Mitochondrial DNA mutations: The good, the bad, and the ugly

January 13, 2015 by John Hewitt report
Mitochondrial DNA. Credit: en.wikipedia.org

(Medical Xpress)—Programmers typically evolve new code by copying and modifying existing code to meet new needs. With the more advanced programming languages, they also make use of something known in the business as polymorphism—the ability to process objects differently depending on their data type or class. Similarly, one way that life evolves is to copy and modify genes. Biologists, however, often use the term polymorphism to mean different things. Sometimes it simply means a non disease-causing change to a base pair, and sometimes it more specifically means a change found at a frequency of 1% or higher in the population.

The word 'mutation' is often associated with something negative, a disease causing variant or a pathogenic subsitution. The problem with these kinds of terms is that despite their different meanings, they can and will be used to describe the exact same change in any number of specific base pair alterations. This is no way to run scientific dialog, let alone research. At the risk of getting bogged down in such ambiguities, we might suggest that the central question of what is the meaning of change in base pairs can be still answered, only not yet for our nuclear DNA. On the other hand, our rapidly mutating mitochondrial DNA (mtDNA) has just 37 genes and therefore provides a much simpler and compact microcosm to explore. Of those genes, 22 encode already familiar tRNAs, two are for rRNAs, and the remaining 13 spots code subunits for just 4 proteins—ATP synthase, NADH dehydrogenase, cytochrome oxidase, and cytochrome b.

A recent review in Neuron provides a nice summary of the current state of affairs for mitochondrial mutations in the central and peripheral nervous system. Why the nervous system you might ask? The simple answer is that due to the high demand for oxygen in the brain, and therefore for mitochondria, this is where the effects of changes tend to show up. The more complex answer for why mitochondrial mutations have disproportionate effects on the brain leads to a possible explanation for the origins of neurons themselves: their spatially-extended structure, having been evolved largely by and for their mitochondria, provides both refuge from a potentially hostile nuclear environment where they are continually threatened with lysosomal degradation, and also a way to select and deliver mitochondrial derivatives and mtDNA nucleoids to parts unknown.

Among the more specific assaults to mtDNA, is a sniper-like ability seen in Leber's hereditary optic neuropathy (LHON) to uniquely target retinal ganglion cells. The most commonly found mutation of this type looks something like this: LHON ND4 m.11778G>A. In keeping with the official Human Genome Variation Society guide this nomenclature would indicate that this particular defect is caused by a subsitution of adenine for guanine at position 11778 in the 4th subunit of mitochondrial NADH dehydrogenase. On an even more interesting note, these same ganglion cells are known to do something that until now would have been called unusual. Within the lamina of the optic nerve head, before the ganglion cell axons pick up a thick coat of myelin, they select specific mitochondria according to their specific markers and membrane potential, and shed them to their surroundings.

This one-two punch, transexudation followed by transmitophagy, delivers mitochondria to a surrounding meshwork of orthogonally oriented astrocytic processes that eagerly consume them. I asked Mark Ellisman and Nicholas Marsh-Armstrong, the researchers who discovered this, if these events are affected in LHONs or other mtDNA disorders. While they have not looked to deeply into this question specifically, they indicated that new work suggests these events are much more widespread in the brain then we might first imagine, and furthermore that there appears to be cyclic or circadian variation.

The brain is not the only place where mtDNA is routed between cells, or for that matter between organs. Mike Berridge just published work in the journal Cell Metabolism showing that tumor cells from the breast and skin fail to thrive when DNA for respiratory proteins is deleted from their mitochondria (creating so-called rho0 mitochondria). When transplanted in mice, these cells somehow later acquire mtDNA, presumably through horizontal transfer from the host. In the absence of any clear mechanism for uptake of the necessary DNA, the best explanation seemed to be that mitochondria are transferrred to the new cells.

