Journal
NATURE COMMUNICATIONS
Volume 11, Issue 1, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41467-019-14276-x
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Funding
- ERC-consolidator grant [ERC-2013-CoG-615638]
- Senior Wellcome Research Fellowship
- Fundacao para a Ciencia e a Tecnologia (FCT) [SFRH/BD/74284/2010]
- Sir Henry Wellcome Fellowship [204747/Z/16/Z]
- Investigador FCT position
- Wellcome Trust [204747/Z/16/Z] Funding Source: Wellcome Trust
- Fundação para a Ciência e a Tecnologia [SFRH/BD/74284/2010] Funding Source: FCT
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Centromeres are defined by a self-propagating chromatin structure based on stable inheritance of CENP-A containing nucleosomes. Here, we present a genetic screen coupled to pulse-chase labeling that allow us to identify proteins selectively involved in deposition of nascent CENP-A or in long-term transmission of chromatin-bound CENP-A. These include factors with known roles in DNA replication, repair, chromatin modification, and transcription, revealing a broad set of chromatin regulators that impact on CENP-A dynamics. We further identify the SUMO-protease SENP6 as a key factor, not only controlling CENP-A stability but virtually the entire centromere and kinetochore. Loss of SENP6 results in hyper-SUMOylation of CENP-C and CENP-I but not CENP-A itself. SENP6 activity is required throughout the cell cycle, suggesting that a dynamic SUMO cycle underlies a continuous surveillance of the centromere complex that in turn ensures stable transmission of CENP-A chromatin.
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