Sandrine Ragu

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The absence of Tsa1, a key peroxiredoxin that functions to scavenge H(2)O(2) in Saccharomyces cerevisiae, causes the accumulation of a broad spectrum of mutations including gross chromosomal rearrangements (GCRs). Deletion of TSA1 also causes synthetic lethality in combination with mutations in RAD6 and several key genes involved in DNA double-strand break(More)
We developed a clonal WI-38hTERT/GFP-RAF1-ER immortal cell line to study RAF-induced senescence of human fibroblasts. Activation of the GFP-RAF1-ER kinase by addition of 4-hydroxy-tamoxifen led to a robust induction of senescence within one population doubling, accompanied by the assembly of heterochromatic foci. At least two pathways contribute in parallel(More)
The absence of Tsa1, a key peroxiredoxin that scavenges H2O2 in Saccharomyces cerevisiae, causes the accumulation of a broad spectrum of mutations. Deletion of TSA1 also causes synthetic lethality in combination with mutations in RAD51 or several key genes involved in DNA double-strand break repair. In the present study, we propose that the accumulation of(More)
The peroxiredoxins (Prx) are conserved antioxidant proteins that use cysteine as the primary site of oxidation during the reduction of peroxides. Many organisms have more than one isoform of Prx. Deletion of TSA1, one of five Prxs in yeast Saccharomyces cerevisiae, results in accumulation of a broad spectrum of mutations including gross chromosomal(More)
Replications forks are routinely hindered by different endogenous stresses. Because homologous recombination plays a pivotal role in the reactivation of arrested replication forks, defects in homologous recombination reveal the initial endogenous stress(es). Homologous recombination-defective cells consistently exhibit a spontaneously reduced replication(More)
The Ogura cytoplasmic male sterility causing protein, ORF138, was found to be part of a complex with an apparent size of over 750 kDa in the inner membrane of mitochondria of sterile plants. ORF138 did not colocalize with any of the oxidative phosphorylation complexes, nor did its presence modify their apparent size or amount, compared to samples from(More)
DNA double-strand breaks (DSBs) are highly lethal lesions that jeopardize genome integrity. However, DSBs are also used to generate diversity during the physiological processes of meiosis or establishment of the immune repertoire. Therefore, DSB repair must be tightly controlled. Two main strategies are used to repair DSBs: homologous recombination (HR) and(More)
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