About us

We, as individuals, are a collective of genes with each gene aiming to maximize its own evolutionary success. As a result, the expression of genes can be detrimental for other genes, expressed in the same individual, and may result in intragenomic conflict. This conflict can rip apart the individual causing among other things health problems. We are interested in all kinds of intragenomic conflict and the detrimental effect these may have in the individual. In particular, we are interested in detrimental effects with medical implications.

Our research focuses on genes that can kill other genes (meiotic drive), genes that can change other genes into copies of themselves (gene conversion), genes that can move around the genome (transposable elements), genes that can move across genomes (endogenous retroviruses) and genes that can keep memories of past hosts (imprinted genes). We apply the gene’s eye view to understand maladaptive processes with medical implications, including infectious diseases, recombination hotspots, genomic imprinting, cancer resistance and speciation.

To explore this range of problems we use mathematical models of different types -including population genetics, kin selection, adaptive dynamics and game theory. We contrast the predictions of our mathematical models against large datasets.

Our Research

Paternally and maternally inherited egoistic or altruistic genes are expressed differentially in humans and other Mammals due to differences in sex-specific dispersion

Genomic Imprinting

Imprinted genes are genes with different patterns of expression when inherited from females as opposed to males. They are found in humans and many other mammals. We are interested in exploring when does natural selection favour the evolution of genes that can remember which parent they came from.

Recombination Hotspots converge either towards an internal equilibrium with strong negative linkage disequilibrium, or towards a limit cycle with weaker negative linkage disequilibrium.

Recombination Hotspots

As part of the recombination mechanism, the sequence that allows recombination is converted into the sequence that prevents recombination. This means that, over evolutionary time, recombination should disappear. Recombination hotspots are regions where recombination is one or two orders of magnitude higher than the average in the genome. Thus recombination hotspots should be doomed, but are not. We are interested in what evolutionary forces make possible the existence and ubiquity of recombination hotspots in mammals.

Phenotypes of P. mexicana - P. latipinna hybrids can be explained by different hypotheses

Evolution of sexual and asexual reproduction

As part of the recombination mechanism, the sequence that allows recombination is converted into the sequence that prevents recombination. This means that, over evolutionary time, recombination should disappear. Recombination hotspots are regions where recombination is one or two orders of magnitude higher than the average in the genome. Thus recombination hotspots should be doomed, but are not. We are interested in what evolutionary forces make possible the existence and ubiquity of recombination hotspots in mammals.

Schematics of a sex-specific epidemiological model

Infectious diseases

Pathogens colonize hosts evolving and co-evolving with their host genomes. We are particularly interested in researching how fundamental differences in the biology of females and males may lead to sex-specific differences in the outcome of infectious diseases. From a broad perspective we are interested in contributing to developing a more effective treatment of infectious diseases in each of the sexes.

Our Members

Drawing of Francisco Ubeda's portrait

Francisco Úbeda de Torres

I am a Reader at the School of Biological Sciences, Royal Holloway, University of London.

My research focuses on developing mathematical models to investigate conflict between genes expressed in the same individual (intra-genomic conflict) and their implications on disease. I am compelled to ensure that my theoretical research has far-reaching impact and broad appeal by applying it to understanding: the epigenetic architecture of imprinted genes, the persistence of recombination hotspots in human populations, the difference in virulence of infections in the sexes and the evolution of sexual reproduction… among other topics.

The joy that research brings to my life (as captured in the picture provided) is only comparable to the happiness that the sun bestows on the estival evenings of London.

Photography of Frederic Fyon' portrait

Frédéric Fyon

I have been a PostDoctorate Research Assitant with Francisco since September 2020. Specialized in the use of multi-locus population genetics models to investigate evolutionary conundrums, lately I have been working on the evolution of asexual reproduction, taking on the puzzling case of the Amazon Molly.

I did my phD at the University of Montpellier under the supervision of Dr. Thomas Lenormand. Together, we developped a theory of an unadaptative, indirect selective force shaping the evolution of cis-regulators. This theory notably led to an alternative explanation for the divergence of sex chromosome .

More generally, I am especially interested in the areas of non-adaptive selection, genomic conflicts, evolution of reproductive systems and evolution of genomic architecture and features. In my research, I predominantly use mathematical analysis and programming (C++) of numerical simulations.

To know more about me, here is my professional website.

Our Papers

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