Biology subjects

Ubeda, F.

Publications and source records attributed to Ubeda, F..

4 recordsLinked to original sources

bioRxiv2026

Ancestral gene flow shaped the singular origin of the Amazon molly

The evolutionary origins of asexuality remain poorly understood, despite extensive research on its ecological and evolutionary consequences. Asexuality often arises through hybridization between species with intermediate genomic divergence, implying that hybrid-induced asexuality may be partly repeatable. The Amazon molly (Poecilia formosa), the first asexual vertebrate known to science, challenges this view: repeated experimental crosses between its extant parental species have failed to recreate a stable Amazon molly-like lineage. This apparent paradox gave rise to the Rare Formation Hypothesis, which proposes that stable asexuality requires an exceptionally specific genomic combination. Here, we combine experimental crosses, molecular cytogenetics, and population genomics to test whether ancestral introgression before the hybrid speciation event set the stage for the singular origin of the Amazon molly. We show that most experimental hybrids are viable but sexual, but that a subset of F1 hybrids produce unreduced eggs through a mechanism distinct from that of the Amazon molly. Population genomic analyses reveal that introgression between parental species likely predated the formation of the Amazon molly, and shared homozygous tracts across Amazon molly genomes support inheritance from admixed progenitors. Together, our findings reconcile the repeatable and contingent views of the origin of asexuality, suggesting that ancestral introgression may be the missing mechanism assembling the rare genomic combinations required for seemingly unrepeatable evolutionary innovations, including the emergence of asexual species.

evolutionary biology↗

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

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↗

bioRxiv2020

Epigenetic inheritance and the evolution of infectious diseases

Genes with identical DNA sequences may show differential expression because of epigenetic marks. These marks in pathogens are key to their virulence and are being evaluated as targets for medical treatment. Where epigenetic marks were created in response to past conditions (epigenetically inherited), they represent a form of memory, the impact of which has not been considered in the evolution of infectious diseases. We fill this gap by exploring the evolution of virulence in pathogens that inherit epigenetic information on the sex of their previous host. We show that memories of past hosts can also provide clues about the sex of present and future hosts when women and men differ in their immunity to infection and/or their interactions with the sexes. These biological and social differences between the sexes are pervasive in humans. We show that natural selection can favour the evolution of greater virulence in infections originating from one sex. Furthermore, natural selection can favour the evolution of greater virulence in infections across sexes (or within sexes). Our results explain certain patterns of virulence in diseases like measles, chickenpox and polio that have puzzled medical researchers for decades. In particular, they address why girls infected by boys (or boys infected by girls) are more likely to die from the infection than girls infected by girls (or boys infected by boys). We propose epigenetic therapies to treat infections by tampering with the memories of infecting pathogens. Counterintuitively, we predict that successful therapies should target pathogens genes that inhibit virulence, rather than those enhancing virulence. Our findings imply that pathogens can carry memories of past environments other than sex (e.g. those related to socioeconomic status) that may condition their virulence and could signify an important new direction in personalised medicine.

evolutionary biology↗