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Beyond the Blueprint

In addition to serving as a set of instructions to build an individual, the genome can influence neighboring organisms and, potentially, entire ecosystems.

By , , and | September 1, 2014

A GENETIC WEB: Interacting species, such as this Gulf fritillary butterfly (Agraulis vanillae) feeding on goldenrod blooms at the edge of a salt marsh on St. Simons Island, Georgia, have an intimate relationship: the genes of one are likely influencing the phenotype of the other.© BEACHCOTTAGEPHOTOGRAPHY/ISTOCKPHOTO.COM

The relationship between an individual’s phenotype and genotype has been fundamental to the genetic analysis of traits and to models of evolutionary change for decades. Of course, scientists have long recognized that phenotype responds to nongenetic factors, such as environmental variation in nutrient availability or the presence of other, competing species. But by assuming that the genetic component of a particular trait is confined to your genes and only yours, scientists overlooked another important input: the genes of your neighbors.

Take field crickets as an example. To identify potential mates, female crickets listen with ears on their forelegs to the males’ songs, produced by the rubbing together of their forewings. Some males emit series of long, trill-like chirps, an advertisement of their fitness that females find very attractive. Songs dominated by short chirps have less pull. But female crickets don’t evaluate songs on their absolute merits; instead, their preferences are influenced by the songs they’ve heard in the past. Female crickets previously exposed only to songs with long chirps are less likely to respond to short-chirp songs than females that have been exposed to the songs of less-fit males already. The insects appear to be retaining information about available males and then using that information to assess the attractiveness of suitors.1

Choosing mates amidst competition is ubiquitous among animals, but the logistics of how such choice evolved is less straightforward: because male song type is largely determined by genetics, female mating behavior is under the influence of male genes. In other words, the females’ decision-making behaviors evolved based on the genetic composition of the entire social group. Such indirect genetic effects (IGEs), also called associative effects or extended phenotypes, are common and have profound implications for evolution. Beyond learning and behavior in social species, IGEs affect how organisms develop, how productive plants are, and whether individuals are attacked by predators, herbivores, and disease.

In some sense, examples of IGEs are intuitively obvious. No individual exists in a vacuum, isolated from the influences of others it encounters. Yet for decades, many prominent evolutionary theories assumed that all of the genetic influences on an individual’s phenotype came from genes within itself. What the field needs now is a clear framework that recognizes IGEs as additional factors in a population’s evolution, allowing for more-accurate predictions about how biological systems will change in the future. The genetic makeup of an individual not only influences phenotypes of individuals in its own species, but can have far-reaching effects on organisms at different trophic levels within its food web, impacting the dynamics of entire ecosystems. The role of commensal microbes in human health is a prime example of how IGEs can transcend species boundaries.

How IGEs affect evolutionary dynamics remains very much an open question. Recent theoretical strides in this area show how IGEs can greatly accelerate evolutionary change and hint at their hitherto unsuspected roles in such varied phenomena as animal mating rituals, the development of human agricultural systems, species range shifts in response to climate change, and even altruism. The influences of IGEs on diverse evolutionary processes are undoubtedly more complicated than most models can capture, and biologists must think creatively about new phenomena that IGEs may drive.

The social network

House cricket© VITALII/ISTOCKPHOTO.COMExamples of IGEs in social learning and behavior, such as cricket mating song preferences, are common. For example, contests between male red deer (Cervus elaphus) determine the population’s dominance hierarchy, such that the fitness of one male affects the outcome of contests with his opponents. Male dancing fiddler crabs (Uca terpsichores) build shelters that differ in quality, some of which provide better protection than others. Shelter quality determines which males are selected by female fiddler crabs, and the fitness of the female is in turn affected by the quality of the shelter, which is partly under the control of the male’s genes.

As a highly social species, humans are no exception. More than 50 years ago, Albert Bandura of Stanford University and his colleagues conducted the now-famous Bobo doll experiment, in which they exposed 3- to 6-year-old children to three different scenarios: an adult peacefully playing with toys while ignoring a weighted, inflatable toy called Bobo (that returns to a standing position after being disturbed); an adult yelling and striking the doll; or no adult present at all. When the children were given the choice of toys, they tended to mimic the actions of the adult they had observed: those who had seen an adult aggressively playing with the doll did the same, but played quietly with the other toys.2 Because behavioral traits such as aggressiveness are partially determined by genetics, this experiment suggested that the phenotypes of adults, and, in part, their genes, are a factor shaping the social choices made by children.

