Team

Research interest

Our research theme is focused on the determination of the genetic impact of spermatid chromatin remodelling. We have highlighted the formation of double strand DNA breaks during this important structural transition and hypothesized that the repair of these breaks is a source of genetic instability since their repair cannot rely on sister chromatid in this haploid context.  

Our objective is thus to map these breaks through high throughput sequence and to determine whether the structural transition really induces de novo polymorphism at break sites, which could highlight a new evolutionary component. We intend to determine the mechanism involved in the repair of transitory breaks as well as the impact of physiological changes, such as aging, on their distribution and mutagenicity. The spermatid chromatin structure change requires the eviction of histones and relies on their massive acetylation.

One of our parallel projects consist in determining the mechanism through which histones become globally, and not specifically, hyperacetylated during chromatin remodelling. We are exploring non enzymatic acetylation which could involve the regulation of acetyl-CoA pools by mitochondrial acetyltransferases relocated to the nucleus. Other projects are currently being developed and involve the etiology of disorders in the spectrum of autism as well as the study of parameters involved in the initiation of genetic instability in carcinogenesis. 

Expertise