they never learned about how biophysically-constrained nutrient-dependent ecological adaptations lead to biodiversity via amino acid substitutions, and why evolutionary events do not.
anonymous_9001
5 / 5 (3) Aug 24, 2014
You appear to think that anyone who mentions mutations, natural selection, or any other pseudoscientific nonsense linked to the evolution of biodiversity supports your ridiculous opinions.


Their mention of selection did not precede "does not exist", so yeah, they do support it.

authors who change terms used from "evolution" to GDE


They didn't change the term. They are saying GDEs are a part of evolution, not replacing it:

Conclusions: Reconstruction of evolution in groups of closely related bacteria and archaea reveals ... demonstrates that ... are the two dominant evolutionary processes...


Koonin's group demonstrates his blatant disregard for the term "evolutionary events."


There are 58 instances of the word "evolution" or some form of "evol-" in that paper, so no, they don't seem to have a problem with it. Again, don't speak for them. Especially an interpretation that is proven wrong by reading their paper.
JVK
1 / 5 (3) Aug 24, 2014
What evolutionary events do they link to the evolution of sex differences in cell types or to the evolution of biodiversity?

I wrote:
You appear to think that anyone who mentions mutations...


You confirmed that when you replied:
There are 58 instances of the word "evolution"

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