Recent research has also shown that when species interact, IGEs can have far-reaching effects. Last year, we published an article about two goldenrod species (Solidago altissima and S. gigantea) whose genomes affected not only neighboring plants, but also associated pollinators, and even the rate at which nutrients in dropped leaves are recycled through the ecosystem.3 We grew genetically identical individuals of each goldenrod species with neighbors of the same or different genetic identity to examine how unique combinations of plants fared. As expected, some clones were more productive than others—both in terms of above- and belowground biomass growth—and the more productive clones received more visits from pollinators. More surprisingly, clones predictably affected the productivity and chemical composition of their neighbors. For example, the neighbors of a particularly productive S. gigantea clone always devoted more resources to belowground biomass, a shift that was accompanied by higher levels of the complex polymer lignin. Increased lignin production by the plants neighboring the productive S. gigantea clone, in turn, made the neighbors’ leaf litter less attractive to microbial decomposers, such that it look longer for those nutrients to be cycled. The effects on pollinators were less clear: focal plants had more pollinators when grown next to particular genotypes, but a subsequent analysis indicated that it wasn’t simply due to plants producing more biomass. It’s possible that differences in the timing of floral displays between neighbors influenced visitation.

Also last year, Darren Rebar and Rafael Rodríguez of the University of Wisconsin–Milwaukee found additional evidence to support the idea that IGEs could have impacts across an ecosystem. They explored the interactions of treehoppers (Enchenopa binotata) and the nannyberry tree (Viburnum lentago), which serves as the insects’ host plant and primary environment.4 On the population level, as evolution acts on the plants’ genes, the treehoppers’ environment changes. And because each plant is genetically different—yielding larger or smaller leaves that provide better or worse hiding places for the arthropods, for example—a different mix of plants may select for different traits in their associated arthropod community.

By assuming that the genetic component of a particular trait is con­fined to your genes and only yours, scientists overlooked another important input: the genes of your neighbors.

For this experiment, the researchers raised a random sample of treehoppers on several clones of V. lentago and found that different clonal lines had varying effects on the arthropods’ traits related to mating and reproduction. Once again, the influence of the plants’ genomes on the treehoppers may seem obvious in retrospect, but this study provides some of the most direct evidence to date that IGEs operate between trophic levels of an ecosystem. This also reinforces the notion that IGEs are ubiquitous in natural systems, but are not always recognized as such. Moreover, this example illustrates an important consequence of IGEs: when an organism’s environment has a genetic component, that environment itself can evolve.

A changing landscape

SHARED GENETIC EFFECTS: Pollinators, such as this honeybee on a thyme flower, are under the influence not just of their own genomes, but the genes of their host plants as well. The genetic underpinnings of a plant’s nectar productivity, for example, could affect an insect’s physiology and behavior.© GREGORY DUBUS/ISTOCKPHOTO.COMOne ecosystem in which IGEs undoubtedly have a major influence is the human gut. Researchers are developing microbes as tools to combat obesity, for example, and some are already used in skin-care products and for the treatment of Clostridium difficile infections. In each case, researchers are exploiting IGEs, targeting the genetic composition of the gut microbial community to effect a phenotypic change in the patient.

Recently, perturbations in the gut microbiome have been linked to cardiovascular disease, the leading cause of death worldwide. Red meat contains a molecule called carnitine that, when broken down by gut microbes, becomes trimethylamine-N-oxide (TMAO), a compound that causes plaque to build up and clog arteries. In April 2013, Stanley Hazen of the Cleveland Clinic and his colleagues enlisted omnivorous and vegan human volunteers to eat red meat and then tested differences in the activity of their gut microbes. The gut microbes of vegans didn’t break down carnitine into TMAO as fast as the bacterial community of meat eaters, suggesting that the function of the gut microbiome has evolved in response to host diet.5 These changes to the gut bacterial community have, in turn, affected people’s ability to digest certain foods, with implications for their health, such as susceptibility to heart disease.

