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Clemente-Blanco, A.* ; Sen, N.* ; Mayan-Santos, M.* ; Sacristán, M.P.* ; Graham, B.* ; Jarmuz, A.* ; Giess, A.* ; Webb, E.* ; Game, L.* ; Eick, D. ; Bueno, A.* ; Merkenschlager, M* ; Aragón, L.*

Cdc14 phosphatase promotes segregation of telomeres through repression of RNA polymerase II transcription.

Nat. Cell Biol. 13, 1450-1456 (2011)
DOI PMC
Open Access Green as soon as Postprint is submitted to ZB.
Kinases and phosphatases regulate messenger RNA synthesis through post-translational modification of the carboxy-terminal domain (CTD) of the largest subunit of RNA polymerase II (ref. 1). In yeast, the phosphatase Cdc14 is required for mitotic exit2, 3 and for segregation of repetitive regions4. Cdc14 is also a subunit of the silencing complex RENT (refs 5, 6), but no roles in transcriptional repression have been described. Here we report that inactivation of Cdc14 causes silencing defects at the intergenic spacer sequences of ribosomal genes during interphase and at Y′ repeats in subtelomeric regions during mitosis. We show that the role of Cdc14 in silencing is independent of the RENT deacetylase subunit Sir2. Instead, Cdc14 acts directly on RNA polymerase II by targeting CTD phosphorylation at Ser 2 and Ser 5. We also find that the role of Cdc14 as a CTD phosphatase is conserved in humans. Finally, telomere segregation defects in cdc14 mutants4 correlate with the presence of subtelomeric Y′ elements and can be rescued by transcriptional inhibition of RNA polymerase II.
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Publication type Article: Journal article
Document type Scientific Article
Keywords no keywords
Language english
Publication Year 2011
HGF-reported in Year 2011
ISSN (print) / ISBN 1465-7392
e-ISSN 1476-4679
Quellenangaben Volume: 13, Issue: 12, Pages: 1450-1456 Article Number: , Supplement: ,
Publisher Nature Publishing Group
Reviewing status Peer reviewed
POF-Topic(s) 30504 - Mechanisms of Genetic and Environmental Influences on Health and Disease
Research field(s) Immune Response and Infection
PSP Element(s) G-501490-001
PubMed ID 22020438
Scopus ID 84856133989
Erfassungsdatum 2011-11-10