Interphase-arrested Drosophila embryos activate zygotic gene expression and initiate mid-blastula transition events at a low nuclear-cytoplasmic ratio.

Interphase-arrested Drosophila embryos activate zygotic gene expression and initiate mid-blastula transition events at a low nuclear-cytoplasmic ratio.
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间期停滞的果蝇胚胎激活合子基因表达并在低核质比下启动中囊胚转变事件

DOI:
10.1371/journal.pbio.3000891
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发表时间:
2020-10
期刊:
影响因子:
9.8
通讯作者:
O'Farrell PH
O'Farrell PH
中科院分区:
生物学1区
文献类型:
--
作者:
Strong IJT;Lei X;Chen F;Yuan K;O'Farrell PH

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外部沉积的卵开始发育时具有巨大的细胞质和单个被淹没的细胞核。随着核质比(N/C)的增加,快速有丝分裂周期恢复正常。一个阈值N/C已被广泛提出激活合子基因组转录和启动形态发生在中期囊胚转换(MBT)。为了测试这些事件是否需要阈值N/C,我们通过下调细胞周期蛋白/Cdk 1来阻止果蝇早期细胞周期的N/C增加。在正常MBT之前两个细胞周期被阻止的胚胎激活了合子基因组的广泛转录,包括先前描述为N/C依赖的基因。这些基因的合子转录在很大程度上保留了它们在空间和时间上的调节特征。此外,合子调节后MBT事件,如细胞化和原肠胚运动发生在这些细胞周期停滞的胚胎。这些结果与表明这些MBT事件与N/C直接耦合的模型不一致。Cyclin/Cdk 1活性通常随着N/C的增加而下降,并受N/C的调节。通过实验促进细胞周期蛋白/Cdk 1的减少,我们将MBT与N/C增加分开,认为N/C引导的细胞周期蛋白/Cdk 1的下调足以促进基因组激活和MBT。
Externally deposited eggs begin development with an immense cytoplasm and a single overwhelmed nucleus. Rapid mitotic cycles restore normality as the ratio of nuclei to cytoplasm (N/C) increases. A threshold N/C has been widely proposed to activate zygotic genome transcription and onset of morphogenesis at the mid-blastula transition (MBT). To test whether a threshold N/C is required for these events, we blocked N/C increase by down-regulating cyclin/Cdk1 to arrest early cell cycles in Drosophila. Embryos that were arrested two cell cycles prior to the normal MBT activated widespread transcription of the zygotic genome including genes previously described as N/C dependent. Zygotic transcription of these genes largely retained features of their regulation in space and time. Furthermore, zygotically regulated post-MBT events such as cellularization and gastrulation movements occurred in these cell cycle–arrested embryos. These results are not compatible with models suggesting that these MBT events are directly coupled to N/C. Cyclin/Cdk1 activity normally declines in tight association with increasing N/C and is regulated by N/C. By experimentally promoting the decrease in cyclin/Cdk1, we uncoupled MBT from N/C increase, arguing that N/C-guided down-regulation of cyclin/Cdk1 is sufficient for genome activation and MBT.
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发表时间: 1986-03-28
期刊: CELL
影响因子: 64.5
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发表时间: 2013-01-21
期刊: CURRENT BIOLOGY
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期刊: CELL
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