論文

査読有り
2017年9月

Identification of three signaling molecules required for calcineurin-dependent monopolar growth induced by the DNA replication checkpoint in fission yeast

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
  • Kazunori Kume
  • ,
  • Tomoyo Hashimoto
  • ,
  • Masashi Suzuki
  • ,
  • Masaki Mizunuma
  • ,
  • Takashi Toda
  • ,
  • Dai Hirata

491
4
開始ページ
883
終了ページ
889
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1016/j.bbrc.2017.07.129
出版者・発行元
ACADEMIC PRESS INC ELSEVIER SCIENCE

Cell polarity is coordinately regulated with the cell cycle. Growth polarity of the fission yeast Schizosaccharomyces pombe transits from monopolar to bipolar during G2 phase, termed NETO (new end take off). Upon perturbation of DNA replication, the checkpoint kinase Cdsl/CHK2 induces NETO delay through activation of Ca2+/calmodulin-dependent protein phosphatase calcineurin (CN). CN in turn regulates its downstream targets including the microtubule (MT) plus-end tracking CLIP170 homologue Tipl and the Casein kinase 1 gamma Cki3. However, whether and which Ca2+ signaling molecules are involved in the NETO delay remains elusive. Here we show that 3 genes (trp1322, vcxl and SPAC6c3.06c encoding TRP channel, antiporter and P-type ATPase, respectively) play vital roles in the NETO delay. Upon perturbation of DNA replication, these 3 genes are required for not only the NETO delay but also for the maintenance of cell viability. Trp1322 and Vcxl act downstream of Cds1 and upstream of CN for the NETO delay, whereas SPAC6c3.06c acts downstream of CN. Consistently, Trp1322 and Vcxl, but not SPAC6c3.06c, are essential for activation of CN. Interestingly, we have found that elevated extracellular Ca2+ per se induces a NETO delay, which depends on CN and its downstream target genes. These findings imply that Ca2+-CN signaling plays a central role in cell polarity control by checkpoint activation. (C) 2017 Elsevier Inc. All rights reserved.

Web of Science ® 被引用回数 : 2

リンク情報
DOI
https://doi.org/10.1016/j.bbrc.2017.07.129
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000411169800004&DestApp=WOS_CPL
ID情報
  • DOI : 10.1016/j.bbrc.2017.07.129
  • ISSN : 0006-291X
  • eISSN : 1090-2104
  • Web of Science ID : WOS:000411169800004

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