Florence MARGOTTIN-GOGUET HIV Group leader

Course and current status

1993-PhD in Cellular and Molecular biology, Pierre and Marie Curie University, Paris (study of transcription in yeast, CEA, Saclay)

1993-1994-Research in Pasteur Institute, French Guyana (malaria)

1994-2000-Research in Cochin Institute, Paris, France (mechanism of CD4 degradation mediated by HIV-1 Vpu, role of beta-TrCP ubiquitin ligase)

2000-2003-Research in Stanford University, California, USA (regulation of entry into mitosis)    

Since 2004-Group leader at Cochin Institute, Paris, France (mechanism of action of viral auxiliary proteins, restriction factors)

Since 2012-Member of the scientific committee of the french association SIDACTION.

Scientific summary

Florence Margottin-Goguet (or Florence Margottin) graduated in 1993 with a doctorate in Cellular and Molecular Biology from the University Pierre and Marie Curie in Paris. During her PhD, she studied basic transcription in the yeast model. She published pioneering work on how gene transcription occurs through a common mechanism for all genes. Starting from 1993, she got interested in infectious diseases, first malaria at the Pasteur Institute of French Guyana, second AIDS at the Cochin Institute in Paris under the supervision of R. Benarous. During this postdoctoral period, she unraveled how HIV-1 Vpu triggers the degradation of the CD4 receptor of the virus. This was the first example of "ubiquitin ligase hijacking" in the HIV field. Additionally, she cloned the gene of the ubiquitin ligase hijacked by Vpu, beta-TrCP, and identified the first cellular substrates of this enzyme. In 2000, she undertook research training in the cell cycle laboratory of Peter Jackson in Stanford University. During this time, she identified beta-TrCP as the ubiquitin ligase responsible for the degradation of the mitotic inhibitor Emi1, a critical step for entry into mitosis. Back to France (end of 2004), she established her own group at Cochin Institute in Paris (group "AVENIR" of INSERM) and concentrated her efforts on the study of host-pathogen interactions with a focus on viral auxiliary proteins and their ability to counteract host restriction factors. In 2007, her group was the first to unravel a molecular link between HIV-1 Vpr and G2 arrest and to propose that HIV-2 Vpx could use the same "ubiquitin ligase hijacking" strategy as HIV-1 Vpr. Later on in 2012, her group, within an international collaboration, identified the mechanism of action of SAMHD1, a restriction factor inactivated by Vpx. Her group also identified a new cellular target degraded by HIV-1 Vpr in primary cells, the HLTF DNA translocase. More recently, her group highlighted a new function of HIV-2 Vpx that is able to reactivate latent HIV-1 through its abilility to antagonize the HUSH complex. 

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