Berridge was able to show that this is the case by comparing mtDNA polymorphism between different mouse strains and cell lines. I also asked him if he thought his results might reflect a similar process to that going on in opic nerve transmitophagy. He noted that the packaging of questionable mitochondria for astrocytic recycling is complimentary to his study and raised the question of whether astrocytes could in turn be a source of yound mitochondria for synapses, especially those at considerable distance from the cell body.

The above observations regarding mitochondria in neurons and mitochondria in tumor cells might be tied together by considering their role in the generation of oocyte and its subsequent differentiation into unique cells in the development of the early embryo. Cancer cells invariably show increased glucose utilization and decreased mitochondrial respiration. This so-called 'Warburg effect' makes them stand out in PET scans where their rapid glucose uptake provides a convenient way to diagnose and track their response to treatment. One explanation of this effect is that cancer-related genes shut down mitochondria that would normally be involved in the apoptosis program that normally kills tumor cells. Crippled or reduced numbers of mtDNA copies could also be an adaptation to the low-oxygen environment in tumor cells.

More convincing perhaps, is the idea that cancer cells shift towards glycolysis despite the presence of oxygen because glycolysis directly provides the building blocks needed for cell proliferation in the right place and proportion. A similar situation may be seen during cell proliferation in the initial stages of the developing embryo where mtDNA replication is temporarily halted for a number of cell division cycles that depends on the particular species. This comes after a phase of mitochondrial proliferation in the maturing oocyte which was preceeded by an even more dramatic mitochondrial genetic bottleneck where the number of mtDNA copies per mitochondria, and per cell was decimated. This restriction-amplification-restriction process is one way the oocyte, and the organism, selects the right mix or heteroplasmy from a pristine population of virginal mitochondrial templates to contribute to the offspring. This embryological Santa Claus, which apportions mitochondria according to an as yet fully seen mechanism may reflect much the same purification and quality control processes we noted in neurons above.

In this view, a mitochondrium effectively wears a given mtDNA variant given its sleeve—it represents the entire organelle which offers itself whole for selection in a way that a single nuclear or germline mutation, amidst a huge background of nuclear DNA variance in each generation, rarely can. But here there is another even more powerful angle of attack to consider. Many ideas in life are best understood by their exceptions, and paternal inheritance of mitochondria is certaining exceptional. Some species of mussels, in particular, do their mitochondrial inheritance a bit differently from the rest of us, and therein lies the magic. At first glance it would appear that they violate the rule of uniparental inheritance because (at least in males), they don't block or target mitochondria donated by sperm for degradation. In most other species, the question is not if, but when and where sperm mitochondria will eventually be eliminated.

However, this apparent violation of uniparental inheritance vanishes when we observe that independent segregation is still maintained; namely, the female type mitochondria are transmitted from mothers in both sexes while the male type is only transmitted from fathers to sons. The important thing for us is that while sperm mitochondria are evenly dispersed among subsequent developing blastomeres to generate females, to make males, sperm mitochondria are concentrated specifically in a blastomere known as 4d. What this means is that not only does the developing embryo have the ability to distinguish mitochondria, but it can accurately position them as well. For example, after fertilization some sperm mitochondria are released in the area where division will later occur, and in other instances they have been observed to concentrate at the cleavage furrow at the 2-4 cell stage.

Since early embryos asynchronously split just one cell at a time, setting a universal speed limit via controlling mtDNA replication and therefore energy available to the embryo enables cells to individually be given identity. As we mentioned, every species has its own differention program, closely regulating the total number of mtDNA copies per cell, and per embryo, up to some given level. For mice that level is the 2 cell stage, and for pigs and cattle the 8 cell stage, while in others it can variously be the blastula, morula or gastrulation stage.

Many of the other specific disease-causing mutations mentioned in the review are not surprisingly found in the tRNA genes. One outstanding question is that considering the similarity of some nuclear encoded tRNAs (like met-tRNA) to mito-tRNAs, what would it take for mitochondrial to utilize nuclear tRNAs, and similarly vice-versa? In other words, do we know that this does not happen? Many of the proteins associated with nucleoids of mtDNA have been shown to be surprisingly versatile. For example, in yeast, both aconitase and Ilv5 are bifunctional with distinct activities both as metabolic proteins and in maintaining mitochondrial nucleoids. Of note, they have been linked to mtDNA positioning and segregation as well as mitochondrial translocations, particularly those associated with cell division.

