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  1. AU="Lenden-Hasse, Hélène"
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  1. Article ; Online: Paralogie et redondance : maintenir l’intégrité du génome au cours de la recombinaison V(D)J.

    Lescale, Chloé / Lenden Hasse, Hélène / Deriano, Ludovic

    Medecine sciences : M/S

    2017  Volume 33, Issue 5, Page(s) 474–477

    Title translation Paralogy and redundancy: maintaining genome integrity during V(D)J recombination.
    MeSH term(s) Animals ; Cytoprotection/genetics ; Cytoprotection/immunology ; DNA Cleavage ; DNA Repair/physiology ; Genetic Diseases, Inborn/genetics ; Genetic Diseases, Inborn/immunology ; Genetic Diseases, Inborn/prevention & control ; Genomic Instability/physiology ; Humans ; Immune System Diseases/genetics ; Immune System Diseases/prevention & control ; Mice ; V(D)J Recombination/genetics
    Language French
    Publishing date 2017-06-14
    Publishing country France
    Document type News
    ZDB-ID 632733-3
    ISSN 1958-5381 ; 0767-0974
    ISSN (online) 1958-5381
    ISSN 0767-0974
    DOI 10.1051/medsci/20173305005
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

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  2. Article ; Online: The control of transcriptional memory by stable mitotic bookmarking.

    Bellec, Maëlle / Dufourt, Jérémy / Hunt, George / Lenden-Hasse, Hélène / Trullo, Antonio / Zine El Aabidine, Amal / Lamarque, Marie / Gaskill, Marissa M / Faure-Gautron, Heloïse / Mannervik, Mattias / Harrison, Melissa M / Andrau, Jean-Christophe / Favard, Cyril / Radulescu, Ovidiu / Lagha, Mounia

    Nature communications

    2022  Volume 13, Issue 1, Page(s) 1176

    Abstract: To maintain cellular identities during development, gene expression profiles must be faithfully propagated through cell generations. The reestablishment of gene expression patterns upon mitotic exit is mediated, in part, by transcription factors (TF) ... ...

    Abstract To maintain cellular identities during development, gene expression profiles must be faithfully propagated through cell generations. The reestablishment of gene expression patterns upon mitotic exit is mediated, in part, by transcription factors (TF) mitotic bookmarking. However, the mechanisms and functions of TF mitotic bookmarking during early embryogenesis remain poorly understood. In this study, taking advantage of the naturally synchronized mitoses of Drosophila early embryos, we provide evidence that GAGA pioneer factor (GAF) acts as a stable mitotic bookmarker during zygotic genome activation. We show that, during mitosis, GAF remains associated to a large fraction of its interphase targets, including at cis-regulatory sequences of key developmental genes with both active and repressive chromatin signatures. GAF mitotic targets are globally accessible during mitosis and are bookmarked via histone acetylation (H4K8ac). By monitoring the kinetics of transcriptional activation in living embryos, we report that GAF binding establishes competence for rapid activation upon mitotic exit.
    MeSH term(s) Acetylation ; Animals ; Chromatin/genetics ; Drosophila/genetics ; Histones/genetics ; Histones/metabolism ; Mitosis/genetics ; Transcription Factors/genetics ; Transcription Factors/metabolism
    Chemical Substances Chromatin ; Histones ; Transcription Factors
    Language English
    Publishing date 2022-03-04
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-022-28855-y
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: SHLD1 is dispensable for 53BP1-dependent V(D)J recombination but critical for productive class switch recombination.

    Vincendeau, Estelle / Wei, Wenming / Zhang, Xuefei / Planchais, Cyril / Yu, Wei / Lenden-Hasse, Hélène / Cokelaer, Thomas / Pipoli da Fonseca, Juliana / Mouquet, Hugo / Adams, David J / Alt, Frederick W / Jackson, Stephen P / Balmus, Gabriel / Lescale, Chloé / Deriano, Ludovic

    Nature communications

    2022  Volume 13, Issue 1, Page(s) 3707

    Abstract: SHLD1 is part of the Shieldin (SHLD) complex, which acts downstream of 53BP1 to counteract DNA double-strand break (DSB) end resection and promote DNA repair via non-homologous end-joining (NHEJ). While 53BP1 is essential for immunoglobulin heavy chain ... ...

