Anne-Sophie Armand

Toxicologie, Pharmacologie et Signalisation céllulaire - UMR-S 1124
Université Paris Descartes
45 rue des Saints Pères
75270 Paris Cedex 06

Fax : +33 (0) 1 42 86 38 68

Anne-Sophie ARMAND

Degeneration and neuromuscular plasticity

anne-sophie.armand@-Code a retirer pour éviter le
+33 1 42 86 21 53, room H330

I am interested particularly in the dissection of the molecular mechanisms that control skeletal muscle development during mouse embryogenesis and adulthood. The roles played by protein-protein interactions in these processes are particularly exciting. We identified a new partner of NFAT transcription factors, the muscle specific bHLH protein MyoD. I would now love to define new coding and non coding partners for NFAT signaling components which are involved in skeletal myogenesis.

For many years, I have investigated the molecular mechanisms that control and regulate skeletal muscle differentiation in mice. The NFAT transcription factor family is particularly interesting since the knock out mice for NFATc2 and NFATc3 display distinct muscle phenotypes, muscle atrophy and aplasia, respectively. Indeed, these two transcription factors regulate different aspects of myogenesis by cooperating with other transcription factors. We demonstrated that these two NFAT isoforms are able to interact with a muscle specific transcription factor, MyoD. The NFAT/MyoD interaction controls different aspects of myogenesis, depending on the NFAT isoform involved in the interaction. This protein-protein interaction is crucial for NFATc3 to activate the expression of another muscle specific bHLH transcription factor, myogenin and, therefore, to regulate myogenic differentiation during early embryonic myogenesis in mice (Armand et al., 2008). The other NFAT isoform, NFATc2, also cooperates with MyoD. However, this interaction is involved in another step of myogenesis: the specification of myofibers during late embryonic myogenesis and neonatal development. Indeed, the NFATc2/MyoD complex regulates the expression of a fetal gene, the neonatal myosin heavy chain (neoMyHC) (Daou et al., 2013).

In collaboration with Leon de Windt, we showed the importance of microRNAs for the modulation of NFAT signaling in cardiac failure (da Costa Martins et al., 2010; Dirkx et al., 2013). We now are analyzing the microRNAs which might modulate NFATc2 signaling during skeletal myogenesis and we have started to envisage the functions of NFATc2 in determining the fates of muscle stem cells.

Recent Publications