Literatura académica sobre el tema "Resection des extrémités non homologues"
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Artículos de revistas sobre el tema "Resection des extrémités non homologues"
MULSANT, P. "Glossaire général". INRAE Productions Animales 24, n.º 4 (8 de septiembre de 2011): 405–8. http://dx.doi.org/10.20870/productions-animales.2011.24.4.3273.
Texto completoTesis sobre el tema "Resection des extrémités non homologues"
Nourisson, Antonin. "Étude structurale et fonctionnelle de la fidélité des ADN polymérases X spécialisées dans la réparation des cassures doubles brins programmées chez Paramecium tetraurelia". Electronic Thesis or Diss., Sorbonne université, 2024. http://www.theses.fr/2024SORUS103.
Texto completoThe unicellular eukaryote Paramecium tetraurelia is a binucleate organism, which loses the nucleus required for gene expression (somatic) during reproduction. This nucleus must therefore be regenerated from its other nucleus (germinal), which is diploid. This regeneration involves numerous replications of the genome, but above all massive rearrangements, some of which consist in the programmed introduction of double-strand breaks at thousands of sites in the genome, in order to eliminate insertion sequences that break the reading frame in many genes. Once these breaks have been introduced, they are repaired by a system that relies on proteins involved in non-homologous repair, or NHEJ (Ku70/80, DNA-PKcs, Ligase IV, XRCC4) including 4 DNA polymerases. However, there is a major difference between classical NHEJ, which is known for its high error rate, and NHEJ in paramecium, which makes virtually no errors. The aim of this thesis is to explain the fidelity of this system, focusing on the DNA polymerases involved in this repair in Paramecium tetraurelia.Initially, a bioinformatics approach was used to hypothesize the reasons for the fidelity of these enzymes, by studying in depth the classification of DNA polymerases of family X. Following an enzymatic study of Paramecium tetraurelia DNA polymerases, which demonstrated their similarities to λ and β DNA polymerases, as well as their high fidelity, the existence of two mechanisms that could explain this fidelity was demonstrated. To this end, the enzymatic activity of DNA polymerase λ mutants was tested, and their structure obtained by X-ray crystallography. A first mechanism, similar to that encountered in DNA polymerase β, is based on local conformational changes within the enzyme's catalytic site. The second mechanism, uncharacterized until now, uses a 10-residue loop to stabilize the DNA within the active site, only in the presence of a correct nucleotide, and is found in DNA polymerase λ.These new insights into the molecular basis of X-family DNA polymerase fidelity provide a better understanding of Paramecium tetraurelia NHEJ fidelity, which may lead to a broader understanding of NHEJ and its implications in the immune system and carcinogenesis
Gelot, Camille. "Rôle du complexe de cohésion sur la ligature d'extrémités d'ADN non homologues et la stabilité du génome". Thesis, Paris 6, 2014. http://www.theses.fr/2014PA066300/document.
Texto completoDNA double-strand breaks (DSBs) repair is essential for genome stability/diversity, but can also generate genome rearrangements. Although non-homologous end-joining (NHEJ) is required for genome stability maintenance, the joining of distant double strand ends (DSE) should inexorably lead to genetic rearrangements. We analyzed the efficiency and accurency of close or distal EJ repair. Our data show that global end-joining is more efficient on close ends (34bp) compared to distal ends (3200bp) and that C-NHEJ is favored on close ends, resulting in more accurate outcome, compared to distal ends where more mutagenic A-EJ events takes place. In addition, the joining of distal ends favors the insertion/capture of DNA sequences. These data show only few kb distances between two DSEs are sufficient to jeopardize DSB repair efficiency and accuracy, leading to complex scars at the re-sealed junctions, and cell response is sufficiently sensitive to differently process such distal ends. We next addressed the question of the mechanisms preventing the joining of distant DSE. We show that depletion of the cohesin complex proteins specifically stimulates the end-joining of I-SceI-induced DSBs distant of 3200bp, while the joining of close DSEs (34bp) remained unaffected. Consistently, exome sequencing and cytogenetic analysis revealed that RAD21 ablation generates large chromosome rearrangements and a strong induction of replication stress-induced chromosome fusions. These data reveal a role for the cohesin complex in the protection against profound genome rearrangements arising through ligation of distant DSEs
Rivera-Muñoz, Paola. "Rôle des facteurs de la voie de réparation des extrémités non homologues au cours du processus de commutation de classe des immunoglobulines". Paris 7, 2009. http://www.theses.fr/2009PA077167.