    Abstract SHLD1 is part of the Shieldin (SHLD) complex, which acts downstream of 53BP1 to counteract DNA double-strand break (DSB) end resection and promote DNA repair via non-homologous end-joining (NHEJ). While 53BP1 is essential for immunoglobulin heavy chain class switch recombination (CSR), long-range V(D)J recombination and repair of RAG-induced DSBs in XLF-deficient cells, the function of SHLD during these processes remains elusive. Here we report that SHLD1 is dispensable for lymphocyte development and RAG-mediated V(D)J recombination, even in the absence of XLF. By contrast, SHLD1 is essential for restricting resection at AID-induced DSB ends in both NHEJ-proficient and NHEJ-deficient B cells, providing an end-protection mechanism that permits productive CSR by NHEJ and alternative end-joining. Finally, we show that this SHLD1 function is required for orientation-specific joining of AID-initiated DSBs. Our data thus suggest that 53BP1 promotes V(D)J recombination and CSR through two distinct mechanisms: SHLD-independent synapsis of V(D)J segments and switch regions within chromatin, and SHLD-dependent protection of AID-DSB ends against resection.
    MeSH term(s) DNA Breaks, Double-Stranded ; DNA End-Joining Repair ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Immunoglobulin Class Switching/genetics ; V(D)J Recombination/genetics
    Chemical Substances DNA-Binding Proteins
    Language English
    Publishing date 2022-06-28
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-022-31287-3
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Repair of G1 induced DNA double-strand breaks in S-G2/M by alternative NHEJ.

    Yu, Wei / Lescale, Chloé / Babin, Loelia / Bedora-Faure, Marie / Lenden-Hasse, Hélène / Baron, Ludivine / Demangel, Caroline / Yelamos, José / Brunet, Erika / Deriano, Ludovic

    Nature communications

    2020  Volume 11, Issue 1, Page(s) 5239

    Abstract: The alternative non-homologous end-joining (NHEJ) pathway promotes DNA double-strand break (DSB) repair in cells deficient for NHEJ or homologous recombination, suggesting that it operates at all stages of the cell cycle. Here, we use an approach in ... ...

    Abstract The alternative non-homologous end-joining (NHEJ) pathway promotes DNA double-strand break (DSB) repair in cells deficient for NHEJ or homologous recombination, suggesting that it operates at all stages of the cell cycle. Here, we use an approach in which DNA breaks can be induced in G1 cells and their repair tracked, enabling us to show that joining of DSBs is not functional in G1-arrested XRCC4-deficient cells. Cell cycle entry into S-G2/M restores DSB repair by Pol θ-dependent and PARP1-independent alternative NHEJ with repair products bearing kilo-base long DNA end resection, micro-homologies and chromosome translocations. We identify a synthetic lethal interaction between XRCC4 and Pol θ under conditions of G1 DSBs, associated with accumulation of unresolved DNA ends in S-G2/M. Collectively, our results support the conclusion that the repair of G1 DSBs progressing to S-G2/M by alternative NHEJ drives genomic instability and represent an attractive target for future DNA repair-based cancer therapies.
    MeSH term(s) Animals ; Cell Cycle ; DNA Breaks, Double-Stranded ; DNA End-Joining Repair ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; G1 Phase ; Mice ; Poly (ADP-Ribose) Polymerase-1/genetics ; Poly (ADP-Ribose) Polymerase-1/metabolism
    Chemical Substances DNA-Binding Proteins ; XRCC4 protein, mouse ; Parp1 protein, mouse (EC 2.4.2.30) ; Poly (ADP-Ribose) Polymerase-1 (EC 2.4.2.30)
    Keywords covid19
    Language English
    Publishing date 2020-10-16
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-020-19060-w
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Generation and CRISPR/Cas9 editing of transformed progenitor B cells as a pseudo-physiological system to study DNA repair gene function in V(D)J recombination.

    Lenden Hasse, Hélène / Lescale, Chloé / Bianchi, Joy J / Yu, Wei / Bedora-Faure, Marie / Deriano, Ludovic

    Journal of immunological methods

    2017  Volume 451, Page(s) 71–77

    Abstract: Antigen receptor gene assembly is accomplished in developing lymphocytes by the V(D)J recombination reaction, which can be separated into two steps: DNA cleavage by the recombination-activating gene (RAG) nuclease and joining of DNA double strand breaks ( ...