Researchers currently are unable to manipulate the mitochondrial genome with the same facility that they can manipulate nuclear sequences. However, as the their ability to insert mutation reporters or selectable markers into the mitochondrial genome increases, some of the questions raised above by looking into early devlopmental process for inspiration may be better answered.

A lot of fascinating new results regarding single mitochondrial mutations and their amplified macroscopic effects on the nervous system were left out. They have names like Twinkle, Polg, MELAS, and MERRF. With any luck we can do another review called, Everything you wanted to know about mitochondrial mutations but were afraid to ask.

Explore further: Inheritance of mitochondrial disease determined when mother is still an embryo

More information: — Mitochondrial DNA: Impacting Central and Peripheral Nervous Systems, Neuron, Volume 84, Issue 6, p1126–1142, 17 December 2014. dx.doi.org/10.1016/j.neuron.2014.11.022

— Mitochondrial Genome Acquisition Restores Respiratory Function and Tumorigenic Potential of Cancer Cells without Mitochondrial DNA, Cell Metabolism, Volume 21, Issue 1, p81–94, 6 January 2015. dx.doi.org/10.1016/j.cmet.2014.12.003

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JVK
1.4 / 5 (7) Jan 13, 2015
International Union of Basic and Clinical Pharmacology. XCII. Urotensin II, Urotensin II–Related Peptide, and Their Receptor: From Structure to Function http://pharmrev.a...abstract

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

Taken together, the differences between mutations and amino acid substitutions are clear.

Mutations perturb protein folding and lead to pathophysiology.

Amino acid substitutions link the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man. They are manifested as variation in morphological phenotypes and behavioral phenotypes that arise during cell type differentiation in all cells of all individuals of all species via conserved molecular mechanisms

http://www.ncbi.n...24693353 is a model of cell type differentiation sans mutations.
Vietvet
4.3 / 5 (6) Jan 13, 2015
Yet again Jamie K posts a long comment without referencing the article but does, like he always does, provides a self-referencing link.
JVK
1 / 5 (7) Jan 13, 2015
Excerpt: "The word 'mutation' is often associated with something negative, a disease causing variant or a pathogenic subsitution. The problem with these kinds of terms is that despite their different meanings, they can and will be used to describe the exact same change in any number of specific base pair alterations. This is no way to run scientific dialog, let alone research."

John Hewitt is attempting to explain, without offending, the difference between "mutations" and "amino acid substitutions".

"Vietvet" and any other antagonists who will no doubt add their ridiculous comments here -- as they always do, may still delay the understanding of cell type differentiation that researchers are trying to move forward in the context of the two articles Hewitt reviews.

As always, however, scientific progress will have no impact on science idiots who cannot understand why I took the time to provide across-species examples of cell type differentiation in my model.
JVK
1 / 5 (7) Jan 13, 2015
See what happened the last time John Hewitt tried to help others understand the basic principles of biology and levels of biological organization required to link nutrient-dependent pheromone-controlled RNA-mediated protein folding from amino acid substitutions to cell type differentiation.

http://phys.org/n...ton.html
Origin of the Eukaryotic cell: Part II - Cytoskeleton, membranes, and beyond

Science idiots insist that differences in the cytoskeleton, membranes, and beyond arise via accumulated mutations that lead to the evolution of new species.
Vietvet
4.3 / 5 (6) Jan 13, 2015
If Jamie K's "model" had any merit he wouldn't have to endlessly self-promote it.
JVK
1 / 5 (7) Jan 13, 2015
I wrote:
John Hewitt is attempting to explain, without offending, the difference between "mutations" and "amino acid substitutions".