We should not be surprised if future research continues to affirm the relationship between the genetic contents of our commensal bacterial communities and our own health. (See “The Body’s Ecosystem,” The Scientist, August 2014.) Indeed, humans have long recognized that altering the microbial composition of the gut may be beneficial. The idea of using fecal material to treat digestive issues dates as far back as the 4th century, when ancient Chinese practitioners created soups that included fecal material from healthy individuals for those suffering from digestive problems. Modern methods in fecal bacteriotherapy are more sophisticated in how the material is transferred, but the basic principle is the same. Use of these procedures in recalcitrant cases of C. difficile infection is approved as a treatment and has already produced positive outcomes for patients: Els van Nood of the University of Amsterdam, along with a group of other researchers, showed in 2013 that fecal transplants could be more effective at treating C. difficile than the antibiotic vancomycin.6

IGEs also may play a role in the migration of species to different geographic ranges as the Earth’s climate continues to change. In a paper published earlier this year, we showed that plants typically found at high elevations grow better when near other high-elevation individuals of the same species, harboring different high-elevation-adapted genotypes. The same was not true of low-elevation plants, which do not perform better in the presence of other low-elevation varieties.7 Mathematical models published earlier this year by one of us (Schweitzer) confirmed this by showing that plant-soil interactions—through which plants alter bacterial and fungal soil communities with subsequent impacts on plant fitness—can lead to soil properties that favor some individuals over others, thereby selecting for different plant and microbial traits over time.8

In addition, the feedback that can occur as a consequence of IGEs may affect the rate and direction of evolution, possibly speeding the process of local adaptation to novel environmental conditions. (See “Seeds of Hopelessness,” The Scientist, August 2014.) Global climate change is causing significant shifts in environmental conditions worldwide by altering temperature and precipitation patterns and fragmenting once-intact habitats. These changing environments are a hotbed for IGEs; we just have to know where to look and how to detect them.

Remodeling evolution

IT TAKES A VILLAGE: Indirect genetic effects (IGEs) are ubiquitous in all ecosystems. Animals that feed or live on other species, for example, are under the influence of that species’ genes. And looking closely at any ecosystem will reveal hundreds more IGEs, which are overlooked by the majority of evolutionary models. It’s time for researchers to consider all the genes in an environment when exploring the evolution of a single species, rather than simply the genome of the focal organism.
See full infographic: JPG | PDF
© LINDSAY HOLLADAY
When it comes to modeling IGEs to explore their influence on evolution, scientists must develop a framework that is both conceptual—drawing from examples across scientific fields to develop a cohesive theory of how IGEs influence genetic change—and mathematical, allowing researchers to make precise, testable predictions. Although the idea that social interactions could accelerate evolution dates back to 1915, interest in the evolutionary importance of IGEs surged in the late 1950s, and some four decades later, scientists finally began writing mathematical models to formalize these predictions. In particular, papers from Allen Moore, then based at the University of Kentucky, and Jason Wolf, first at Kentucky and later at Indiana University, developed evolutionary models that incorporated IGEs and quantified how these affected rates of evolution. Moore and Wolf showed that for certain traits, such as behaviors that involve reciprocal responses like escalating aggression between individuals, IGEs can greatly accelerate the rate of evolutionary change.9,10 Because traits in a focal individual are also part of the “environment” for an interacting individual, when the focal individual’s traits change, so does the environment for an interacting individual—and vice versa. When traits of the focal and interacting individuals both change in the same direction, a positive feedback loop forms that accelerates evolutionary change.

Evolutionary models that incorporate IGEs have developed to the point that they can inform how some societies have developed egalitarian or altruistic tendencies over time. Most animal populations are composed of genetically diverse organisms, some weaker and some stronger, resulting in the adoption of rigid dominance hierarchies. But this is not a universal structure of animal societies. Diverse species, from invertebrates to humans, have complex social structures in which individuals make sacrifices for the good of the group, or for the good of others.

When an organism’s environment has a genetic component, that environment itself can evolve.

According to mathematical models, the answer may involve genetically determined, group-level aversion to inequity that counteracts the tendency of strong individuals to demand tribute from the weak. Sergey Gavrilets of the University of Tennessee, Knoxville, modeled such a system in which the evolution of “helping” behavior was an emergent property of the model.11 In this model, a group of imagined organisms of the same species interact and are ranked from strongest to weakest. When an individual finds a resource, a competitor may demand that resource, and the finder must then decide whether to give in or resist. Gavrilets’s model assumes that there are significant risks associated with losing a contest for possession of the resource, suggesting that the weaker individual will often give in. But the distribution of resources throughout a large group affects every individual in that group, not just a bully and its victims. If the demanding individual has more resources, and is therefore likely to be stronger than the resisting individual, it can be beneficial for an observer to intercede on behalf of the resisting individual, provided that the risk of injury or other costs are not prohibitive. In other words, in Gavrilets’s model, the selfish impulse turns out to be an individual-level aversion to inequality—a desire that no one else be stronger than oneself. Such behavior represents an IGE through which the ultimate share of resources in a population depends on the simultaneous expression of genes in many interacting individuals.