    Abstract Antigen receptor gene assembly is accomplished in developing lymphocytes by the V(D)J recombination reaction, which can be separated into two steps: DNA cleavage by the recombination-activating gene (RAG) nuclease and joining of DNA double strand breaks (DSBs) by components of the nonhomologous end joining (NHEJ) pathway. Deficiencies for NHEJ factors can result in immunodeficiency and a propensity to accumulate genomic instability, thus highlighting the importance of identifying all players in this process and deciphering their functions. Bcl2 transgenic v-Abl kinase-transformed pro-B cells provide a pseudo-physiological cellular system to study V(D)J recombination. Treatment of v-Abl/Bcl2 pro-B cells with the Abl kinase inhibitor Imatinib leads to G1 cell cycle arrest, the rapid induction of Rag1/2 gene expression and V(D)J recombination. In this system, the Bcl2 transgene alleviates Imatinib-induced apoptosis enabling the analysis of induced V(D)J recombination. Although powerful, the use of mouse models carrying the Bcl2 transgene for the generation of v-Abl pro-B cell lines is time and money consuming. Here, we describe a method for generating v-Abl/Bcl2 pro-B cell lines from wild type mice and for performing gene knock-out using episomal CRISPR/Cas9 targeting vectors. Using this approach, we generated distinct NHEJ-deficient pro-B cell lines and quantified V(D)J recombination levels in these cells. Furthermore, this methodology can be adapted to generate pro-B cell lines deficient for any gene suspected to play a role in V(D)J recombination, and more generally DSB repair.
    MeSH term(s) Animals ; Apoptosis/drug effects ; CRISPR-Associated Proteins/genetics ; CRISPR-Associated Proteins/metabolism ; CRISPR-Cas Systems ; Cell Line, Transformed ; Clustered Regularly Interspaced Short Palindromic Repeats ; DNA Breaks, Double-Stranded ; DNA End-Joining Repair ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; G1 Phase Cell Cycle Checkpoints/drug effects ; Gene Editing/methods ; Genotype ; Homeodomain Proteins/genetics ; Homeodomain Proteins/metabolism ; Imatinib Mesylate/pharmacology ; Mice, Inbred C57BL ; Oncogene Proteins v-abl/antagonists & inhibitors ; Oncogene Proteins v-abl/genetics ; Oncogene Proteins v-abl/metabolism ; Phenotype ; Precursor Cells, B-Lymphoid/drug effects ; Precursor Cells, B-Lymphoid/metabolism ; Precursor Cells, B-Lymphoid/pathology ; Protein Kinase Inhibitors/pharmacology ; Proto-Oncogene Proteins c-bcl-2/genetics ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Recombinational DNA Repair/drug effects
    Chemical Substances CRISPR-Associated Proteins ; DNA-Binding Proteins ; Homeodomain Proteins ; Oncogene Proteins v-abl ; Protein Kinase Inhibitors ; Proto-Oncogene Proteins c-bcl-2 ; Rag2 protein, mouse ; Bcl2 protein, mouse (114100-40-2) ; RAG-1 protein (128559-51-3) ; Imatinib Mesylate (8A1O1M485B)
    Language English
    Publishing date 2017-09-04
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 120142-6
    ISSN 1872-7905 ; 0022-1759
    ISSN (online) 1872-7905
    ISSN 0022-1759
    DOI 10.1016/j.jim.2017.08.007
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 795: Show issues Location:
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    Jg. 1995 - 2021: Lesesall (1.OG)
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  6. Article ; Online: Specific Roles of XRCC4 Paralogs PAXX and XLF during V(D)J Recombination.

    Lescale, Chloé / Lenden Hasse, Hélène / Blackford, Andrew N / Balmus, Gabriel / Bianchi, Joy J / Yu, Wei / Bacoccina, Léa / Jarade, Angélique / Clouin, Christophe / Sivapalan, Rohan / Reina-San-Martin, Bernardo / Jackson, Stephen P / Deriano, Ludovic

    Cell reports

    2016  Volume 16, Issue 11, Page(s) 2967–2979

    Abstract: Paralog of XRCC4 and XLF (PAXX) is a member of the XRCC4 superfamily and plays a role in nonhomologous end-joining (NHEJ), a DNA repair pathway critical for lymphocyte antigen receptor gene assembly. Here, we find that the functions of PAXX and XLF in V( ... ...

    Abstract Paralog of XRCC4 and XLF (PAXX) is a member of the XRCC4 superfamily and plays a role in nonhomologous end-joining (NHEJ), a DNA repair pathway critical for lymphocyte antigen receptor gene assembly. Here, we find that the functions of PAXX and XLF in V(D)J recombination are masked by redundant joining activities. Thus, combined PAXX and XLF deficiency leads to an inability to join RAG-cleaved DNA ends. Additionally, we demonstrate that PAXX function in V(D)J recombination depends on its interaction with Ku. Importantly, we show that, unlike XLF, the role of PAXX during the repair of DNA breaks does not overlap with ATM and the RAG complex. Our findings illuminate the role of PAXX in V(D)J recombination and support a model in which PAXX and XLF function during NHEJ repair of DNA breaks, whereas XLF, the RAG complex, and the ATM-dependent DNA damage response promote end joining by stabilizing DNA ends.
    MeSH term(s) Animals ; Ataxia Telangiectasia Mutated Proteins/metabolism ; B-Lymphocytes/metabolism ; CRISPR-Cas Systems/genetics ; DNA Damage ; DNA Repair ; DNA Repair Enzymes/metabolism ; DNA-Binding Proteins/chemistry ; DNA-Binding Proteins/metabolism ; Gene Deletion ; Gene Editing ; Gene Rearrangement, B-Lymphocyte ; Immunoglobulins/genetics ; Ku Autoantigen/metabolism ; Models, Biological ; Oncogene Proteins v-abl/metabolism ; Sequence Homology, Amino Acid ; V(D)J Recombination/genetics
    Chemical Substances DNA-Binding Proteins ; IgK ; Immunoglobulins ; Oncogene Proteins v-abl ; Ataxia Telangiectasia Mutated Proteins (EC 2.7.11.1) ; Ku Autoantigen (EC 4.2.99.-) ; DNA Repair Enzymes (EC 6.5.1.-)
    Language English
    Publishing date 2016-09-02
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2016.08.069
    Database MEDical Literature Analysis and Retrieval System OnLINE

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