Evaluating evolutionary rates could shed light into functions of uncharacterized genes

Feb 08, 2013

Genes that have roles in the same biological pathways change their rate of evolution in parallel, a finding that could be used to discover their functions, said a researcher at the University of Pittsburgh School of Medicine in the February issue of Genetics.

Humans have nearly 21,000 genes that make as many proteins, but the functions of most of those genes have not been fully determined, said lead investigator Nathan Clark, Ph.D., assistant professor of computational and at the Pitt School of Medicine. Knowing what a particular gene does could help unravel the workings of the body, foster understanding of disease processes and identify targets for new drugs.

"For our study, we took a close look at the way genes evolved between species and we found an interesting signature," he said. "Genes that perform together have similar evolutionary histories in that the rates at which they change parallel each other. This could allow us to identify partner genes that we might never have suspected to work together in ."

The researchers studied the evolving genomes of 18 and 22 , looking particularly at genes that are involved in meiosis, a cell division process, and in DNA repair. They found parallel changes, such as acceleration or deceleration, in evolutionary rates among not only genes encoding proteins that physically interact with each other, but also among those that had no direct contact but still participated in meiosis or .

All genes mutate over time, which can be beneficial, harmful or meaningless. Some yeast species evolved a different method of reproduction and meiosis stopped as it was no longer essential for survival, Dr. Clark said. Through subsequent generations, the rate of change in the genes involved in making meiosis proteins accelerated, leading to deterioration of the unnecessary .

"A key question is: How important is that gene at that time?" he said. "If a species encounters a new challenge in its environment, the genes associated with it might have to evolve through subsequent generations in order to adapt that important pathway and ensure species survival."

By tracking those complementary rate changes, it could be possible to identify which genes participate in the same important pathways, providing clues to their function.

"In the future, a researcher studying a particular disease process might be able to plug in a couple of known genes in a database of evolutionary rate changes to find others that have a parallel history," Dr. Clark said. "That could provide new insight into the workings of the of interest."

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Tausch
1 / 5 (1) Feb 09, 2013
In before JVK.
If all genes mutate over time, then no other mechanism need be considered other than epigenetic effects of nutrients and pheromones [as] causing adaptive evolution.

Let's see if JVK has a problem with that.
JVK
1 / 5 (1) Feb 09, 2013
Is there a model for mutation-caused adaptive evolution? If so, we could compare it to my model of nutrient-dependent pheromone-controlled adaptive evolution, especially given the common molecular mechanisms of alternative splicings in yeast species at the advent of nutrient-dependent sexual reproduction.

So, let's hear it: How did mutations cause organisms to develop their nutrient-dependent sexual orientation, their ability to find a mate, and ability to conjugate? Is there a different model for that in some species compared to other species? Or must the model include nutrient-dependent alternative splicings like mine does?
RealScience
5 / 5 (1) Feb 09, 2013

Is there a model for mutation-caused adaptive evolution?

@JVK - There is a model for mutations CONTRIBUTING to adaptive evolution. Mutations create heritable variety, and selection operating on heritable variety causes adaptive evolution.

Have you updated you updated your model yet to include mutations contributing to adaptive evolution, or are you still ignoring real-world examples?

How did mutations cause organisms to develop their nutrient-dependent sexual orientation, their ability to find a mate, and ability to conjugate?

Because organisms with mutations that aided these attributes reproduced better on the average than those without such mutations.

Or must the model include nutrient-dependent alternative splicings like mine does

There is no conflict between a role for mutations and a role for nutrient-dependent alternative splicings.
JVK
1 / 5 (1) Feb 09, 2013
There is no conflict between a role for mutations and a role for nutrient-dependent alternative splicings.


What role did mutations play in the transition from asexual to sexual reproduction? How was epistasis achieved in mutant males and females?
RealScience
5 / 5 (1) Feb 09, 2013
Both mutations and epigenetics played roles in the transitions from asexual to sexual. Mutations played a role in the divergence of the X and Y chromosomes (or their corresponding chromosomes in sexual groups other than mammals), largely by eliminating genes from the Y chromosome, while RNA-managed epistasis kept the changes from being fatal. Without epigenetics providing some level of epistasis this could not have happened.

Mutations also increased the benefits of sexual reproduction by providing greater opportunity to for mutations that were beneficial together to meet and be selected for.

Epistatis in females versus males is epigenetics. Epigenetics play a huge role which most biologists are far from fully appreciating.
JVK
1 / 5 (1) Feb 10, 2013
Epigenetics play a huge role which most biologists are far from fully appreciating.

Really? Would that be anything like the huge role that I have modeled in Kohl, J.V. (2012) Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors. Socioaffective Neuroscience & Psychology, 2: 17338. DOI: 10.3402/snp.v2i0.17338.
"Olfaction and odor receptors provide a clear evolutionary trail that can be followed from unicellular organisms to insects to humans." -- you ignorant buffoon.
http://dx.doi.org...i0.17338
RealScience
not rated yet Feb 10, 2013
@JVK - I don't disagree with you on "Olfaction and odor receptors provide a clear evolutionary trail that can be followed from unicellular organisms to insects to humans." If not disagreeing with you on that makes me an 'ignorant buffoon', what does that make you?

JVK
1 / 5 (1) Feb 10, 2013
@JVK - I don't disagree with you on "Olfaction and odor receptors provide a clear evolutionary trail that can be followed from unicellular organisms to insects to humans." If not disagreeing with you on that makes me an 'ignorant buffoon'...?


What makes you an ignorant buffoon is your belief in an evolutionary theory where mutations are somehow involved in selection that is adaptive, at a time when adaptive evolution via ecological, social, neurogenic, and socio-cognitive niche construction that is nutrient-dependent and pheromone-controlled has been detailed sans mutations. I thought I had clarified that.
RealScience
not rated yet Feb 10, 2013
What makes you an ignorant buffoon is your belief in an evolutionary theory where mutations are somehow involved in selection that is adaptive

So then you consider anyone who thinks that mutations contribute to evolution to be an ignorant buffoon?

What make your theory incomplete is that it does not acknowledge that mutations play a role in adaptive evolution. Natural selection will operate on any heritable variety, and mutations exist so natural selection WILL operate on them. Human-created genetic algorithms use mutations and selection to drive algorithm evolution, so it is clear that mutations CAN be used. And if you are at all familiar with the field, you will know that there are literally thousands of papers that support that nature DOES use mutations in evolution through mutations that are selected for.