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果蝇细胞周期蛋白依赖性激酶2同源物的遗传分析。

Genetic analysis of the Drosophila cdc2 homolog.

作者信息

Stern B, Ried G, Clegg N J, Grigliatti T A, Lehner C F

机构信息

Friedrich-Miescher-Laboratorium der Max-Planck-Gesellschaft, Tübingen, FRG.

出版信息

Development. 1993 Jan;117(1):219-32. doi: 10.1242/dev.117.1.219.

DOI:10.1242/dev.117.1.219
PMID:8223248
Abstract

We have identified mutations in the Drosophila cdc2 gene. The recessive lethality of these mutant alleles was rescued after P-element-mediated transformation with a genomic cdc2 fragment. Sequence analysis of amorphic alleles revealed non-conservative exchanges in evolutionary conserved positions. These alleles caused lethality at the larval-pupal interphase due to the absence of imaginal tissues. Embryonic lethality resulted when the maternal Dm cdc2 contribution was reduced through the use of a temperature-sensitive allele. Dm cdc2 function, therefore, is essential for cell proliferation throughout development. Dm cdc2 function is clearly required for mitosis, but no evidence for a requirement in S-phase was obtained. The reversible block of the mitotic proliferation which was observed in the PNS of mutant embryos occurred exclusively in the G2-phase. Moreover, while the mitotic proliferation of imaginal cells was blocked in the amorphic mutant larvae, non-imaginal larval cells continued to grow and endoreplicate their DNA. The Dm cdc2 mutant phenotype could neither be rescued with Dm cdc2c (encoding a cdc2-like kinase) nor enhanced by a reduction of the Dm cdc2c gene dose. These results indicate that the Dm cdc2- and Dm cdc2c-kinases control different processes.

摘要

我们已经在果蝇的cdc2基因中鉴定出了突变。在用基因组cdc2片段进行P因子介导的转化后,这些突变等位基因的隐性致死性得到了挽救。对无义等位基因的序列分析揭示了进化保守位置上的非保守交换。由于缺乏成虫盘组织,这些等位基因在幼虫-蛹间期导致致死。当通过使用温度敏感等位基因降低母体Dm cdc2的贡献时,胚胎出现致死。因此,Dm cdc2功能对于整个发育过程中的细胞增殖至关重要。Dm cdc2功能显然是有丝分裂所必需的,但未获得其在S期发挥作用的证据。在突变胚胎的外周神经系统中观察到的有丝分裂增殖的可逆阻滞仅发生在G2期。此外,虽然无义突变幼虫中的成虫细胞的有丝分裂增殖被阻断,但非成虫幼虫细胞继续生长并进行DNA的核内复制。Dm cdc2突变表型既不能用Dm cdc2c(编码一种cdc2样激酶)挽救,也不会因Dm cdc2c基因剂量的减少而增强。这些结果表明,Dm cdc2激酶和Dm cdc2c激酶控制不同的过程。

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