Gavrilets’s model indicates that helping behavior can evolve in just 1,000 generations, a very short time span in the history of human culture, and can ensure a more equitable, although not perfectly even, distribution of resources even in the presence of oppressive individuals. Moreover, because the tendency of an individual to participate in a conflict is genetically determined, these “escalation thresholds” can evolve over time.

Such helping is one of many examples of behavior that could be described as moral decisions, a topic that has attracted the attention of scholars for millennia. Some of the most convincing work on the evolution of morality suggests that it is not only the intelligence of humans that promotes moral behavior, but the demands of social groups in which humans find themselves embedded—the expectation to behave a certain way and to follow certain rules. If this is indeed the case, many of these social demands likely evolved due to impacts of IGEs. Whether we study crickets, microbes, plants, or humans, IGEs are important components of many biological systems and key drivers of evolution of all life. 

Mark A. Genung is a postdoctoral researcher in the lab of Joseph K. Bailey, who is an associate professor of ecology and evolutionary biology at the University of Tennessee, Knoxville. Jennifer A. Schweitzer is also an associate professor in the department.

References

  1. N.W. Bailey, M. Zuk, “Field crickets change mating preferences using remembered social information,” Biol Lett, 5:449-51, 2009.
  2. A. Bandura et al., “Transmission of aggression through imitation of aggressive models,” J Abnorm Soc Psych, 63:575-82, 1961.
  3. M.A. Genung et al., “The afterlife of interspecific indirect genetic effects: genotype interactions alter litter quality with consequences for decomposition and nutrient dynamics,” PLOS ONE, 8:e53718, 2013.
  4. D. Rebar, R.L. Rodríguez, “Trees to treehoppers: genetic variation in host plants contributes to variation in the mating signals of a plant-feeding insect,” Ecol Lett, 17:203-10, 2014.
  5. R.A. Koeth et al., “Intestinal microbiota metabolism of l-carnitine, a nutrient in red meat, promotes atherosclerosis,” Nat Med, 19:576-85, 2013.
  6. E. van Nood et al., “Duodenal infusion of donor feces for recurrent Clostridium difficile,” New Engl J Med, 368:407-15, 2013.
  7. J.K. Bailey et al., “Indirect genetic effects: an evolutionary mechanism linking feedbacks, genotypic diversity and coadaptation in a climate change context,” Func Ecol, 28:87-95, 2014.
  8. J.A. Schweitzer et al., “Are there evolutionary consequences of plant-soil feedbacks along gradients?” Func Ecol, 28:55-64, 2014.
  9. A.J. Moore et al., “Interacting phenotypes and the evolutionary process. 1. Direct and indirect genetic effects of social interactions,” Evolution, 51:1352-62, 1997.
  10. J.B. Wolf et al., “Evolutionary consequences of indirect genetic effects,” Trends Ecol Evol, 13:64-69, 1998.
  11. S. Gavrilets, “On the evolutionary origins of the egalitarian syndrome,” PNAS, 109:14069-74, 2012.

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Posts: 0

September 3, 2014

Three published reviews link what was known about molecular epigenetics in 1996 to nutrient-dependent amino acid substitutions that differentiate cell types and to the pheromone-controlled physiology of reproduction in species from microbes to man via conserved molecular mechanisms of alternative splicings of pre-mRNA. Nutrient-dependent/pheromone-controlled adaptive evolution: a model. (2013) Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors. (2012) From fertilization to adult sexual behavior. (1996)

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

Evolutionary models lack experimental evidence of evolutionary events that are required to link the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man.

It is time to examine evidence that attests to the biologically-based cause of cell type differences in all cells of all tissues in all organs of all organisms and to stop claiming that the differences in morphological and behavioral phenotypes "evolved." 

Ecological variation leads to nutrient-dependent pheromone-controlled ecological adaptations manifested in biodiversity. There are too many model organisms that exemplify that fact. Evolutionary models must either include events associated with cell type differentiation or the models will only continue to add theories to theories all the while the evolutionary models dismiss experimental evidence of biologically-based cause and effect.