Science idiots who don't understand the difference criticize me for promoting the only model of biologically-based cause and effect that links the epigenetic landscape to the physical landscape of DNA in species from microbes to man.

See also: "In certain respects, my article reflects some of the points made over 30 years ago by Ho and Saunders (Ho and Saunders, 1979), who wrote: 'The intrinsic dynamical structure of the epigenetic system itself, in its interaction with the environment, is the source of non-random variations which direct evolutionary change, and that a proper study of evolution consists in the working out of the dynamics of the epigenetic system and its response to environmental stimuli as well as the mechanisms whereby novel developmental responses are canalized.' " http://jeb.biolog...abstract
JVK
1 / 5 (7) Jan 13, 2015
It will not become clearer that novel developmental responses are canalized in the context of the nutrient-dependent pheromone-controlled physiology of reproduction. It is not going to become clearer that canalization requires RNA-mediated amino acid substitutions that differentiate all cell types of all individuals of all species.

It will not become clearer that only science idiots continue to believe in ridiculous theories like this: "...genomic conservation and constraint-breaking mutation is the ultimate source of all biological innovations and the enormous amount of biodiversity in this world." http://www.amazon...99661731

What will become clearer is that RNA-mediated epigenetic regulation of gene expression links nutrient uptake to the pheromone-controlled physiology of reproduction and to biodiversity via the conserved molecular epigenetics of the mechanisms we detailed in our 1996 review: http://www.ncbi.n.../9047261
johnhew
5 / 5 (2) Jan 13, 2015
Seems strange to report temperature-dependent comparative secondary structure of urotensins using Kelvins as a unit?
Steve 200mph Cruiz
5 / 5 (5) Jan 13, 2015
JVK:
www.khanacademy.o.../biology

You need to watch every video on here
JVK
1.3 / 5 (6) Jan 13, 2015
using Kelvins as a unit


I don't know enough about the measurements to understand why you think the reporting is strange. Could it be due to the fact that this comes from an International Group?
JVK
1 / 5 (7) Jan 13, 2015
You need to watch every video on here


You need to respond to John Hewitt's review; to the comments on his review; or to the cited works.

Anything other comments assure others that you are just one more science idiot, and there are too many of those here already.
Steve 200mph Cruiz
5 / 5 (5) Jan 13, 2015
No JVK,

You're the one with the "theories", that means YOU'RE the one who has to prove you have a high school education.
JVK
1.5 / 5 (6) Jan 13, 2015
You're the one with the "theories"


We detailed what was known about RNA-mediated epigenetic regulation of gene expression in our 1996 review. http://www.hawaii...ion.html See the section on molecular epigenetics.

What aspect of cell type differentiation in species from microbes to man do you think is based on some ridiculous theory?
anonymous_9001
5 / 5 (4) Jan 13, 2015
Mutagenesis studies irrefutably show mutations having beneficial effects on enzymes. If you disagree with this, Kohl, either you have an issue with calling the changes in the genes mutations or you have an issue with whether the resulting changes in the enzymes were beneficial. If it's the former, keep in mind that the only things present in mutageneis studies like the ones I've cited are the genes, replicative enzymes, and precursor molecules. The changes in the genes are due to the inherent error rate of the replicative enzymes themselves.
JVK
1 / 5 (4) Jan 13, 2015
See what John Hewitt wrote (above) "The word 'mutation' is often associated with something negative, a disease causing variant or a pathogenic subsitution. The problem with these kinds of terms is that despite their different meanings, they can and will be used to describe the exact same change in any number of specific base pair alterations. This is no way to run scientific dialog, let alone research."

Attempting to discuss anything with someone who thinks his research shows that mutations have beneficial effects, is a waste of time. Andrew Jones (aka anonymous_9001) has trapped himself in his thesis. http://www.scribd...s#scribd

Only a science idiot would claim that he or any other science idiot could create a system of heredity and evolution through natural selection based on mutagenesis experiments. Mutations perturb protein folding and cause physiopathology -- not biodiversity.
Vietvet
3 / 5 (2) Jan 14, 2015
Seems strange to report temperature-dependent comparative secondary structure of urotensins using Kelvins as a unit?


