Science (New York, N.Y.) · 2002
Genomic instability in mice lacking histone H2AX.
СтатьяПоддержка исследования: вне правительства СШАПоддержка службы здравоохранения СШАНазвание и аннотация: Перевод в очереди
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Celeste Arkady, Petersen Simone, Romanienko Peter J, Fernandez-Capetillo Oscar, Chen Hua Tang, Sedelnikova Olga A, Reina-San-Martin Bernardo, Coppola Vincenzo, Meffre Eric, Difilippantonio Michael J, Redon Christophe, Pilch Duane R, Olaru Alexandru, Eckhaus Michael, Camerini-Otero R Daniel, Tessarollo Lino, Livak Ferenc, Manova Katia, Bonner William M, Nussenzweig Michel C, Nussenzweig André
Аннотация
Higher order chromatin structure presents a barrier to the recognition and repair of DNA damage. Double-strand breaks (DSBs) induce histone H2AX phosphorylation, which is associated with the recruitment of repair factors to damaged DNA. To help clarify the physiological role of H2AX, we targeted H2AX in mice. Although H2AX is not essential for irradiation-induced cell-cycle checkpoints, H2AX-/- mice were radiation sensitive, growth retarded, and immune deficient, and mutant males were infertile. These pleiotropic phenotypes were associated with chromosomal instability, repair defects, and impaired recruitment of Nbs1, 53bp1, and Brca1, but not Rad51, to irradiation-induced foci. Thus, H2AX is critical for facilitating the assembly of specific DNA-repair complexes on damaged DNA.
Предметные рубрики MeSH
Amino Acid SequenceAnimalsB-LymphocytesBase SequenceCell CycleCells, CulturedCellular SenescenceChromosome AberrationsDNA DamageDNA RepairFemaleGene TargetingHistonesImmunoglobulin Class SwitchingInfertility, MaleLymphocyte CountMaleMeiosisMiceMice, KnockoutMolecular Sequence DataMutationPhosphorylationRecombination, GeneticSpermatocytesT-Lymphocytes