Biology subjects

Fyon, F.

Publications and source records attributed to Fyon, F..

3 recordsLinked to original sources

bioRxiv2023

Why Do Hybrids Turn Down Sex?

Asexual reproduction is ancestral in prokaryotes; the switch to sexuality in eukaryotes is one of the major transitions in the history of life. The study of the maintenance of sex in eukaryotes has raised considerable interest for decades and is still one of evolutionary biologys most prominent question. The observation that many asexual species are of hybrid origin have led some to propose that asexuality in hybrids results from sexual processes being disturbed because of incompatibilities between the two parental species genomes. This proximate theory appears difficult in real life, as it requires fundamental reproductive traits to be profoundly altered without collapsing individuals fertility. Repeated failures to produce asexual Amazon Molly in the lab through crossing experiments show that we are still in need of an evolutionary explanation. Here, we present a mathematical model and propose an adaptive route for the evolution of asexuality from previously sexual hybrids. Under smaller reproductive alterations, we show that asexuality can evolve to rescue hybrids reproduction. Importantly, we highlight that when incompatibilities only affect the fusion of sperm and eggs genomes, unreduced meiosis and paternal genome elimination can evolve separately, greatly facilitating the overall evolutionary route.

evolutionary biology↗

bioRxiv2022

The evolutionary fate of divergent genomes in hybrid zones between selfing and outcrossing species

Hybridization is a natural process whereby two diverging evolutionary lineages reproduce and create offspring of mixed ancestry. Differences in mating systems (e.g., self-fertilization and outcrossing) are expected to affect the direction and extent of hybridization and introgression in hybrid zones. Among other factors, selfers and outcrossers are expected to differ in their mutation loads. This has been studied both theoretically and empirically; however, conflicting predictions have been made on the effects mutation loads of parental species with different mating systems can have on the genomic composition of hybrids. Here we develop a multi-locus, selective model to study how the different mutation load built up in selfers and outcrossers as a result of selective interference and homozygosity impact the long-term genetic composition of hybrid populations. Notably, our results emphasize that genes from the parental population with lesser mutation load get rapidly over-represented in hybrid genomes, regardless of the hybrids own mating system. When recombination tends to be more important than mutation, outcrossers genomes tend to be of higher quality and prevail. When recombination is small, however, selfers genomes may reach higher quality than outcrossers genomes and prevail. Taken together these results provide concrete insights into one of the multiple factors influencing hybrid genome composition and introgression patterns in hybrid zones with species containing species with different mating systems.

evolutionary biology↗

bioRxiv2022

Mutation and the Recombination Hotspot Paradox

Recombination often concentrates in small regions called recombination hotspots where recombination is much higher than the genomes average. In many vertebrates, including humans, gene PRDM9 specifies which DNA motifs will be the target for breaks that initiate recombination ultimately determining the location of recombination hotspots. Because the sequence that breaks (allowing recombination) is converted into the sequence that does not break (preventing recombination), the latter sequence is over-transmitted to future generations and recombination hotspots are self-destructive. Given their self-destructive nature, recombination hotspots should eventually become extinct in genomes they are observed. While empirical evidence shows that individual hotspots do become inactive over time (die), hotspots are abundant in many vertebrates: a contradiction called the Recombination Hotspot Paradox. What saves recombination hotspots from their foretold extinction? Here we formulate a co-evolutionary model of the interaction among sequence specific gene conversion, fertility selection and recurrent mutation. We find that when fertility selection is weaker than gene conversion, fertility selection cannot stop individual hotspots from dying but can save them from extinction by driving their re-activation (resuscitation). It can also save them from extinction by driving the birth of new hotspots in target sites with small allelic variation. The amount of allelic variation that can result in the birth of a hotspot depends on the strength of fertility selection and the mutation rate. In our model mutations balance death and resuscitation of hotspots maintaining their numbers over time. Interestingly we find that mutations are responsible for the oscillation of individual hotspots being asynchronous across the genome such that the average recombination across the genome remains constant. Our model thus contributes to better understanding how new hotspots may be formed thus explaining the Recombination Hotspots Paradox. From a more applied perspective our work provides testable predictions regarding the relation between mutation and fertility with life expectancy of hotspots.

evolutionary biology↗