I like your question. It led me to research something I had only thought about in cosmological terms without appreciating how it applies to biology.
Vietvet
3.7 / 5 (3) Jan 14, 2015
using Kelvins as a unit


I don't know enough about the measurements to understand why you think the reporting is strange. Could it be due to the fact that this comes from an International Group?


Once you understand the difference between measuring HEAT and measuring molecular activity you'll have the answer.
alfie_null
5 / 5 (3) Jan 14, 2015
. . . Only a science idiot would claim that he or any other science idiot . . .

You, by your lonely self are clearly in the minority. We'll continue to call what they do science and call them scientists. Call yourself something else.

Universally reviled and mocked, yet you return for more. Aberrant behavior. Is it nature or nurture?
JVK
1.5 / 5 (4) Jan 14, 2015
Universally reviled and mocked...


Why would anyone claim such nonsense when two of my published works have won awards, and the majority of serious scientists now realize how the epigenetic landscape is linked to the physical landscape of DNA in organized genomes of species from microbes to man via the conserved molecular mechanisms we detailed in our 1996 review?

http://www.hawaii...ion.html
JVK
1 / 5 (3) Jan 14, 2015
Once you understand the difference between measuring HEAT and measuring molecular activity you'll have the answer.


Thank you for explaining how much you know about this. It is everything I expect from a science idiot.
JVK
1.7 / 5 (3) Jan 14, 2015
Mutagenesis studies irrefutably show mutations having beneficial effects on enzymes.


Please try to link the studies to what is known about links between metabolic networks and genetic networks in the context of the enzymes measured in the study that supports pharmacogenomics testing.

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

I suspect everyone at the Mayo Clinic knows that mutations are not beneficial, but watch this video so that you are prepared to convince them that your experiment showed some mutations are beneficial.

https://www.youtu...G_9EEeeA
JVK
1 / 5 (3) Jan 14, 2015
Once you understand the difference between measuring HEAT and measuring molecular activity....


http://www.jneuro...abstract

This report makes it imperative that "Vietvet" or someone else like him explain how thermodynamic cycles of protein biosynthesis and degradation can be linked via mutations to the chemoreceptors that actively maintain pH in a carefully controlled range that links biological energy from the sun to the life of every organism that requires oxygen to survive.

In case "Vietvet" chooses to not explain anything about how to "...understand the difference between measuring HEAT and measuring molecular activity..." I hope another science idiot will do it so that their theories about mutations and evolution can be placed into the context of life-saving measures that sometimes require artificial ventilation to maintain the pH balance.

Alternatively, science idiots can continue to kill people with their ridiculous claims.
anonymous_9001
5 / 5 (2) Jan 15, 2015
Nothing about metabolic and genetic networks changes the fact that we can directly observe beneficial mutations. You're trying to obfuscate. We can mutate libraries of genes, transcribe and translate them, and observe better enzymes emerge as a consequence. Cut and dried.
JVK
1 / 5 (3) Jan 15, 2015
You're trying to obfuscate.


You're trying to stick with your pseudoscientific nonsense based on de Vries definition of "mutation."

John Hewitt wrote: "The word 'mutation' is often associated with something negative, a disease causing variant or a pathogenic subsitution. The problem with these kinds of terms is that despite their different meanings, they can and will be used to describe the exact same change in any number of specific base pair alterations. This is no way to run scientific dialog, let alone research."

Why don't you address that fact, or any other fact associated with cell type differentiation in species from microbes to man?

I wrote: "Only a science idiot would claim that he or any other science idiot could create a system of heredity and evolution through natural selection based on mutagenesis experiments. Mutations perturb protein folding and cause physiopathology -- not biodiversity."

