What Role Do Non-Coding RNAs Play in Gene Regulation and Evolution?

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Discussion Overview

The discussion revolves around the role of non-coding RNAs (ncRNAs) in gene regulation and evolution, exploring the mechanisms of gene mutations, their implications for survival and adaptation, and the complexities of genetic and epigenetic interactions. Participants raise questions about the randomness of mutations, the potential for genes to "learn," and the evolutionary reasons behind reproduction and mortality.

Discussion Character

  • Exploratory
  • Technical explanation
  • Conceptual clarification
  • Debate/contested

Main Points Raised

  • Some participants suggest that most mutations are random mistakes during cell division, while others propose that most mutations have no effect and can survive without conferring an advantage.
  • There is a question about whether genes can "learn" to adapt to environments or if all mutations are purely random, with one participant noting that mutation is random but selection is not.
  • One participant discusses the philosophical implications of determinism in relation to the randomness of mutations, particularly in the context of the Bohmian interpretation of quantum mechanics.
  • Another participant highlights recent advancements in sequencing technology that have led to the discovery of numerous novel lincRNAs and their potential roles in gene regulation and developmental processes.
  • There is speculation about the biological purpose of lincRNAs and their involvement in chromatin remodeling and gene regulation pathways, with a suggestion that the understanding of these processes may evolve over time.
  • One participant humorously references Lamarckian principles in the context of evolving understandings of genetics and epigenetics.

Areas of Agreement / Disagreement

Participants express a mix of agreement and disagreement regarding the nature of mutations, with some asserting randomness and others questioning this notion. The discussion remains unresolved on the extent to which non-coding RNAs influence gene regulation and the implications for evolutionary theory.

Contextual Notes

Participants acknowledge limitations in current understanding, particularly regarding the definitions and roles of non-coding RNAs, the complexity of gene regulation, and the philosophical implications of randomness in mutations.

Avalon
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I know random gene mutations determine which animals will survive and which will die out in their environment.

I have some questions though,

What usually causes the gene mutations?

Is it possible for the genes to "learn", if you will, to program an animal so it is better off suited for its environment or is it all just random?

Does evolution give any answers as to why we (animals) reproduce and then die instead of living on forever like bacteria and cells?
 
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Most mutations are just mistakes that occur during cell division.

http://www.sciencemuseum.org.uk/on-line/lifecycle/82.asp

It is pretty much just random.
Most mutations die out, but some convey an advantage.
 
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Thank you.
 
Xnn said:
Most mutations die out, but some convey an advantage.

Actually, it is probably more likely that most mutations have no effect and survive.
 
Avalon said:
Is it possible for the genes to "learn", if you will, to program an animal so it is better off suited for its environment or is it all just random?

Does evolution give any answers as to why we (animals) reproduce and then die instead of living on forever like bacteria and cells?

Mutation is random, selection is not. Mutations will induce variation in a particular organism. Depending on the environmental circumstances, certain variations will be preferentially selected for or against. These variations produce more or less offspring, and the corresponding genetic information will be amplified or restricted in that population.

Not even bacteria or cells live on forever. Genes do. Genes build their host organisms to produce more copies of the genes, even to the detriment of the individual organism. Although individuals die, the original replicators have been around for billions of years.
 
If the Bohmian interpretation of QM is correct, would this not lead one to suspect that mutation is not random? Or is this apples and oranges?
 
Descartz2000 said:
If the Bohmian interpretation of QM is correct, would this not lead one to suspect that mutation is not random? Or is this apples and oranges?

Pretty much apples and oranges. The random shunts and bumps of molecules (not least biological macromolecules) are so far removed from the quantum domain that the quantum variety of uncertainty doesn't play into it directly. It's essentially random anyway due to the sheer amount of molecules, collisions, and chaos.

So whether or not it's 'truly' random boils down to the philosophical question of determinism.
 
alxm said:
So whether or not it's 'truly' random boils down to the philosophical question of determinism.

I just ran across this article http://www.bio-itworld.com/news/02/05/09/lander-advances-genome-sequencing-AGBT.html" that I found quite interesting. The talk (at the AGBT conference), was mainly about advancements in sequencing technology, but he brushed over a few discoveries being made with the help of these advancements.


Until now, only about a dozen functional large non-coding RNAs (ncRNA)s have been found, such as the XIST gene in X-chromosome inactivation. Rinn and colleagues identified two specific epigenomic modifications, lysine methylations of histone H3 known as K4 (in the promoter region) and K36 (along the transcript). “If you see a K4 and a K36, it marks a gene,” said Lander. By studying DNA regions marked with this K4/K36 pattern, the group found a staggering 1600 novel intergenic transcribed K4-K36 regions.

What is the biological purpose of these lincRNAs? The genes can be associated with known pathways, such as fatty acid metabolism, p53, and developmental process, e.g. gametogenesis, brain development, immune response, cell cycle. Recently, the group has identified lincRNAs regulated by p53. Lander said that no-one has been able to identify the protein presumed to repress genes regulated by the p53 tumor suppressor. But, he said, “there’s a lincRNA, near p21, when you knock it out, it causes up-regulation of those genes that were suppressed in the p53 pathway.”

Like some of the best characterized ncRNAs, more than 50% lincRNAs have been implicated in chromatin remodeling, a glimpse of a new world of gene regulation, “anti-transcription factors that play distinct roles in shutting down genes as part of pathways.” Interestingly, lincRNAs would be excellent candidates for those GWAS hits that land in gene deserts.

These are the regions of the genome that were previously thought of as "junk" DNA (at least when I was going to high school).

IMHO as we learn and discover more and more about the intricate details of epigenetics, gene regulation and expression patterns as it relates to development and the production of gametes, we may come to realize that the process is far more complex than previously thought.

Who knows, maybe we will even revisit some Lamarckian principles?
:rolleyes:shame on me! (<--slaps himself on the wrist)
 
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