|Mouse Molecular Genetics - CNRS URA2578|
|HEAD||AVNER Philip / email@example.com|
|MEMBERS||ATTIA Mikaël / Dr CHANTALAT Sophie / CHUREAU-POMMIER Corinne
Dr CLERC Philippe / Dr NAVARRO Pablo / OLDFIELD Andrew / Dr ROGNER Ute
Dr ROUGEULLE Claire / VALLOIS David / VIGNEAU Sébastien
The research activities of the Mouse Molecular Genetics Unit are organised around three themes. The first concerns the epigenetic mechanisms of cellular and transcriptional control. Our studies on X-inactivation and the Nap112 (Nucleosomal assembly protein) gene fall under this heading through the central importance of chromatin structure and modification to their action. The second research theme concerns the genetics of polygenic and multifactorial inheritance. The model that we have studied for over a dozen years now concerns the genetic predisposition of the NOD (Non-obese diabetic) mouse to develop Type 1 diabetes. A third research theme concerns mouse genomic studies. These studies are undertaken as collaborative efforts often in association with the French National Sequencing Centre (CNS) and the National Genotyping Centre (CNG).
Major recent advances in our research on X-inactivation have concerned the demonstration that the Xist gene critical to eutherian X-inactivation is absent from methatherians such as marsupials in which X-inactivation also occurs and that the non-coding Xist has evolved, at least in part, from the Lnx3 protein coding gene. X-inactivation in marsupials is therefore Xist independent and may be a carry-over from the meiotic silencing of the X chromosome occurring in the male germline. Potentially highly important aspects of X-inactivation have been opened up both through our implication of the nonsense-mediated decay pathway in Xist regulation and processing, and by our studies on Xist regulation by the Tsix antisense which have shown this occurs in part by altering the structure of the chromatin surrounding the Xist promoter. Our diabetes studies have been marked by the finding that the Arntl2 circadian rhythm gene is a candidate for the mouse type 1 diabetes locus, Idd6. Other studies have shown that, at least part of the resistance due to the Idd6 locus is mediated via a modulation of regulatory T cell activity. In the field of mouse genomics, the mutagenesis ES cell resource we have set up with our collaborators has proved its worth in pilot studies and provided a source of allelic series complementing existing mouse knock-out resources.
|Publications 2006 of the unit on Pasteur's references database|
Activity Reports 2006 - Institut Pasteur
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