-- and yet, here you are AGAIN!
anonymous_9001
5 / 5 (2) Jan 15, 2015
Why don't you address that fact


The fact that people get confused because "mutation" can refer to both good and bad changes? You exemplify that perfectly. It can be easily remedied by qualifiers, e.g.- "good mutation" and "bad mutation". Neutral mutations also exist.

How about we address you agreeing with Hewitt when he uses the term "pathogenic subsitution"?

According to you, all negative changes are mutations and all positive changes are substitutions.

Mutations perturb protein folding and cause physiopathology -- not biodiversity


All mutagenesis/directed evolution studies contradict this directly.
JVK
1 / 5 (3) Jan 15, 2015
Hewitt:
Programmers typically evolve new code by copying and modifying existing code to meet new needs.


Is he trying to politely tell the biologically uninformed that Francis Collin's "Language of God" (i.e.. DNA) did not evolve via mutations. Each mutation can be considered to be a change to a letter of the code that would make the language useless. No information could be conveyed from the epigenetic landscape to the physical landscape of DNA that would enable its biophysically constrained chemistry of protein folding.

That's why there is no point to discussion of positive mutations. You invent them for use in your thesis, as have other science idiots, but your definition and assumptions about what mutations do are useless to serious scientists.

According to you, all negative changes are mutations and all positive changes are substitutions.


Stop trying to put words in my mouth. Start trying to make sense of the ridiculous language you use.
anonymous_9001
5 / 5 (2) Jan 16, 2015
Stop trying to put words in my mouth.


I'm not. You consistently refer to all positive base changes as substitutions and all negative ones as mutations.

What about duplications? What do you call positive and negative duplications?
JVK
1 / 5 (3) Jan 16, 2015
What do you call positive and negative...


Thanks for asking. I don't call them anything. I modeled the difference between nutrient-dependent amino acid substitutions, which are fixed by the metabolism of nutrients to species-specific pheromones that control the physiology of reproduction. The model clarifies the fact that mutations perturb protein folding and that amino acid substitutions link the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man via the biophysically constrained chemistry of protein folding and RNA-mediated cell type differentiation.

You reviewed the model http://www.ncbi.n...24959329 and claimed:

...James Kohl presents an unsupported challenge to modern evolutionary theory and misrepresentations of established scientific terms and others' research. It was a mistake to let such a sloppy review through to be published.


Only a science idiot would say that.
JVK
1 / 5 (3) Jan 16, 2015
John Hewitt wrote:
Similarly, one way that life evolves is to copy and modify genes. Biologists, however, often use the term polymorphism to mean different things. Sometimes it simply means a non disease-causing change to a base pair, and sometimes it more specifically means a change found at a frequency of 1% or higher in the population.


The sun's biological energy is linked via amino acid substitutions to gene duplication in plants and animals. That is the basis for this claim: "Life is physics and chemistry and communication" http://dx.doi.org...as.12570

Science idiots like Andrew Jones base their claims on mutagenesis experiments. See his thesis: http://www.scribd...s#scribd

Rarely do science idiots get reviews of serious scientists works published. Jones thinks because his review was published that others do not think he is a science idiot.

What do you think?
JVK
1 / 5 (2) Jan 16, 2015
See also: Environment, not genes, dictates human immune variation, research finds
http://medicalxpr...une.html

My comment: http://www.sfgate...8629.php

Excerpt: David Raulet... said in an e-mail that there is a "large body of evidence that genetic differences affect susceptibility to infections." He's also not ready to declare that environment trumps genetics in either the immune system or overall health.

Others at Berkeley have always refused to accept any experimental evidence that refutes their ideas about mutations and evolution.
-------
Clearly, it is not only the fault of Andrew Jones that he became a science idiot. Someone taught him to become one. And someone may also be teaching your descendants to also become science idiots.

Perhaps you should complain about that before you encounter more science idiots like Andrew Jones.
rockwolf1000
5 / 5 (1) Jan 16, 2015
Clearly, it is not only the fault of Andrew Jones that he became a science idiot. Someone taught him to become one. And someone may also be teaching your descendants to also become science idiots.

