Evidence of long-term directionality in origination of human mutation: study | Hacker News Reader

Evidence of long-term directionality in origination of human mutation: study

phys.org

47 pointsgmays18 comments

Some species of mycorrhizal fungi have been observed to have a fascinating stress response to being exposed to a new soil/environment. The mycellium will somehow ramp up it's rate of HGT (horizontal gene transfer) and therefore borrow genes from other soil organisms in that soil. These genes are borrowed across phylums from even bacteria or microalgae.

Essentially, it's a natural mechanism to rapidly increase its rate of evolution.

Source?

- Elevated rates of HGT in the industrialized human microbiome. Transferred gene functionality reflect the lifestyle of their hosts[0]

- HGT from bacteria and plants to mycorrhizal fungi. These genes are functional[1]

- More about fungi sharing genes[2][3]

- Lab experiment showing HGT can act as a directional evolutionary force in bacteria adapting to antibiotics[4]

- A species of fungi used HGT (mostly from bacteria and some from eukaryotes) in order to adapt to colonize apple trees[5]

- A call for a replacement of neo-Darwinism with a new evolutionary synthesis that takes into account the role of HGT (among other things)[6]

Ok, so I didn't save the actual paper I was paraphrasing. I thought I'd read it in Annual Reviews, but I can't seem to find it. However, I hope I provided enough sources to show that: (1) fungi often share genes across phylums, (2) we have clear examples of elevated rates of HGT in microbiota faced with a new environment, and (3) HGT can play a critical role in adaptation

[0] https://www.sciencedirect.com/science/article/pii/S009286742...

[1] https://www.frontiersin.org/articles/10.3389/fpls.2018.00701...

[2] https://massivesci.com/articles/fungi-gene-plants-mutualism/

[3] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6643240/

[4] https://www.pnas.org/content/117/43/26868

[5] https://www.nature.com/articles/srep33129

[6] https://royalsocietypublishing.org/doi/10.1098/rspb.2009.167...

The biggest thing in ecology right now is niche construction theory. It's the realization that organisms don't just respond to their environment, but also shape it and reproduce it

I think it's high time for the equivalent perspective to reach evolutionary molecular biology and realize that organisms aren't just gonna sit idly by and wait for the random process of mutation to let them adapt. As shown by the recent studies on the prevalence of genes being shared across animals,[0] there's clearly many mechanisms of action missing from our molecular analysis toolbox. One recent finding was the discovery of epigenetic inheritance. If epigenetics allows organisms to adapt to environments in their lifetimes and these adaptations can, in some capacity, be passed down. In addition, we've already shown a number of factors to increase the rates of mutation. Given these findings, I don't think it's far-fetched to imagine some level of "~~niche~~[gene] construction" happening at the molecular level

[0] https://www.quantamagazine.org/dna-jumps-between-animal-spec...

Lamarck and Lysenko got a raw deal.

https://en.wikipedia.org/wiki/Lamarckism

https://en.wikipedia.org/wiki/Lysenkoism

Lysenko was a fraud and a disgusting human being who cheerfully saw scientists condemned to death to further his take science.

Lamarck's theories were unsupported by the evidence available at the time. Current research indicates that inheritance of acquired traits, if it does exist, is in its details quite unlike what was described in Lamarck's theories.

So no, neither got a raw deal.

I was speaking more to the heritability of acquired traits, as that was the context of the discussion. I’m open to learning more about their negative aspects also.

Excellent reply. And absolutely fascinating research. Thanks.

If anyone is here who works in the field of evolutionary biology can answer this: The article seems to be saying this result goes against the mainstream thinking that mutations are entirely random. But is that really the mainstream thinking of modern evolutionary scientists? Or just the simple high-school explanation which is devoid of a lot of known nuance?

I don't work in evolutionary biology, but I found this paper calling for a replacement of neo-Darwinism to be a really helpful overview (it also sites many similar works)

https://royalsocietypublishing.org/doi/10.1098/rspb.2009.167...

I know with some bacteria (which I work with for evolutionary biology) they can intentionally mutate at higher rates when under stress.

The article states that mutations arise randomly (de novo mutations), but the rate of of these mutations differ based on populations experiencing differing environmental pressures.

The naïve hypothesis would be to expect that de novo mutations, being random, should arise in differing populations -- even in different environments -- at the same rate; apparently this isn't the case.

The article doesn't explain the underlying mechanism, so I assume this is just premilitary observational science? The authors say this challenges neo-Darwinism, how?

One explanation is that environmentally selected genes (meta genes?) that promote mutation of de novo genes in regions of the genome under environmental pressure. These meta genes dispersed in a population would prime that population for the synthesis of new adaptations.

The underlying paper lists 3 different hypotheses that could explain the results.

1. Unrelated fragility of this particular sequence in Africans

2. Modifier theory

3. Having mutations makes future generations more susceptible to nearby mutations. This what the authors are suggesting.

There's a sort of soft-assumption in modern biology that mutations are approximately random, which underlies things like the molecular clock. It's well-known to be wrong, but at scale the experimental evidence suggests that it still holds in many useful situations.

Combine a paper pointing out a limitation of that assumption with popsci press and you get the breathless headline above.

> One explanation is that environmentally selected genes (meta genes?) that promote mutation of de novo genes in regions of the genome under environmental pressure.

This has been studied. They’re DNA repair pathways. Put a bunch of E. coli in a bioreactor and trace the lineages. As soon as one lineage loses a DNA repair pathway, new mutations explode and out-compete the old lineages (and each other).

Besides cancer and viability concerns, highly stable DNA is mainly beneficial in cyclical conditions (as adaptive memory). In the stable—but highly competitive—environment of a bioreactor, sacrificing DNA stability for adaptive pace is a very beneficial mutation.

Is that survivorship bias here? surely people in Africa should have higher rate of the mutation. because people who didn't have it died from malaria.

This study measures the rate of de novo (not inherited) HbS mutation, and finds it occurs at significantly greater than random chance in populations where malaria is prevalent. So there is a survivorship bias, but not just for the inheritance of the specific downstream adaptively relevant mutation, but also for some meta-process that controls the rate at which that mutation appears anew without inheritance. They're able to observe this through a new method that can measure the rate of de novo mutations in specific areas of interest in the genome, as opposed to prior methods which were constrained to measuring the rate of mutations in general across the whole genome.

Thanks for explaining that. The article just jumps right into using "de novo" all over the place with minimal explanation, but the link they highlight it with is broken.

> "We hypothesize that evolution is influenced by two sources of information: External information that is natural selection, and internal information that is accumulated in the genome through the generations and impacts the origination of mutations,"

But how was that internal information accumulated? Through natural selection? Couldn't people in Africa have a higher rate of generating the HbS mutation de novo, because other parts of their parents genome encodes that information? Like when a zygote is getting spliced up you're more likely to get errors where HbS gene is in Africa because they've inherited another gene that causes those errors because of natural selection.

I don't understand the distinction they're making between "natural selection" and "internal information that is accumulated in the genome through the generations". To me that sounds the same. But perhaps I've been thinking about natural selection all wrong.

Reply on news.ycombinator.com