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Transcription factor Atf1‐dependent degradation of the mitotic cyclin Cdc13 is regulated by multiple factors in Schizosaccharomyces pombe
The bZIP transcription factor Atf1 is a key player in the transcriptional programme of Schizosaccharomyces pombe cell cycle. It also controls both expression and degradation of mitotic cyclin Cdc13. Temporal regulation of these opposing functions of Atf1 is critical for fidelity of cell division. Ou...
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Published in: | FEBS letters 2022-08, Vol.596 (16), p.2021-2030 |
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Main Authors: | , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | The bZIP transcription factor Atf1 is a key player in the transcriptional programme of Schizosaccharomyces pombe cell cycle. It also controls both expression and degradation of mitotic cyclin Cdc13. Temporal regulation of these opposing functions of Atf1 is critical for fidelity of cell division. Our investigations revealed that an increase in the activity of mitogen‐activated protein kinase (MAPK) Spc1 during mitotic exit and the consequent phosphorylation of Atf1 along with the prevailing high activity of cyclin‐dependent kinase Cdc2 regulate Cdc13 degradation. Our results also indicate the possibility of a complex interplay between Cdc2 inhibitory kinase Wee1, the anaphase‐promoting complex and Atf1 during mitotic exit. These observations provide evidence of new regulatory mechanisms of mitotic exit.
This study reports that enhanced Spc1 mitogen‐activated protein kinase activity leading to phosphorylation of the bZIP transcription factor Atf1 is associated with degradation of the mitotic cyclin Cdc13 by the anaphase‐promoting complex (APC) during metaphase to anaphase transition in Schizosaccharomyces pombe. This event is also dependent on the activity of the cyclin‐dependent kinase Cdc2 (Cdk1). Complex regulatory communication between Atf1, Wee1 (Cdc2 inhibitor) and APC also influences this phenomenon. |
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ISSN: | 0014-5793 1873-3468 |
DOI: | 10.1002/1873-3468.14439 |