Annabel Quinet

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150px-Annabel.jpg PhD student of Biology at University of São Paulo and University of Paris-Sud 11, France under the supervision of Prof. Dr. Carlos F.M. Menck and Dr. Anne Stary. The scientific project entitled “Characterization of alternative response pathways to DNA damage induced by ultraviolet irradiation in the xeroderma pigmentosum syndrome” is financially supported by Ministère de l’Education Supérieure et de la Recherche (MESR, France).

Research Project

The genetic disorder xeroderma pigmentosum (XP) is characterized by UV hypersensitivity and early cancer in sun-exposed body sites. UV�induced DNA damage interferes with DNA replication and can result in cell death or mutagenesis. These lesions are normally eliminated by nucleotide excision repair (NER) and tolerated by specialized polymerases such as Polη (Trans-Lesional Synthesis, TLS). Defects in NER are responsible for the XP syndrome and Polη deficiency is associated with the variant form of XP. It is established that TLS is the UV damage tolerance pathway in human cells, but in other organisms such as S. cerevisiae, the homologous recombination (HR) also plays an important role. Furthermore, it was suggested that non homologous end joining (NHEJ) could be activated in UV�damaged cells. In this PhD project, we seek to determine the involvement of HR and NHEJ pathways in the cellular responses to UV injuries in XP�C human fibroblasts.


Fig.1. γH2AX, DNA damage marker, immunostaining as a function of the cell cycle. After a low UVC dose, 2 J/m², XP-C cells present more γH2AX formation than XP-C + fibroblasts.

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