The transcription factor Atf1 is known to promote cell survival during various stress conditions in Schizosaccharomyces pombe by activating the expression of appropriate genes. It can also activate transcription of other important genes responsible for cell cycle progression. An Atf1-dependent increase in the expression of cell division promoting genes will oppose activation of checkpoints necessary to ensure repairs and cell survival during stress. Hence, selective inhibition of the cell cycle-related functions of Atf1 would be indispensable for cellular survival during stress. Here we present evidence in favour of selective inhibition of Atf1's ability to activate cdc13+ transcription. We show that the transcription factor Pcr1 can specifically inhibit the recruitment of Atf1 on cdc13 promoter and thereby prevent Atf1-mediated mitotic acceleration. We also show that this opposition of Atf1 functions by Pcr1 extends to the G1-S transition event as well. Altogether these results suggest a previously unknown antagonistic function of Atf1 and Pcr1 in regulating Cdc13 expression during cell cycle progression.

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.

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