Bandyopadhyay Sushobhana, Ghosh Protiti Maiti, Basu Sohini, Paul Madhurima, Alam Syed Benazir, Das Elizabeth, Sundaram Geetanjali
Department of Biochemistry and Centre for Research in Nanoscience and Nanotechnology, University of Calcutta, 35, Ballygunge Circular Road, Kolkata-700019, West Bengal, India.
FEMS Microbiol Lett. 2017 Aug 1;364(14). doi: 10.1093/femsle/fnx132.
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.
已知转录因子Atf1通过激活适当基因的表达，在粟酒裂殖酵母的各种应激条件下促进细胞存活。它还可以激活负责细胞周期进程的其他重要基因的转录。Atf1依赖性的细胞分裂促进基因表达增加，将对抗在应激期间确保修复和细胞存活所必需的检查点的激活。因此，选择性抑制Atf1与细胞周期相关的功能对于应激期间的细胞存活将是不可或缺的。在此，我们提供证据支持选择性抑制Atf1激活cdc13+转录的能力。我们表明，转录因子Pcr1可以特异性抑制Atf1在cdc13启动子上的募集，从而防止Atf1介导的有丝分裂加速。我们还表明，Pcr1对Atf1功能的这种拮抗作用也延伸到G1-S转换事件。总之，这些结果表明Atf1和Pcr1在细胞周期进程中调节Cdc13表达方面存在以前未知的拮抗功能。
