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Aberrant association of chromatin with nuclear periphery induced by Rif1 leads to mitotic defect and cell death

View ORCID ProfileYutaka Kanoh, Seiji Matsumoto, View ORCID ProfileMasaru Ueno, View ORCID ProfileMotoshi Hayano, Satomi Kudo, View ORCID ProfileHisao Masai
doi: https://doi.org/10.1101/2022.05.13.491604
Yutaka Kanoh
1Department of Genome Medicine, Tokyo Metropolitan Institute of Medical Science, Setagaya-ku, Tokyo, Japan;
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Seiji Matsumoto
1Department of Genome Medicine, Tokyo Metropolitan Institute of Medical Science, Setagaya-ku, Tokyo, Japan;
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Masaru Ueno
2Graduate School of Integrated Sciences for Life, Hiroshima University, 1-3-1 Kagamiyama, Higashi-Hiroshima 739-8530, Japan;
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Motoshi Hayano
3Department of Neuropsychiatry, Keio University, 35 Shinano-machi, Shinjuku-ku, Tokyo, Japan
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Satomi Kudo
1Department of Genome Medicine, Tokyo Metropolitan Institute of Medical Science, Setagaya-ku, Tokyo, Japan;
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Hisao Masai
1Department of Genome Medicine, Tokyo Metropolitan Institute of Medical Science, Setagaya-ku, Tokyo, Japan;
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  • For correspondence: masai-hs@igakuken.or.jp
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Abstract

Chromatin is compartmentalized in nuclei and its architecture and nuclear location may have impacts on chromatin events. Rif1, identified as a potent suppressor of hsk1-null mutation (defective in initiation of DNA replication) in fission yeast, recognizes G-quadruplex structures and inhibits origin firing in their 50∼100-kb vicinity, leading us to postulate that Rif1 may generate chromatin higher-order structures inhibitory for initiation. However, effects of Rif1 on chromatin localization in nuclei have not been known. We show here that overexpression of Rif1 causes growth inhibition and eventually cell death in fission yeast. Chromatin binding activities of Rif1, but not recruitment of phosphatase PP1, are required for growth inhibitory effect. Overexpression of a PP1 binding site mutant of Rif1 does not delay S-phase, but still causes cell death, indicating that cell death is caused not by S-phase problems but by issues in other phases of cell cycle, most likely M-phase. Indeed, Rif1 overexpression generates cells with unequally segregated chromosomes. Rif1 overexpression relocates chromatin near nuclear periphery in a manner dependent on its chromatin-binding ability, and this correlates with growth inhibition and cell death induction. Thus, regulated Rif1-mediated chromatin association with nuclear periphery is important for coordinated progression of S- and M-phases.

Competing Interest Statement

The authors have declared no competing interest.

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The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. All rights reserved. No reuse allowed without permission.
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Posted May 13, 2022.
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Aberrant association of chromatin with nuclear periphery induced by Rif1 leads to mitotic defect and cell death
Yutaka Kanoh, Seiji Matsumoto, Masaru Ueno, Motoshi Hayano, Satomi Kudo, Hisao Masai
bioRxiv 2022.05.13.491604; doi: https://doi.org/10.1101/2022.05.13.491604
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Aberrant association of chromatin with nuclear periphery induced by Rif1 leads to mitotic defect and cell death
Yutaka Kanoh, Seiji Matsumoto, Masaru Ueno, Motoshi Hayano, Satomi Kudo, Hisao Masai
bioRxiv 2022.05.13.491604; doi: https://doi.org/10.1101/2022.05.13.491604

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