Avatar of: James V. Kohl

James V. Kohl

Posts: 184

September 5, 2014

Re: "Evolutionary models must either include events associated with cell type differentiation..."

Two companion papers have done what evolutionary theorists have not done. See:

1) Altered proteostasis in aging and heat shock response in C. elegans revealed by analysis of the global and de novo synthesized proteome

2) Bio-orthogonal labeling as a tool to visualize and identify newly synthesized proteins in Caenorhabditis elegans

The de novo Creation of proteins via nutrient-dependent amino acid substitutions is antithetical to claims that mutations and natural selection somehow lead to the evolution of biodiversity. Indeed, claims that link auditory input to "...indirect genetic effects (IGEs), also called associative effects or extended phenotypes..." fail to link nutrient-dependent cell type differentiation to behavioral phenotypes.

We are left with examples of nutrient-dependent morphological phenotypes that appear to have somehow evolved  in the absence of pheromone-controlled behavior. So far as I know, there is no model for that.

I encourage comments from theorists who think there is experimental evidence of biologically-based cause and effect that supports their beliefs. Support for my model includes evidence from crickets that links ecological variation to biodiversity via cell type differentiation of mandibles and genitalia:

"Differentiation in the mandibles and male genitalia (figure 2) is quantified and used as a proxy for the presence of divergent selection 7. 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." -- Ecological selection as the cause and sexual differentiation as the consequence of species divergence?

In yeasts and nematodes, sexual differentiation of cell types is clearly nutrient-dependent and pheromone-controlled. It would be extremely unusual if the conserved molecular mechanisms of cell type differentiation that we detailed in our 1996 Hormones and Behavior review did not extend from what is known about yeasts, flies, and nematodes to what is known about primates.

Avatar of: James V. Kohl

James V. Kohl

Posts: 184

Replied to a comment from James V. Kohl made on September 5, 2014

September 5, 2014

The Erotic Endurance of Whale Hips

Excerpt: "Over the course of about ten million years, the ancestors of today’s whales moved into the water. They evolved seal-like bodies with stout limbs; later, their forelegs became flippers and their hind legs dwindled away. They lost their fur and their nostrils migrated from the tip of their head to above their eyes, where it became a blow hole. (I wrote about this transition in my book At the Water’s Edge.)"

These are the transitions attributed to evolution by theorists who typically seem to think in mutations and natural selection the leads to the evolution of biodiversity. However, science journalists who write about such transitions refuse to acknowlede what is known by serious scientists. See, for example:

A universal trend of amino acid gain and loss in protein evolution Excerpt: "We cannot conceive of a global external factor that could cause, during this time, parallel evolution of amino acid compositions of proteins in 15 diverse taxa that represent all three domains of life and span a wide range of lifestyles and environments. Thus, currently, the most plausible hypothesis is that we are observing a universal, intrinsic trend that emerged before the last universal common ancestor of all extant organisms."

The universal trend argues against evolutionary events that Zimmer continues to report as if experimental evidence of biologically-based cause and effect supported his misrepresentations. Clearly, "Ecological variation is the raw material by which natural selection can drive evolutionary divergence 1–4."

However, nutrient uptake does not typically result in mutations. That is why mutations cannot be linked to evolutionary events. Anyone who understands the difference between effects of perturbed protein folding in diseases and disorders can compare the effects to epigenetic effects on amino acid substitutions that stablize protein biosynthesis and the DNA of organized genomes in species from microbes to whales.

Avatar of: James V. Kohl

James V. Kohl

Posts: 184

Replied to a comment from James V. Kohl made on September 5, 2014

September 5, 2014

Re: "Ecological variation is the raw material by which natural selection can drive evolutionary divergence 1–4."


"DNA might have initially evolved for the purpose of storing phosphate, and the various genetic benefits evolved later,"

If ecological variation drives ecological adaptations manifested in morphological and behavioral phenotypes, biodiversity arises via the nutrient-dependent pheromone-controlled physiology of reproduction in species from microbes to man.

It does not seem biologically plausible for DNA to evolve and for various genetic benefits to evolve after genes evolved. The problem is one of cell  type differentiation, which appears to be nutrient-dependent because the role of amino acid substitutions in cell type differentiation extends to self vs non-self recognition in species from yeasts to mammals.

