Antonio Conconi

PhD

Professeur titulaire, Département de microbiologie et d’infectiologie, Faculté de médecine et des sciences de la santé, Université de Sherbrooke

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Non esitate d’andare contro corrente.

Conconi A and Bell B (NATURE 2017)
The long and short of a DNA-damage response (cited 11 times).

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 20 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 82 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 103 times).

Smerdon M and Conconi A (Progress in Nucl Acids Res and Mol Biol 1999)
Modulation of DNA Damage and Repair in Chromatin (cited 152 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 310 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 464 times).

Students

Alexia Muguet

PhD Student

PROTEIN FACTORS PARTICIPATING IN NUCLEOTIDE EXCISION REPAIR

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Subir des échecs n’est pas une défaite, mais un enseignement de valeur.

AqME

Audrey Paillé

PhD Student

NER IN CHROMATIN of ACTIVE rRNA GENE

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It always seems impossible, until it’s done.

Nelson Mandela

Quentin Dholandre

Master Student

THE ROLE OF RIBOSOMAL GENES COPY NUMBER IN UV SENSITIVITY

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