論文

査読有り 国際誌
2010年1月1日

The p150 subunit of CAF-1 causes association of SUMO2/3 with the DNA replication foci.

Biochemical and biophysical research communications
  • Junsuke Uwada
  • ,
  • Niina Tanaka
  • ,
  • Yutaro Yamaguchi
  • ,
  • Yasuhiro Uchimura
  • ,
  • Kei-ichi Shibahara
  • ,
  • Mitsuyoshi Nakao
  • ,
  • Hisato Saitoh

391
1
開始ページ
407
終了ページ
13
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1016/j.bbrc.2009.11.071
出版者・発行元
ACADEMIC PRESS INC ELSEVIER SCIENCE

The small ubiquitin-related modifier 2/3 (SUMO2/3) can be post-translationally conjugated to a wide variety of proteins constituting chromatin, the platform for genetic and epigenetic regulation. Nevertheless, it is unclear how SUMO2/3 and SUMO2/3-modified proteins are delivered to the chromatin fibers. Here we report that the largest subunit of chromatin assembly factor 1 (CAF-1), human p150, interacts directly and preferentially with SUMO2/3. Amino acid residue of 98-105 in p150 is essential and sufficient for SUMO2/3 interaction. p150-SUMO2/3 interaction coincided with regions that replicate chromatin fibers, because accumulation of the proliferating cell nuclear antigen (PCNA), and incorporation of bromodeoxyuridine (BrdU) were detected at foci co-localized with both p150 and SUMO2/3 during the S-phase in a cell line expressing epitope-tagged p150. Although inhibition of SUMO2/3 expression had only a small effect on p150 deposition on the replication sites, depletion of p150 led to delocalization of SUMO2/3 from the replication foci. Furthermore, p150 mutants deficient in SUMO2/3 interaction, caused a major reduction of SUMO2/3 at the replication foci. Thus, our findings suggest an expanded role of p150 as a SUMO2/3-interacting factor, and raise the intriguing possibility that p150 plays a role in promoting delivery of SUMO2/3 or SUMO2/3-modified proteins (or both) on chromatin fibers during replication.

リンク情報
DOI
https://doi.org/10.1016/j.bbrc.2009.11.071
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/19919826
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000273624500072&DestApp=WOS_CPL
ID情報
  • DOI : 10.1016/j.bbrc.2009.11.071
  • ISSN : 0006-291X
  • PubMed ID : 19919826
  • Web of Science ID : WOS:000273624500072

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