Perhaps you should complain about that before you encounter more science idiots like Andrew Jones.


I'm not concerned.

We've all met the worst science idiot in James Van Kohl.

Go away. No one is buying your BS or your stinky love potions.

It's not surprising someone like you would try to sell such garbage. It's obvious that a bonafide autoclave operator such as yourself has no social skills and thus you would need to administer a chemical (drug/pheromone) in order to pick up a woman. Do you also employ roofies in the same manner?

http://en.wikiped...trazepam

Very sad indeed.
JVK
2 / 5 (2) Jan 16, 2015
John Hewitt wrote: "On the other hand, our rapidly mutating mitochondrial DNA (mtDNA) has just 37 genes and therefore provides a much simpler and compact microcosm to explore. Of those genes, 22 encode already familiar tRNAs, two are for rRNAs, and the remaining 13 spots code subunits for just 4 proteins—ATP synthase, NADH dehydrogenase, cytochrome oxidase, and cytochrome b."

Does anyone know what NADH dehydrogenase does? Could it link hydrogen atoms to ecosystems via light-induced amino acid substitutions in plants and animals and nutrient-dependent amino acid substitutions that differentiate all the cell types of all individuals of all species that have not arisen via mutations, which is what de Vries named the energy jumps?

http://en.wikiped...inone%29 It is one of the "entry enzymes" of cellular respiration or oxidative phosphorylation in the mitochondria.[1][2]
FainAvis
not rated yet Jan 17, 2015
@JVK tl;dr
JVK
2 / 5 (2) Jan 17, 2015
Science is not for those with short attention spans.

Our 1996 review detailed everything known about the nature/nurture debate. In 1997, our co-author exposed the 'textbook' misrepresentations made by John Money who bastardized the entire field of sex research with claims that nurture trumped nature.

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

http://hawaii.edu...ent.html
This was later expanded into a full-length book As Nature Made Him: The Boy Who Was Raised as a Girl,[4]

"White Matter Microstructure in Transsexuals and Controls..." http://www.jneuro...abstract rehashes every aspect of what we detailed in 1996 and reaches the same obvious conclusions.

Re:
...not ready to declare that environment trumps genetics in either the immune system...


Many researchers continue their support of the evolution industry and cannot face the truth.
anonymous_9001
5 / 5 (1) Jan 17, 2015
Does anyone know what NADH dehydrogenase does?


As the name implies, it dehydrogenates NADH to produce NAD+, H+, and 2 electrons.

light-induced amino acid substitutions


How many times do you have to be informed that nothing in that paper suggested light CAUSED the substitution? That paper was about the effect the substitution had on the enzyme, not the cause of the substitution. Visible light does not have the necessary energy to break bonds.
jsdarkdestruction
5 / 5 (2) Jan 18, 2015
Jvk, we see through your appeal to authority to avoid answering questions and prove your ideas. I Know you are desperate for someone, anyone, to support your ideas but your nose is turning brown from kissing johns bottom so much.

John, what happened to your declaration that if anyone insulted or bad mouthed another user in the comment section on one of your "articles" you'd do everything in your power to get them banned?
Did you realize that you were deluding yourself as to how important you are to the site and how how much power you wield ? Was it because your buddy jvk does it all the time, usually first and with no provocation?
JVK
1 / 5 (2) Jan 18, 2015
John, what happened to your declaration that if anyone insulted or bad mouthed another user in the comment section on one of your "articles" you'd do everything in your power to get them banned?


What happened to Captain Stumpy and Uncle Ira?

That paper was about the effect the substitution had on the enzyme, not the cause of the substitution.


I mentioned before that John Hewitt may have decided to let the biologically uninformed continue to expose their own ignorance. Obviously, removing one science idiot simply encourages another one to take their place.

Thanks to 'jsdarkdestruction' for providing an example of that.