Avatar of: James V. Kohl

James V. Kohl

Posts: 184

Replied to a comment from James V. Kohl made on September 5, 2014

September 6, 2014

Quote James V. Kohl

...the role of amino acid substitutions in cell type differentiation extends to self vs non-self recognition in species from yeasts to mammals.

Article excerpt: "To identify potential mates, female crickets listen with ears on their forelegs to the males' songs, produced by the rubbing together of their forewings."

Evidently, this pseudoscientific nonsense is being taught to biology students attending college at UT Knoxville. If so, I wonder if the students are being taught about the physiology of reproduction.

All invertebrates identify potential mates via the nutrients they ingest because the nutrients are metabolized to species-specific pheromones that vary with sex differences and all other cell type differences in species from yeasts to mammals. In our 1996 review, we wrote:


"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 (Runge and Zakian, 1996; Wu and Haber, 1995)."

Are biology teachers at other universities still teaching pseudoscientific nonsense that defies accurate representations of biologically-based facts like this: "The diverse social behaviors that are enabled by the functional flexibility of the secrete-and-sense circuits (Fig. 5C) may explain the frequent occurrence of this class of circuits in nature."

What are your descendants being taught to believe by biology teachers who were taught to believe in neo-Darwinian theory? " What Haldane, Fisher, Sewell Wright, Hardy, Weinberg et al. did was invent.... The anglophone tradition was taught. I was taught, and so were my contemporaries, and so were the younger scientists. 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.... No, it wasn't dishonesty. I think it was wish fulfillment and social momentum. Assumptions, made but not verified, were taught as fact."

It's time that biological facts were taught as fact!

Quote James V. Kohl

...the role of amino acid substitutions in cell type differentiation extends to self vs non-self recognition in species from yeasts to mammals.

Avatar of: James V. Kohl

James V. Kohl

Posts: 184

Replied to a comment from James V. Kohl made on September 6, 2014

September 7, 2014

Why I am the only person commenting on the ridiculous assertions in this artcle? Do students at UT Knoxville know their professors are teaching evolutionary theory as if it could be linked by biologically-based cause and effect to ecology? Do their professors known the difference between theories and biological facts? Do the students discuss what they expect to be taught about biology and ecology by their professors?

For example: "...rearing larvae on an artificial diet containing different concentrations of the crude alkaloid extract decreased pupal viability and adult size in a concentration-dependent manner."

In crickets and flies, that fact can be epigenetically linked to nutrient-dependent differences in the morphology of male genitalia via the conserved molecular mechanisms of pheromone-controlled reproduction in species from microbes to man. That fact might help students understand the rather obvious nutrient-dependent link to ecological adaptations manifested in the genital morphology of all species that  reproduce via internal fertilization.

For examples, see: From Fertilization to Adult Sexual Behavior, which links what was known about the nutrient-dependent molecular epigenetics of alternative splicings of pre-mRNA to sex differences in cell types that are manifested in sex differences in morphology and behavior.

The nutrient-dependent pheromone-controlled sex differences in cell types exemplify how the epigenetic landscape is linked to the physical landscape of DNA by fixed amino acid substitutions in the organized genomes of all species. See for example, what's known about flies. Rapid Divergent Evolution of Male Genitalia Among Populations of Drosophila buzzatii.

Are UT Knoxville students permitted to ask their professors why sexual selection for divergence in male genitalia appears to occur too quickly to be attributed to mutations, natural selection, and the evolution of biodiversity? If not, they may never learn why the theory of evolution is now being taught in Israeli middle-schools: "...learning about evolution is not the primary function of the decision, but rather to use it as a building block for students to learn more about their ecology."

If UT Knoxville students do not learn about the differences between what's known about how ecological variation leads to ecological adaptations and how evolutionary theories misrepresent those facts, they may never learn how to compare what's known about molecular epigenetics to the pseudoscientific nonsense represented in reports of studies based on population genetics. The problem for our descendants is that another generation of researchers will not be as productive as those taught to ignore ridiculous theories and focus on what they learn about ecology.

Conclusion: "Specifically, we show how miRNAs of the miR-106b-25 cluster, involved in the inhibition of several apoptotic pathways can be differentially expressed."

Nutrient dependent miRNAs that inhibit apoptosis may be important links from ecological variation to ecological adaptations. If so, biological facts could be compared to what UT Knoxville students are taught about how evolutionary theory links the sounds that male crickets make to nutrient-dependent pheromone-controlled ecological adaptations. Biological facts might then also limit what UT Knoxville students are willing to believe about evolutionary theories.  But perhaps all the UT Knoxville biology students are silently preparing to move to Israel to learn more about accurate representations of biologically-based cause and effect. If so, they will already be several years behind students who have been taught the difference between theories and biological facts from the time they start middle-school.

