P
Peter J. Romanienko
Researcher at National Institutes of Health
Publications - 14
Citations - 4075
Peter J. Romanienko is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Meiosis & Medicine. The author has an hindex of 8, co-authored 8 publications receiving 3847 citations. Previous affiliations of Peter J. Romanienko include Memorial Sloan Kettering Cancer Center.
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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.
Journal ArticleDOI
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.
Journal ArticleDOI
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.
Journal ArticleDOI
The mouse X chromosome is enriched for sex-biased genes not subject to selection by meiotic sex chromosome inactivation.
Pavel P. Khil,Natalya A Smirnova,Peter J. Romanienko,Peter J. Romanienko,R. Daniel Camerini-Otero +4 more
TL;DR: It is shown that mouse spermatogenesis genes are relatively under-represented on the X chromosome and female-biased genes are enriched on it, which may be a universal driving force for X-chromosome demasculinization.