Gene repair and sex
The gene repair theory
The status of the gene repair theory of the evolution of sex is one of
the active areas of modern evolutionary biology.
The theory's prominent supporters include Richard Michod and
Alexei Kondrashov.
Kondrashov describes the theory in the paper: "Deleterious
mutations and the evolution of sexual reproduction" 1988.
Kondrashov's theory is widely believed to require "synergetic
mutations" to work.
Problems
The main problem with the gene repair theory is that it
faces competition with the 'Red Queen' theory - which
explains a similar range of phenomena, but does it rather
better.
However, the concern of this essay is narrower than that -
it looks at the significance of dysergetic epistasis to the
gene repair theory.
Model
In an attempt to throw some light on the area, I wrote a
computer simulation of single-celled organisms, reproducing
both sexually and asexually.
Directly modelling the effect of mutations on fitness has
some realism problems - since it fails to take into account
issues such as the fact that late mutations have less impact
on reproductive success than early ones - so to avoid this
problem I chose to allow mutations to affect mortality.
Increases in mortality automatically compromise reproductive
success - by decreasing the organism's remaining lifespan.
I modelled zero epistasis, synergetic epistasis and dysergetic
epistasis.
I measured the number of deaths in the population, the
average lifespan, the number of mutations each new-born
organism carried - and the number of mutations present in
each living individual at the end of the run. Mutations
were measured since they are a useful proxy for the
population's general state of health.
Conclusions so far
My initial conclusions are as follows:
In this model, sexual recombination usually reduces the
death rate, reduces the number of mutations in newborns and
typical adults, and extends the lifespan of members of the
population (as compared to asexual populations).
It does this in a range of cases - including the case of
zero epistasis. This doen't directly contradict
Kondrashov's model - since in his model mutations are
considered to directly affect fitness - whereas in my model
(which I hope is more realistic) the mutations affect
mortality - and thus can have different effects on fitness
depending on the age at which they occur.
Also, it is thought that the balance between synergetic and
dysergetic epistasis is matters - since dysergetic epistasis
favours asexual reproduction. [e.g. see Mark Ridley's
"Evolution" textbook, [Figure 12.6, p. 323 (3rd
edition)].
My model suggests that not all types of dysergetic
epistasis favour asexual reproduction; and that - that of
those that do - the effect appears to be incredibly
small.
Therefore, the idea that there is some sort of balance
between synergetic and dysergetic epistasis may prove to be
worth reexamining. If synergetic interactions favour sex -
while finding dysergetic interactions that offer more than a
tiny advantage to asexual reproduction seems rather
challenging - then the issue of how much dysergetic
epistasis occurs may not matter - and the viability of the
mutation repair theory would depend only on whether the
interactions that favour sex are common enough to offset
its costs.
Future work
The most obvious next thing to do with this model is to put
the sexual individuals and asexual individuals into the same
population - and allow them to compete with one another - to
examine the circumstance under which sex is favoured.
Source code
The (public domain) source code is available
here.
Raw results
Here's the raw data from one run of the program:
Zero epistasis: effects of mutations on mortality are independent
Asexual experiment
Deaths: 1040406 - Average lifespan:1.9221448
Average mutations at birth:7.3622866
Average mutations per individual at end of run:7.52
Sexual experiment
Deaths: 889552 - Average lifespan:2.2480564
Average mutations at birth:5.746793
Average mutations per individual at end of run:5.03
Dysergetic epistasis: mutations have diminishing effect on mortality
Asexual experiment
Deaths: 1437500 - Average lifespan:1.3912237
Average mutations at birth:11.261751
Average mutations per individual at end of run:16.9
Sexual experiment
Deaths: 1052413 - Average lifespan:1.9002084
Average mutations at birth:1.1641209
Average mutations per individual at end of run:0.67
Dysergetic epistasis: mutations have diminishing effect on mortality
Asexual experiment
Deaths: 1005376 - Average lifespan:1.9890469
Average mutations at birth:0.54179233
Average mutations per individual at end of run:0.28
Sexual experiment
Deaths: 1033338 - Average lifespan:1.9352545
Average mutations at birth:0.55689037
Average mutations per individual at end of run:0.14
Synergetic epistasis: mutations have an increasingly negative effect on mortality
Asexual experiment
Deaths: 60790 - Average lifespan:32.847622
Average mutations at birth:12.590755
Average mutations per individual at end of run:12.82
Sexual experiment
Deaths: 60048 - Average lifespan:33.24732
Average mutations at birth:12.433553
Average mutations per individual at end of run:12.34
Synergetic epistasis: mutations have an increasingly negative effect on mortality
Asexual experiment
Deaths: 602897 - Average lifespan:3.3168137
Average mutations at birth:9.951496
Average mutations per individual at end of run:11.15
Sexual experiment
Deaths: 571718 - Average lifespan:3.4977016
Average mutations at birth:9.355055
Average mutations per individual at end of run:10.14
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