Sex favours polyploidity
The gene repair theory
Why do some organisms maintain more than one copy of their
There are several possible answers to this question.
Here we examine the last theory - that polyploidity can
assist with the process of gene repair.
- One is that evolution proceeds by a process of duplication
and modification - and that polyploidity is a common result of
- Another points out that changes in ploidity often result in
speciation. Speciation is the species-level equivalent of
reproduction - and this is often thought to be beneficial to
- In the special case of diploidity, having two copies of
the genome is tied up with the process of sexual
- One possibilty is inertia - organisms may have multiple
copies of their genomes simply because their parents did.
- Lastly - and most obviously - polyploidity results in
organisms having a back-up copy of their genetic material -
and this may help with the process of gene repair.
In theory, the idea seems simple - if you have several back-up
copies of your genome, you can compare them, and use the majority
vote to eliminate any mutations.
However - as far as is known, no polyploid organisms have
mastered this trick yet.
Are the "backup" copies still helpful at repairing genes in
the absence of such technology?
The answer appears to be "yes" - a combination of
sexual recombination and synergetic epistasis caused by
recessive deleterious genes is sufficient to provide
several selective benefits to polyploidity in a population.
To illustate this, we have developed a computer model:
In an attempt to throw some light on the area, I wrote a
computer simulation of sexual single-celled organisms,
which exhibit variable levels of ploidity.
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.
My initial conclusions are as follows:
In this model, increasing polyploidity results in
reductions in the death rate, fewer mutations in newborns and
typical adults, and an increased lifespan.
The (public domain) source code is available
Here's the raw data from one run of the program:
Zero epistasis: effects of mutations on mortality are independent
Total number of deaths: 585205
Average expressed mutations at birth:12.779196
Average expressed mutations per individual at end of run:12.33
Total number of deaths: 408973
Average expressed mutations at birth:8.02542
Average expressed mutations per individual at end of run:7.16
Total number of deaths: 255346
Average expressed mutations at birth:5.098525
Average expressed mutations per individual at end of run:3.79