Professeur agrégé, Département de microbiologie et d’infectiologie, Faculté de médecine et des sciences de la santé, Université de Sherbrooke
Non esitate d’andare contro corrente.
Tremblay M, Charton R et al (Nucl Acids Res 2014)
Gene transcription abruptly stops when RNA polymerase-II encounters a DNA lesion on the transcribed strand. What happens to stalled RNA polymerases-II is not well understood, they could: (i) transcribe through the lesion, (ii) remain at the damaged site and undergo conformational changes to allow repair, (iii) be moved from the damaged site by reverse translocation without separating from the DNA strand, (iv) be released from the DNA. Even less is known about the fate of stalled RNA polymerase-I at DNA lesions, and how the arrest affects the structure open rDNA chromatin. In this study the two forms of rDNA chromatin were separated during NER and analyzed by various assyas. We showed for the first time in vivo that RNA polymerases-I were displaced from the damaged transcribed strand and replaced by nucleosomes. Moreover, the newly inactivated rDNA chromatin retained the signature of active rRNA genes and was readily reopened when UV induced photoproducts were removed by NER (cited 6 times).
Toussaint M and Conconi A (NATURE Prot 2006)
High-throughput and sensitive assay to measure yeast cell growth: a bench protocol for testing genotoxic agents (cited 41 times).
Conconi A et al (PNAS 2002)
UV-induced DNA lesions are removed from the DNA by nucleotide excision repair (NER). Active genes are repaired faster than inactive DNA by a process called transcription-coupled repair (TCR). TCR is not completely understood but it is thought that RNA polymerase II elongation is necessary for TCR. Using yeast as a model, this study shows that TCR also occurs in RNPI transcribed genes (cited 84 times).
Smerdon M and Conconi A (Progress in Nucl Acids Res and Mol Biol 1999)
Modulation of DNA Damage and Repair in Chromatin (cited 113 times).
Conconi A et al (NATURE 1996)
Some mammalian genes associated with tissue injuries and inflammations are activated by UV light. There is a remarkable analogy between the induction pathway of one plant defense mechanism (the wound-inducible proteinase inhibitor-I and -II genes) and the inflammatory response in animals. This study shows that a lipid-based pathway is part of the UV response, adding important information on how UV irradiation induces stress responses in cells. Moreover, damaged DNA could participate in the UV response. This study was introduced by a commentary (Nature 1996, 383, p.763) (cited 246 times).
Conconi A et al (CELL 1989)
To investigate what happens to nucleosomes during transcription, investigators used ribosomal genes (rDNA) as model. Contradictory results were reported: one group of studies suggested that nucleosomes were present during transcription, another suggested that nucleosomes were absent and a third model proposed that nucleosomes were largely modified during RNPI elongation. This study: 1) explained why reported results in the literature yielded opposing conclusions, 2) showed for the first time that two different populations of rDNA are present in the same cell (an inactive packaged with nucleosomes, and an actively transcribed depleted of nucleosomes), 3) demonstrated that nucleosomes are not present in the coding regions of highly transcribed rDNA. This work was described as an innovative study in a commentary in Cell (1989, 59, pp. 243-244) (cited 316 times).
François PeyresaubesPhD Student
REPAIR OF UV INDUCED DNA LESIONS IN THE rDNA LOCUS
A person who never made a mistake never tried anything new.
– 2011-2013: MSc Structural and Functional Biochemistry – Université de Lyon (France)
– 2008-2011: BSc Earth and Environment Biochemistry – Université de Reims (France)
– 2006-2008: Medical School – Université de Médecine de Reims (France)
– 2015: Peyresaubes F, D’Amours A, Leduc F, Grégoire MC, Boissonneault G, Conconi A. Immuno-capture of UVDE generated 3’-OH ends at UV photoproducts. DNA Repair 36, 156-161
– 2015: Guintini L, Charton R, Peyresaubes F, Thoma F, Conconi A. Nucleosome positioning, nucleotide excision repair and photoreactivation in Saccharomyces cerevisiae. DNA Repair 36, 98-104
– 2015: Charton R, Guintini L, Peyresaubes F, Conconi A. Repair of UV induced DNA lesions in ribosomal gene chromatin and the role of “Odd” RNA polymerases (I and III). DNA Repair 36, 49-58
Musique (guitare, clarinette)
Voyage (Italie, Irlande, USA, Autriche, République-Tchèque…)
Alexia MuguetPhD Student
PROTEIN FACTORS PARTICIPATING IN NUCLEOTIDE EXCISION REPAIR
Subir des échecs n’est pas une défaite, mais un enseignement de valeur.
– 2014-2015: Master in Fondamentale and Applied Microbiology – Université de Bretagne Occidentale (France)
– 2012-2014: Master in Oceanography and Marine Environments – Université Pierre et Marie Curie / Paris VI (France)
– 2011-2012: Licence in Microbiology – Université de Montpellier (France)
– 2009-2011: Classes préparatoires – Montpelier (France)
– 2018: Bourse de mobilité scientifique – relation Québec-Bavière, Ministère des Relations Internationales du Québec
– 2009-2015: Bourse aux études, CROUS (France)
– 2009-2011: Bourse au mérite, CROUS (France)
– 2016: Abadie E, Muguet A, Berteaux T, Chomérat N, Hess P, Roque D’OrbCastel E, Masseret E, Laabir M. Toxin and Growth Responses of the Neurotoxic Dinoflagellate Vulcanodinium rugosum to Varying Temperature and Salinity. Toxins 8, 136
Tango argentin / Argentine tango, Jive
Audrey PailléPhD Student
NER IN ACTIVE rRNA GENE CHROMATINE
It always seems impossible, until it’s done.
– 2015-2017: Master in Biology, Health and Medical Science, BioHealth and Ingeneering Research, Cell Ingeneering speciality – Université de Poitiers (France)
– 2012-2015: Licence in Life Science, Neuroscience and Physiology speciality – Univeristé de Poitiers (France)
– 2011-2012: First year of Medical school – Université de Poitiers (France)
Food and Pâtisserie
Travel (France, Italy, Sweden, England, Belgium, Spain, Canada, Andorre….)