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Regulation of Multiple Fission and Cell-Cycle-Dependent Gene Expression by CDKA1 and the Rb-E2F Pathway in Chlamydomonas.
Current Biology ( IF 9.2 ) Pub Date : 2020-04-02 , DOI: 10.1016/j.cub.2020.03.019
Frederick R Cross 1
Affiliation  

The green alga Chlamydomonas proliferates by "multiple fission": a long G1 with >10-fold cell growth followed by multiple rapid divisions. Cells above a critical size threshold are "committed" and will divide independent of light and further cell growth. The number of divisions carried out depends on the initial size of the committed mother cell. Here, I show that CDKA1, the ortholog of the yeast and animal mitotic inducer CDK1, regulates the critical size for commitment. The Rb/E2F/Dp1 pathway regulates division number as well as commitment size. Epistasis analysis indicated that CDKA1 and Rb/E2F/Dp1 regulate multiple fission by distinct mechanisms. Rb-E2F/Dp1 regulates G1/S gene expression in animals and land plants. Transcriptome analysis showed that mat3 or dp1 disruption altered regulation of a large group of cell-division-associated genes with respect to cell size, but not with respect to synchronization timing. In contrast, cdka1 inactivation disturbed both temporal and cell-size regulation of expression. These defects were enhanced by double inactivation of cdka1 and dp1, suggesting interaction between CDKA1 and the Rb-E2F/Dp1 pathways in regulating cell-cycle-specific gene expression and cell-cycle initiation. In the context of a theoretical model for regulation of Chlamydomonas multiple fission, these results suggest that CDKA1 may promote a switch into a division-competent state, and E2F/Dp1 may promote maintenance of this state.

中文翻译:

衣藻中 CDKA1 和 Rb-E2F 通路对多重裂变和细胞周期依赖性基因表达的调节。

绿藻衣藻通过“多次裂变”增殖:一个长 G1,细胞生长超过 10 倍,然后多次快速分裂。超过临界尺寸阈值的细胞被“提交”并且将独立于光和进一步的细胞生长而分裂。进行的分裂次数取决于提交母细胞的初始大小。在这里,我展示了 CDKA1,酵母和动物有丝分裂诱导剂 CDK1 的直向同源物,调节了承诺的临界大小。Rb/E2F/Dp1 通路调节分裂数量和承诺大小。上位性分析表明 CDKA1 和 Rb/E2F/Dp1 通过不同的机制调节多重裂变。Rb-E2F/Dp1 调节动物和陆地植物的 G1/S 基因表达。转录组分析表明,mat3 或 dp1 中断改变了一大群细胞分裂相关基因在细胞大小方面的调节,但在同步时间方面没有改变。相比之下,cdka1 失活扰乱了表达的时间和细胞大小调节。这些缺陷因 cdka1 和 dp1 的双重失活而增强,表明 CDKA1 和 Rb-E2F/Dp1 通路在调节细胞周期特异性基因表达和细胞周期起始方面存在相互作用。在调节衣藻多次裂变的理论模型的背景下,这些结果表明 CDKA1 可能促进转变为可分裂状态,而 E2F/Dp1 可能促进这种状态的维持。cdka1 失活扰乱了表达的时间和细胞大小调节。这些缺陷因 cdka1 和 dp1 的双重失活而增强,表明 CDKA1 和 Rb-E2F/Dp1 通路在调节细胞周期特异性基因表达和细胞周期起始方面存在相互作用。在调节衣藻多次裂变的理论模型的背景下,这些结果表明 CDKA1 可能促进转变为可分裂状态,而 E2F/Dp1 可能促进这种状态的维持。cdka1 失活扰乱了表达的时间和细胞大小调节。这些缺陷因 cdka1 和 dp1 的双重失活而增强,表明 CDKA1 和 Rb-E2F/Dp1 通路在调节细胞周期特异性基因表达和细胞周期起始方面存在相互作用。在调节衣藻多次裂变的理论模型的背景下,这些结果表明 CDKA1 可能促进转变为可分裂状态,而 E2F/Dp1 可能促进这种状态的维持。
更新日期:2020-04-02
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