Our first line of research focuses on the regulation of recombination events involving a single DNA end. These events are known to generate chromosomal rearrangements (GCRs) and are particularly mutagenic.

Although these events are generally repressed, they can occur as a last resort to repair damaged DNA. They also play a key role in maintaining chromosome ends, known as telomeres, in a significant fraction of ALT cancers.

Our second line of research focuses on the regulation of recombination during meiosis, the cell division that generates gametes and is essential for sexual reproduction.

Meiotic recombination is part of a rigorously controlled cellular program. It plays a key role in the correct segregation of chromosomes and contributes to genetic mixing. Having studied in detail the dynamics of exchanges between DNA molecules during meiotic recombination, we now turn our attention to the impact of DNA polymorphism on the efficiency of this process.

DNA polymorphism, naturally present in populations, generates base mismatches during recombination. These mismatches are detected by a protein machinery that can either repair them or eliminate the recombination intermediates. This mechanism ensures efficient allelic recombination while preventing recombination between homologous non-allelic sequences, potential sources of chromosomal rearrangements (GCRs).

A third line of research focuses on the study of meiotic recombination in budding yeasts related to Saccharomyces cerevisiae.

We are particularly interested in an as-yet-unknown mechanism that inhibits meiotic recombination on the entire arm of the chromosome carrying the sex-type locus in the yeast Lachancea kluyveri.

This mechanism could shed new light on a pathway for the emergence of **sex chromosomes**, which are often characterized by a massive extinction of meiotic recombination.

The laboratory's fourth theme is the regulation of recombination between sex chromosomes during male meiosis in the mouse. Unlike autosome pairs, the challenge for the X and Y chromosomes in male mammals is to recombine in their region of very limited homology, called pseudoautosomal region (PAR), to ensure their correct segregation at meiosis I.

To ensure this recombination, the mo-2 minisatellite present in the PAR and thehyperaccumulation of pro-recombination factors establish respectively a cis- and trans-regulation.

We aim to further characterize the proteome associated with PAR, to refine the characterization of its particular chromatin structure and to study its evolution since its associated minisatellite mo-2 probably favors rapid evolution.