期刊
JOURNAL OF CELL BIOLOGY
卷 201, 期 1, 页码 49-63出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.201207183
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资金
- National Cancer Institute(NCI) [P30 CA23074]
- GI SPORE (NCl/National Institutes of Health) [P50 CA95060]
- NIH [GM069462, GM068675, GM090150]
- Arizona Center on Aging
- American Cancer Society [RSG-07-040-01]
- Burroughs Wellcome Fund
- Div Of Biological Infrastructure
- Direct For Biological Sciences [1039423] Funding Source: National Science Foundation
Condensin complexes play vital roles in chromosome condensation during mitosis and meiosis. Condensin II uniquely localizes to chromatin throughout the cell cycle and, in addition to its mitotic duties, modulates chromosome organization and gene expression during interphase. Mitotic condensin activity is regulated by phosphorylation, but mechanisms that regulate condensin II during interphase are unclear. Here, we report that condensin II is inactivated when its subunit Cap-H2 is targeted for degradation by the SCFslimb ubiquitin ligase complex and that disruption of this process dramatically changed interphase chromatin organization. Inhibition of SCFslimb function reorganized interphase chromosomes into dense, compact domains and disrupted homologue pairing in both cultured Drosophila cells and in vivo, but these effects were rescued by condensin II inactivation. Furthermore, Cap-H2 stabilization distorted nuclear envelopes and dispersed Cid/CENP-A on interphase chromosomes. Therefore, SCFslimb- mediated down-regulation of condensin II is required to maintain proper organization and morphology of the interphase nucleus.
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