Function and regulation of transcription factors during mitosis-to-G1 transition.
Function and regulation of transcription factors during mitosis-to-G1 transition.
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在细胞分裂期间，有丝分裂特征性的剧烈细胞变化导致转录机制的失活和转录的整体下调。因此，序列特异性转录因子（TF）被认为仅仅是旁观者，在有丝分裂过程中没有任何调节功能。近年来，这种观点发生了重大变化，因为许多TF在细胞分裂期间与浓缩的染色体相关联，甚至占据了有丝分裂染色质中的一小部分基因组靶位点。这一发现是TF有丝分裂书签概念的起源，提出了一种通过促进特定书签基因的重新激活来跨细胞分裂传播基因调控信息的机制。虽然这种模型的潜在机制和生物学意义仍然难以捉摸，但这个快速发展的领域的最新进展为有丝分裂期间的TF活性带来了新的曙光，超越了书签的作用。在这里，我们首先回顾了最近的研究结果的复杂性质的TF-染色质相互作用在有丝分裂过程中，和机制，可能会调节它们。接下来，根据最近的报道，描述了转录是如何重新启动在时间上不同的波在有丝分裂到G1过渡，我们探讨如何TF可能有助于定义这个层次的基因表达过程。最后，我们讨论了如何TF活动在有丝分裂退出可能会影响收购的细胞身份后，细胞分裂，并提出了一个模型，集成在TF-染色质相互作用的动态变化，在此细胞周期期间，与执行细胞命运的决定。
During cell division, drastic cellular changes characteristic of mitosis result in the inactivation of the transcriptional machinery, and global downregulation of transcription. Sequence-specific transcription factors (TFs) have thus been considered mere bystanders, devoid of any regulatory function during mitosis. This view changed significantly in recent years, upon the conclusion that many TFs associate with condensed chromosomes during cell division, even occupying a fraction of their genomic target sites in mitotic chromatin. This finding was at the origin of the concept of mitotic bookmarking by TFs, proposed as a mechanism to propagate gene regulatory information across cell divisions, by facilitating the reactivation of specific bookmarked genes. While the underlying mechanisms and biological significance of this model remain elusive, recent developments in this fast-moving field have cast new light into TF activity during mitosis, beyond a bookmarking role. Here, we start by reviewing the most recent findings on the complex nature of TF–chromatin interactions during mitosis, and on mechanisms that may regulate them. Next, and in light of recent reports describing how transcription is reinitiated in temporally distinct waves during mitosis-to-G1 transition, we explore how TFs may contribute to defining this hierarchical gene expression process. Finally, we discuss how TF activity during mitotic exit may impact the acquisition of cell identity upon cell division, and propose a model that integrates dynamic changes in TF–chromatin interactions during this cell-cycle period, with the execution of cell-fate decisions.
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