A new study from New Zealand, which is published in the Proceedings of the Royal Society B, lends support to the idea that “selfish” genes may have encouraged individuals to mate so they could infect other genomes.
Birds do it and bees do it, but why does so much of nature engage in sexual reproduction? Some might say because it is pleasurable, but from an evolutionary view, this aspect did not emerge until long after the process of mixing genes among individuals to produce new offspring arose.
“Selfish” or parasitic genes are those that thwart the principles of Mendel’s rules of inheritance, which is the way in which traits are passed from one generation to the next.
Thanks to sexual reproduction, these selfish genes become overrepresented in offspring. Plus, they bring no benefits to their hosts; they have their own agenda.
Selfish genes have been well studied, and biologists and geneticists know a lot about the molecular processes behind their evolution.
However, what they do not know so much about is the effect they have on their hosts, which is what this new study, by researchers Paulina Giraldo-Perez and Matthew R. Goddard of the University of Auckland, investigates.
The New Zealand researchers explored the idea that since selfish genes may only spread through sex with different partners, it would be to their advantage if promiscuity among their hosts were to increase.
They studied a family of genes known as Homing endonuclease genes (HEGs) in a species of yeast called Saccharomyces cerevisiae, which has been used in baking, winemaking and brewing since ancient times.
Previous studies have already shown that HEGs appear to spread more than other genes in the genome by inducing “a biased gene-conversion event,” known as “homing,” so they are inherited by a disproportionate number of offspring.
Without such a bias in sexual reproduction, a gene would spread according to Mendelian inheritance principles, giving it a 50% chance of being passed on to the next generation.
But one type of HEG “has been shown to display super-Mendelian inheritance of between 75 and 90%, rather than the Mendelian 50%,” write the authors, adding that:
“HEGs may very quickly spread in populations and this has been shown in experiments with microbes and insects.”
The first thing they did in their study was to show HEGs are selfish genes and not benign, as previously thought. Their hosts appear to accrue no benefit from the cost of carrying them in their genome, which the researchers estimated to be “a selective load of approximately 1-2% in ‘natural’ niches.”
They then looked at the ability of HEGs to affect the sexual behavior of their host, since, as they explain:
“As all selfish genes critically rely on sex for spread, then any selfish gene correlated with increased host sexuality will enjoy a transmission advantage.”
And this is what their data showed, leading them to conclude that a selfish gene may increase its host’s disposition to have sex. They did not explore what the underlying mechanisms for such an effect might be.
Thus, the study shows evidence that selfish genes have a vested interest in maintaining the process of sexual reproduction of their hosts:
“The data presented here show that a selfish element may increase the propensity of its eukaryote host to undergo sex and along with increased rates of non-Mendelian inheritance, this may counterbalance mitotic selective load and promote spread.”
But the authors also suggest their findings support the – separate, though related – idea that selfish genes may have encouraged sex to evolve in the first place.