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Induction of string rescues the neuroblast proliferation defect in trol mutant animals.

作者信息

Park Youngji, Ng Cristina, Datta Sumana

机构信息

Department of Biochemistry and Biophysics, Texas A&M University, College Station, Texas 77843, USA.

出版信息

Genesis. 2003 Aug;36(4):187-95. doi: 10.1002/gene.10216.

DOI:10.1002/gene.10216
PMID:12929089
Abstract

In trol mutants, neuroblasts fail to exit G1 for S phase. Increasing string expression in trol mutants rescues the number of S phase neuroblasts without an increase in M phase neuroblasts. Decreasing string expression further decreased the number of S phase neuroblasts. Coexpression of cyclin E and string did not produce additional S phase cells. Unlike cyclin E, cdk2, and cdk2AF, elevated expression of neither cyclin A, cyclin D, nor cdk1AF was able to promote S phase progression in arrested neuroblasts, indicating that String-induced activity of a Cyclin A or Cyclin D complex is unlikely to drive trol neuroblasts into S phase. Biochemical analyses revealed a rapid increase of Cyclin E-Cdk2 kinase activity to wild-type levels upon increased string expression. These results suggest that Drosophila Cdc25 may directly or indirectly increase the kinase activity of Cyclin E-Cdk2 complexes in vivo, thus driving arrested neuroblasts into cell division.

摘要

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Mutations in String/CDC25 inhibit cell cycle re-entry and neurodegeneration in a Drosophila model of Ataxia telangiectasia.在共济失调毛细血管扩张症的果蝇模型中,String/CDC25的突变会抑制细胞周期重新进入和神经退行性变。
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