Texto completoThe non homologous end-joining (NHEJ) is a predominant pathway for double-strand break (DSB) repair in mammalian cells. NHEJ repair factors (Ku70, Ku80, DNA-PKcs, Artemis, XRCC4 and DNA ligase IV) defect causes a defective V(D)J recombination exhibiting a severe combined immune-deficiency and usually associated with a pronounced hypersensitivity towards ionizing radiation. Although DSB are essential intermediates in CSR, NHEJ intervention has not been established unequivocally yet. To bypass the V(D)J recombination defect and analyse XRCC4 and Artemis involvement in CSR, we developed a conditional knock-out mouse model. For the XRCC4 model we used a novel lentiviral transgenic technology to abolish its synthesis in mature B cells, whereas the classical homologous recombination was employed to achieve the Artemis conditional model. The partial CSR defect obtained in the absence of XRCC4 enabled us to conclude unambiguously the involvement of the NHEJ pathway during CSR, but also revealed a new alternative NHEJ repair pathway. For Artemis the results showed its function for repairing a subset of DSB induced during CSR. Finally, the Cernunnos KO mouse model exposed a "normal" immune System development associated with a partial CSR defect. These results suggest that as a NHEJ factor, Cernunnos is not essential for the V(D)J recombination but has a role during the repair of the CSR DSB. Furthermore, the hypocellularity of every lymphoid organ analysed brings to consideration a cell viability function in a NHEJ independent pathway
Le, Guyader Gwenaël. "Analyse du rôle joué par les protéines de la voie de réparation par jonction des extrémités non-homologues de l'ADN au cours du processus de commutation de classe des immunoglobulines". Paris 7, 2007. http://www.theses.fr/2007PA077122.
Texto completoThe immune System is the site of intense DNA damage. Indeed, DNA double-strand breaks (DSBs) are a constant threat to ail living cells. Mammalian cells tend to utilize mainly the non-homologous end-joining pathway (NHEJ) to repair DSBs. Lack of one of the NHEJ proteins (Artemis or XRCC4) leads to a severe combined immune deficiency with radiosensitivity in mammals. Mature B cells migrate to secondary lymphoid organs, where they undergo antigen-driven immunoglobulin-gene diversification through somatic hypermutation and class-switch recombination (CSR). So far, XRCC and DNA Ligase IV are the only proteins required for ail types of NHEJ reactions that have no reported roles outside NHEJ. Therefore, although most available evidence points to a role for NHEJ factors in CSR, elucidation of the role of XRCC4 would provide the most unequivocal proof. To bypass the embryonic lethality and the V(D)J recombination defect of knockout models, we tried to develop four differents strategies to identify the role of Artemis and XRCC4 in CSR. The purpose of one of these strategies was to bring about conditional inactivation of Artemis murine gene in mature germinal center B cells. We found that Artemis-deficient B cells undergo robust CSR, indicating that NHEJ pathway functions mostly in CSR via an Artemis-independent mechanism. To formally implicate NHEJ process in CSR, we built up a strategy of conditional invalidation of XRCC4 gene in mature B cells. Our results connect XRCC4 and NHEJ pathway to CSR while reflecting the use of an alternative pathway using microhomologies in the repair of CSR DSB in the absence of XRCC4
Grabarz, Anastazja. "Réparation des cassures double brin de l'adn chez les mammifères : rôle des protéines MRE11 et BLM dans l’initiation de la ligature d’extrémités non homologues (NHEJ )". Thesis, Paris 11, 2011. http://www.theses.fr/2011PA112172.
