作者: Akira Inoue , Judith Hyle , Mark S. Lechner , Jill M. Lahti
DOI: 10.1016/J.YEXCR.2011.08.006
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摘要: The ChlR1 DNA helicase, encoded by DDX11 gene, which is responsible for Warsaw breakage syndrome (WABS), has a role in sister-chromatid cohesion. In this study, we show that human deficient cells exhibit abnormal heterochromatin organization. While constitutive discretely localized at perinuclear and perinucleolar regions control HeLa cells, ChlR1-depleted showed dispersed localization of accompanied disrupted centromere clustering. Cells isolated from Ddx11(-/-) embryos also exhibited diffuse centromeres foci. Similar abnormalities were found depleted combinations HP1α HP1β. Immunofluorescence chromatin immunoprecipitation decreased level pericentric cells. Trimethyl-histone H3 lysine 9 (H3K9-me3) was modestly sequences. abnormality further supported methylation within major satellite repeats embryos. Furthermore, micrococcal nuclease (MNase) assay revealed density the telomeres. These data suggest addition to cohesion, involved proper formation heterochromatin, turn contributes global nuclear organization pleiotropic effects.