Avatar of: Roy Niles

Roy Niles

Posts: 62

Replied to a comment from James V. Kohl made on September 7, 2014

September 13, 2014

Kohl asks: Why I am the only person commenting on the ridiculous assertions in this artcle?

Bexause it's making your ridiculous versions of evolution by smell look more ridiculous than ever.

 

 

 

 

 

 

 

 

 

 

 

 

Kohl asks: Why I am the only person commenting on the ridiculous assertions in this artcle?

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Bexause it's making your ridiculous versions of evolution by smell look more ridiculous than ever

 

 

 

 

 

Avatar of:

Posts: 0

Replied to a comment from Roy Niles made on September 13, 2014

September 14, 2014

RNA and dynamic nuclear organization just linked the RNA-mediated events from our 1996 review of cell type differentiation in species from microbes to man to nutrient-dependent pheromone-controlled chromosomal rearrangements in a unicellular animal to a primate.

Although Roy Niles doesn't like the representations of those facts in my model, it does not refute any of my accurate representations of biologically based cause and effect, which refute the pseudoscientific nonsense of evolutionary theorists. The theorists have never described an evolutionary event that could be compared to biophysically-constrained RNA-mediated events that link cell type differentiation from microbes to man in my model.

See also: Combating Evolution to Fight Disease Help others to stop the evolutionary theorists from killing more of us with their ignorance of biology.

Avatar of:

Posts: 0

September 20, 2014

H3K27me and PRC2 transmit a memory of repression across generations and during development

Is there biologically-based experimental evidence of an evolutionary event  for comparison to the nutrient-dendent RNA-mediated events that differentiate the cell types of all individuals of all species via amino acid substitutions? Could mutations somehow become fixed like amino acid substitutions that stabilize DNA in the organized genomes of species from microbes to man via the nutrient-depenedent pheromone-controlled physiology of reproduction?  

If not, what evolutionary event is Carl Zimmer calling "...a tremendous evolutionary event, giving rise to a huge diversity of animal forms and even changing the chemistry of the oceans and atmosphere."  I wonder if it one that 'just happens' as he reported in The Surprising Origins of Evolutionary Complexity. " "Others maintain that as random mutations arise, complexity emerges as a side effect, even without natural selection to help it along. Complexity, they say, is not purely the result of millions of years of fine-tuning through natural selection—the process that Richard Dawkins famously dubbed “the blind watchmaker.” To some extent, it just happens."

 

For comparison to what's known about how ecological variation leads to organismal complexity via ecological adaptations see:

See: Maleszka et al (2013) http://bfg.oxfordjournals.org/content/early/2013/12/12/bfgp.elt050.long

They link oxidation of 5Mc to 5hmC from the main pathway that removes methyl tags from the genome to brain-increased levels of 5hmC in gene bodies that correlate with active transcription.

"Within the neuronal function-related genes, gain of 5hmC is accompanied by loss of H3K27me3..."

Taken together with what is known about nutrient-dependent pheromone-controlled cell type differentiation via amino acid substitutions in the honeybee and other model organisms, a model of RNA-mediated cause and effect suggests learning and memory of food odors and species-specific pheromones links transgenerational epigenetic inheritance via the molecular mechanisms that transmit a 'memory of repression,' which can be linked to behavior.

The link from conserved molecular mechanisms to transgenerational epigenetic inheritance of behavior appears to occur in the context of the systems complexity of nutrient-dependent changes in the microRNA/messenger RNA balance and the overwhelming influence of all epigenetic effects on cell type differentiation in all cells of all individuals of all organisms (i.e., of all genera). It is now clearer that control of cell type differentiation occurs via the combination of epigenetic effects on the development of morphological phenotypes and on the development of behavioral phenotypes during life history transitions via amino acid substitutions that stabilize DNA in organized genomes via nutrient-dependent pheromone-controlled ecological adaptations to nutrient availability. See also: Starvation-Induced Transgenerational Inheritance of Small RNAs in C. elegans http://www.cell.com/cell/abstract/S0092-8674%2814%2900806-X

 

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Mettler Toledo
Mettler Toledo
Life Technologies