R
R. Daniel Camerini-Otero
Researcher at National Institutes of Health
Publications - 97
Citations - 10158
R. Daniel Camerini-Otero is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Homologous recombination & Meiosis. The author has an hindex of 45, co-authored 97 publications receiving 9288 citations. Previous affiliations of R. Daniel Camerini-Otero include Laboratory of Molecular Biology.
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Journal ArticleDOI
Genomic instability in mice lacking histone H2AX.
Arkady Celeste,Simone Petersen,Peter J. Romanienko,Oscar Fernandez-Capetillo,Hua Tang Chen,Olga A. Sedelnikova,Bernardo Reina-San-Martin,Vincenzo Coppola,Eric Meffre,Michael J. Difilippantonio,Christophe E. Redon,Duane R. Pilch,Alexandru Olaru,Michael Eckhaus,R. Daniel Camerini-Otero,Lino Tessarollo,Ferenc Livak,Katia Manova,William M. Bonner,Michel C. Nussenzweig,André Nussenzweig +20 more
TL;DR: Higher order chromatin structure presents a barrier to the recognition and repair of DNA damage, and H2AX is critical for facilitating the assembly of specific DNA-repair complexes on damaged DNA.
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The mouse Spo11 gene is required for meiotic chromosome synapsis.
TL;DR: The Spo11 protein initiates meiotic recombination by generating DNA double-strand breaks (DSBs) and is required for meiotic synapsis in S. cerevisiae, but it is speculated that there is an additional role for Spo11, after it generates DSBs, insynapsis.
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DNA damage-induced G2-M checkpoint activation by histone H2AX and 53BP1.
Oscar Fernandez-Capetillo,Hua Tang Chen,Arkady Celeste,Irene M. Ward,Peter J. Romanienko,Julio C. Morales,Kazuhito Naka,Zhengfang Xia,R. Daniel Camerini-Otero,Noboru Motoyama,Phillip B. Carpenter,William M. Bonner,Junjie Chen,André Nussenzweig +13 more
TL;DR: It is proposed that at threshold levels of DNA damage, H2AX-mediated concentration of 53BP1 at double-strand breaks is essential for the amplification of signals that might otherwise be insufficient to prevent entry of damaged cells into mitosis.
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H2AX Is Required for Chromatin Remodeling and Inactivation of Sex Chromosomes in Male Mouse Meiosis
Oscar Fernandez-Capetillo,Shantha K. Mahadevaiah,Arkady Celeste,Peter J. Romanienko,R. Daniel Camerini-Otero,William M. Bonner,Katia Manova,Paul S. Burgoyne,André Nussenzweig +8 more
TL;DR: It is shown that the X and Y chromosomes of histone H2AX-deficient spermatocytes fail to condense to form a sex body, do not initiate MSCI, and exhibit severe defects in meiotic pairing.
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Genetic recombination is directed away from functional genomic elements in mice
TL;DR: It is shown that PRDM9 determines the positions of practically all hotspots in the mouse genome, with the exception of the pseudo-autosomal region (PAR)—the only area of the genome that undergoes recombination in 100% of cells.