Human CCR4-NOT complex: regulation and effects on pathologies

The degradation of functional eukaryotic mRNAs is initiated by the shortening of their poly (A) tail. This step is mainly catalyzed by the CCR4-NOT complex, a phylogenetically conserved assembly, of which 2 subunits have deadenylase activities. Recent studies have revealed a major role of the CCR4-NOT complex in mechanisms linking translation and mRNA stability. Alterations of the human CCR4-NOT complex have also been implicated in the development of pathologies such as cancer and rare genetic diseases. We seek to elucidate the functions of the CCR4-NOT complex in the control of translation and mRNA stability in mammals including their regulation by specific partners. We are in particular interested in understanding the roles of these factors in human pathologies or during viral infections.