| Item type |
デフォルトアイテムタイプ_（フル）(1) |
| 公開日 |
2023-03-18 |
| タイトル |
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|
タイトル |
Casein kinase 1γ acts as a molecular switch for cell polarization through phosphorylation of the polarity factor Tea1 in fission yeast |
|
言語 |
en |
| 作成者 |
Koyano, Takayuki
Barnouin, Karin
Snijders, Ambrosius P.
Kume, Kazunori
Hirata, Dai
Toda, Takashi
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| アクセス権 |
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アクセス権 |
open access |
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アクセス権URI |
http://purl.org/coar/access_right/c_abf2 |
| 権利情報 |
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権利情報 |
© 2015 The Authors. Genes to Cells published by Molecular Biology Society of Japan and Wiley Publishing Asia Pty Ltd. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
| 内容記述 |
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内容記述 |
Fission yeast undergoes growth polarity transition from monopolar to bipolar during G2 phase, designated NETO (New End Take Off). It is known that NETO onset involves two prerequisites, the completion of DNA replication and attainment of a certain cell size. However, the molecular mechanism remains unexplored. Here, we show that casein kinase 1γ, Cki3 is a critical determinant of NETO onset. Not only did cki3∆ cells undergo NETO during G1‐ or S‐phase, but they also displayed premature NETO under unperturbed conditions with a smaller cell size, leading to cell integrity defects. Cki3 interacted with the polarity factor Tea1, of which phosphorylation was dependent on Cki3 kinase activity. GFP nanotrap of Tea1 by Cki3 led to Tea1 hyperphosphorylation with monopolar growth, whereas the same entrapment by kinase‐dead Cki3 resulted in converse bipolar growth. Intriguingly, the Tea1 interactor Tea4 was dissociated from Tea1 by Cki3 entrapment. Mass spectrometry identified four phosphoserine residues within Tea1 that were hypophosphorylated in cki3∆ cells. Phosphomimetic Tea1 mutants showed compromised binding to Tea4 and NETO defects, indicating that these serine residues are critical for protein–protein interaction and NETO onset. Our findings provide significant insight into the mechanism by which cell polarization is regulated in a spatiotemporal manner. |
|
言語 |
en |
| 内容記述 |
|
|
内容記述タイプ |
Other |
|
内容記述 |
T.K. was the recipient of a JSPS fellowship (PD) and was partly supported by ‘Strategic Young Researcher Overseas Visits Program for Accelerating Brain Circulation’ from JSPS. This work was supported by Cancer Research UK (T.T. and A.P.S) and the Ministry of Education, Culture, Sports, Science and Technology (D.H.). |
| 出版者 |
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出版者 |
Wiley |
| 言語 |
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|
言語 |
eng |
| 資源タイプ |
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資源タイプ識別子 |
http://purl.org/coar/resource_type/c_6501 |
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資源タイプ |
journal article |
| 出版タイプ |
|
|
出版タイプ |
VoR |
|
出版タイプResource |
http://purl.org/coar/version/c_970fb48d4fbd8a85 |
| 関連情報 |
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識別子タイプ |
DOI |
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関連識別子 |
10.1111/gtc.12309 |
| 関連情報 |
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識別子タイプ |
PMID |
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関連識別子 |
26525038 |
| 関連情報 |
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|
識別子タイプ |
DOI |
|
|
関連識別子 |
https://doi.org/10.1111/gtc.12309 |
| 収録物識別子 |
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|
収録物識別子タイプ |
ISSN |
|
収録物識別子 |
1356-9597 |
| 収録物識別子 |
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収録物識別子タイプ |
ISSN |
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収録物識別子 |
1365-2443 |
| 開始ページ |
|
|
開始ページ |
1046 |
| 書誌情報 |
Genes to Cells
Genes to Cells
巻 20,
号 12,
p. 1046-1058,
発行日 2015-12-07
|
| 旧ID |
48969 |
GenesCells_20_1046.pdf (2.4 MB)