Did anyone see the news about the latest SICB meeting, where presenters linked behavior, immunity, and life history via chemosensory genes that diversify through protein-sequence changes? It linked crustaceans to insects via conserved molecular mechanisms, not mutations. http://www.scienc...20.short
JVK
1 / 5 (2) Jan 18, 2015
Re: "It linked crustaceans to insects...."

The presenters may not realize what they did because Billie Swalla, the SICB president, encourages biological ignorance. She co-authored http://dx.doi.org...re13400, which claims "...ctenophore neural systems, and possibly muscle specification, evolved independently from those in other animals."

Six months later, those findings were refuted by an accurate representation of biologically-based cause and effect that indirectly links species from microbes to man: http://dx.doi.org...omms6536

Two weeks later SICB presenters linked crustaceans to insects but were left with questions about how they could all be part of one big family (organisms of "like kind").

"But researchers have learned that production of both hormones depends on the same rate-limiting enzymes... And Jerome Hui... found that in both insects and crustaceans, the same set of micro RNAs control expression of the genes for those enzymes."
JVK
1 / 5 (2) Jan 18, 2015
That paper was about the effect the substitution had on the enzyme, not the cause of the substitution. Visible light does not have the necessary energy to break bonds.


Why would anyone whose claims about biodiversity are based on mutagenesis experiments attempt to tell others that the sun's biological energy is not essential to life in the context of physics, chemistry, and information about the epigenetic landscape which must be linked to the physical landscape of DNA in the organized genomes of species from microbes to man, for species from microbes to man to survive?

Is it not enough for this science idiot (aka Andrew Jones) to have made his ridiculous thesis available for all to see? http://www.scribd...s#scribd

How can he possibly continue to think that anything he says is relevant to discussion among intelligent people?
anonymous_9001
5 / 5 (2) Jan 18, 2015
Until you stop copying and pasting your catchphrases over and over, nobody can have an intelligent conversation with you. Converse as a normal person would. A phrase often used when speaking with toddlers- Use your words. It applies even more so to you.

http://www.parent...r-words/

It's much easier for a child this age to express herself by hitting, biting, and kicking than by stringing together a polite request with her limited vocabulary


What in that paper suggested that light CAUSED the substitution? The paper was about the effect the substitution had on the enzyme's action, not the cause of the substitution. You pull conclusions out of thin air that have nothing to do with the works you cite.
JVK
1 / 5 (2) Jan 18, 2015
What in that paper suggested that light CAUSED the substitution?


Everything known about physics and the chemistry of protein folding. What does the paper suggest to you? What do you claim caused the amino acid substitution that links biological energy from the sun to plant life and to animal life via the biophysically constrained chemistry of RNA-mediated protein folding?
anonymous_9001
5 / 5 (2) Jan 18, 2015
Everything known about physics and the chemistry of protein folding


That doesn't make any sense and it should be obvious as to why. You're aware folding is the process by which proteins acquire secondary and tertiary structure following translation, right? How does the process of folding make changes to the base sequence of DNA?
JVK
1 / 5 (2) Jan 18, 2015
How can you not realize that your ridiculous mutagenesis experiments led you to assume everything you think you know, when everything you know is based on someone else's definition of "mutation" and others assumptions?

"[W]hat Haldane, Fisher, Sewell Wright, Hardy, Weinberg et al. did was invent.... Evolution was defined as "changes in gene frequencies in natural populations." The accumulation of genetic mutations was touted to be enough to change one species to another.... Assumptions, made but not verified, were taught as fact." http://www.huffin...211.html
anonymous_9001
5 / 5 (2) Jan 18, 2015
ridiculous mutagenesis experiments


You've yet to give a straight answer as to what invalidates said experiments. They're direct observational evidence of mutations occurring replication and altering enzyme activity, in some cases, for the better. What part of that do you disagree with? Do you disagree with the changes in the genes being mutations or do you disagree with the resulting enzymes being improved?

After you answer this, of course:

How does the process of folding make changes to the base sequence of DNA?

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