CSN5/Jab1 controls multiple events in the mammalian cell cycle

Akihiro Yoshida, Noriko Yoneda-Kato, Martina Panattoni, Ruggero Pardi, Jun Ya Kato

Research output: Contribution to journalArticlepeer-review


The COP9 signalosome (CSN) complex is critical for mammalian cell proliferation and survival, but it is not known how the CSN affects the cell cycle. In this study, MEFs lacking CSN5/Jab1 were generated using a CRE-flox system. MEFs ceased to proliferate upon elimination of CSN5/Jab1. Rescue experiments indicated that the JAMM domain of CSN5/Jab1 was essential. CSN5/Jab1-elimination enhanced the neddylation of cullins 1 and 4 and altered the expression of many factors including cyclin E and p53. CSN5/Jab1-elimination inhibited progression of the cell cycle at multiple points, seemed to initiate p53-independent senescence and increased the ploidy of cells. Thus, CSN5/Jab1 controls different events of the cell cycle, preventing senescence and endocycle as well as the proper progression of the somatic cell cycle. Structured summary: MINT- 8046253: Csn1 (uniprotkb: Q99LD4) physically interacts (MI: 0914) with Csn5 (uniprotkb: O35864), Csn8 (uniprotkb: Q8VBV7), Csn3 (uniprotkb: O88543), Csn7b (uniprotkb: Q8BV13) and Csn6 (uniprotkb: O88545) by anti bait coimmunoprecipitation (MI: 0006).

Original languageEnglish
Pages (from-to)4545-4552
Number of pages8
JournalFEBS Letters
Issue number22
Publication statusPublished - Nov 19 2010


  • Cell cycle
  • Cell proliferation
  • COP9 signalosome
  • CSN5/Jab1
  • Endocycle
  • Neddylation
  • Senescence

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Cell Biology
  • Genetics
  • Molecular Biology
  • Structural Biology


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