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First published online 14 April 2009
doi: 10.1242/jcs.046466

Journal of Cell Science 122, 1418-1429 (2009)
Published by The Company of Biologists 2009
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Research Article

Genetic control of cellular quiescence in S. pombe

Kenichi Sajiki1,2, Mitsuko Hatanaka1,3, Takahiro Nakamura3, Kojiro Takeda1, Mizuki Shimanuki1, Tomoko Yoshida1, Yuichiro Hanyu3, Takeshi Hayashi1, Yukinobu Nakaseko3 and Mitsuhiro Yanagida1,2,3,*

1 Okinawa Institute of Science and Technology (OIST), Initial Research Project, Uruma 904-2234, Okinawa, Japan
2 Graduate School of Biological Science, Nara Institute of Science and Technology (NAIST), Ikoma, Nara 630-0192, Japan
3 Graduate School of Biostudies, Kyoto University, Sakyo-ku, Kyoto 606-8501, Japan

* Author for correspondence (e-mail: yanagida{at}kozo.lif.kyoto-u.ac.jp)

Accepted 6 January 2009

Transition from proliferation to quiescence brings about extensive changes in cellular behavior and structure. However, the genes that are crucial for establishing and/or maintaining quiescence are largely unknown. The fission yeast Schizosaccharomyces pombe is an excellent model in which to study this problem, because it becomes quiescent under nitrogen starvation. Here, we characterize 610 temperature-sensitive mutants, and identify 33 genes that are required for entry into and maintenance of quiescence. These genes cover a broad range of cellular functions in the cytoplasm, membrane and nucleus. They encode proteins for stress-responsive and cell-cycle kinase signaling pathways, for actin-bound and osmo-controlling endosome formation, for RNA transcription, splicing and ribosome biogenesis, for chromatin silencing, for biosynthesis of lipids and ATP, for cell-wall and membrane morphogenesis, and for protein trafficking and vesicle fusion. We specifically highlight Fcp1, a CTD phosphatase of RNA polymerase II, which differentially affects the transcription of genes that are involved in quiescence and proliferation. We propose that the transcriptional role of Fcp1 is central in differentiating quiescence from proliferation.

Key words: Cell-cycle control, Protein trafficking, Cortex actin, RNA polymerase II, Protein phosphatase


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