Texto completoDNA double strand breaks (DSBs) are highly cytotoxic lesions, which can lead to genetic rearrangements. Two pathways are responsible for repairing these lesions : homologous recombination (HR) and non homologous end joining (NHEJ). In our laboratory, an intrachromosomal substrate has been established in order to measure the efficiency and the fidelity of NHEJ in living cells (Guirouilh-Barbat 2004). This approach led us to identify a KU-independent alternative pathway, which uses microhomologies in the proximity of the junction to accomplish repair – the alternative NHEJ (Guirouilh-Barbat 2004, Guirouilh-Barbat et Rass 2007). The goal of my thesis consisted in identifying and characterising major actors of this pathway. In the absence of KU, alternative NHEJ would be initiated by ssDNA resection of damaged ends. We showed that the nuclease activity of MRE11 is necessary for this mechanism. MRE11 overexpression leads to a two fold stimulation of NHEJ efficiency, while the extinction of MRE11 by siRNA results in a two fold decrease. Our results demonstrate that the proteins RAD50 and CtIP act in the same pathway as MRE11. Moreover, in cells deficient for XRCC4, MIRIN – an inhibitor of the MRN complex – leads to a decrease in repair efficiency, implicating MRE11 in alternative NHEJ. We also showed that MRE11 can act in an ATM-dependent and independent manner (Rass et Grabarz Nat Struct Mol Biol 2009). The initiation of break resection needs to be pursued by a more extensive degradation of DNA, which is accomplished in yeast by the proteins Exo1 and Sgs1/Dna2. In human cells, in vitro studies have recently proposed a similar model of a two-step break resection. We chose to elucidate the role of one of the human homologs of Sgs1 – the RecQ helicase BLM – in the resection process. Our experiments show, that he absence of BLM decreases the efficiency of end joining by NHEJ, accompanied by an increase in error-prone events, especially long-range deletions (>200nt). This suggests that BLM protects against extensive resection during alternative NHEJ. Furthermore, BLM is implicated in the protection against CtIP-dependent resection at the initiation of HR. In conclusion, our results show a major role of BLM in protecting against an excess of resection, mediated by the MRN cofactor – CtIP. BLM interacts with 53BP1 at sites of damage, in an ATM-dependent manner, in order to regulate the resection process and counteract BRCA1 activity. This underlines the novel role of BLM in the protection against resection and favouring gene conversion events without crossing-over, which is substantial for maintaining genomic integrity
De, Melo Abinadabe Jackson. "Molecular basis for the structural role of human DNA ligase IV". Thesis, Aix-Marseille, 2016. http://www.theses.fr/2016AIXM4040.
Texto completoFailure to repair DNA double-strand breaks (DSBs) may have deleterious consequences inducing genomic instability and even cell death. In most mammalian cells, Non-Homologous End Joining (NHEJ) is a prominent DSB repair pathway. DNA ligase IV (LigIV) is unique in its ability to promote classical NHEJ. It associates with two structurally related proteins called XRCC4 and XLF (aka Cernunnos). LigIV directly interacts with XRCC4 forming a stable complex while the XLF interaction with this complex is mediated by XRCC4. XLF strongly stimulates the ligation activity of the LigIV/XRCC4 complex by an unknown mechanism. Recently, a structural noncatalytic role of LigIV has been uncovered (Cottarel et al., 2013). Here, we have reconstituted the end joining ligation step using recombinant proteins produced in bacteria to explore not only the molecular basis for the structural role of LigIV, but also to understand the mechanism by which XLF stimulates the ligation complex, and how these three proteins work together during NHEJ. Our biochemical analysis suggests that XLF, through interactions with LigIV/XRCC4 complex, could induce a conformational change in LigIV. Rearrangement of the LigIV would expose its DNA binding interface that is able to bridge two independent DNA molecules. This bridging ability is fully independent of LigIV’s catalytic activity. We have mutated this interface in order to attempt to disrupt the newly identified DNA bridging ability. In vitro analysis of this LigIV mutant will be presented as well as a preliminary in vivo analysis