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Cyclin E and Cdk1 regulate the termination of germline transit-amplification process in Drosophila testis.
Cell Cycle ( IF 3.4 ) Pub Date : 2020-06-23 , DOI: 10.1080/15384101.2020.1780381
Purna Gadre 1 , Shambhabi Chatterjee 1 , Bhavna Varshney 1 , Krishanu Ray 1
Affiliation  

An extension of the G1 is correlated with stem cell differentiation. The role of cell cycle regulation during the subsequent transit amplification (TA) divisions is, however, unclear. Here, we report for the first time that in the Drosophila male germline lineage, the transit amplification divisions accelerate after the second TA division. The cell cycle phases, marked by Cyclin E and Cyclin B, are progressively altered during the TA. Antagonistic functions of the bag-of-marbles and the Transforming-Growth-Factor-β signaling regulate the cell division rates after the second TA division and the extent of the Cyclin E phase during the fourth TA division. Furthermore, loss of Cyclin E during the fourth TA cycle retards the cell division and induces premature meiosis in some cases. A similar reduction of Cdk1 activity during this stage arrests the penultimate division and subsequent differentiation, whereas enhancement of the Cdk1 activity prolongs the TA by one extra round. Altogether, the results suggest that modification of the cell cycle structure and the rates of cell division after the second TA division determine the extent of amplification. Also, the regulation of the Cyclin E and CDK1 functions during the penultimate TA division determines the induction of meiosis and subsequent differentiation.



中文翻译:

细胞周期蛋白 E 和 Cdk1 调节果蝇睾丸中种系转运扩增过程的终止。

G1 的延伸与干细胞分化相关。然而,细胞周期调节在随后的转运扩增 (TA) 分裂过程中的作用尚不清楚。在这里,我们首次报告在果蝇雄性种系谱系中,在第二次 TA 分裂之后,传输放大分裂加速。以细胞周期蛋白 E 和细胞周期蛋白 B 为标志的细胞周期阶段在 TA 期间逐渐改变。大理石袋的拮抗作用Transforming-Growth-Factor-β 信号调节第二次 TA 分裂后的细胞分裂率和第四次 TA 分裂期间细胞周期蛋白 E 期的程度。此外,在第四个 TA 循环期间细胞周期蛋白 E 的损失会延迟细胞分裂并在某些情况下诱导过早减数分裂。在此阶段,Cdk1 活性的类似降低会阻止倒数第二次分裂和随后的分化,而 Cdk1 活性的增强将 TA 延长一轮。总之,结果表明细胞周期结构的改变和第二次 TA 分裂后细胞分裂的速率决定了扩增的程度。此外,在倒数第二次 TA 分裂期间对细胞周期蛋白 E 和 CDK1 功能的调节决定了减数分裂和随后的分化的诱导。

更新日期:2020-07-08
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