通过RNA干扰鉴定调控细胞大小和细胞周期进程的信号通路
Identification of pathways regulating cell size and cell-cycle progression by RNAi.
作者信息
Björklund Mikael, Taipale Minna, Varjosalo Markku, Saharinen Juha, Lahdenperä Juhani, Taipale Jussi
机构信息
Molecular and Cancer Biology Program, Biomedicum Helsinki, PO Box 63 (Haartmaninkatu 8), FI-00014 University of Helsinki, Finland.
出版信息
Nature. 2006 Feb 23;439(7079):1009-13. doi: 10.1038/nature04469.
Many high-throughput loss-of-function analyses of the eukaryotic cell cycle have relied on the unicellular yeast species Saccharomyces cerevisiae and Schizosaccharomyces pombe. In multicellular organisms, however, additional control mechanisms regulate the cell cycle to specify the size of the organism and its constituent organs. To identify such genes, here we analysed the effect of the loss of function of 70% of Drosophila genes (including 90% of genes conserved in human) on cell-cycle progression of S2 cells using flow cytometry. To address redundancy, we also targeted genes involved in protein phosphorylation simultaneously with their homologues. We identify genes that control cell size, cytokinesis, cell death and/or apoptosis, and the G1 and G2/M phases of the cell cycle. Classification of the genes into pathways by unsupervised hierarchical clustering on the basis of these phenotypes shows that, in addition to classical regulatory mechanisms such as Myc/Max, Cyclin/Cdk and E2F, cell-cycle progression in S2 cells is controlled by vesicular and nuclear transport proteins, COP9 signalosome activity and four extracellular-signal-regulated pathways (Wnt, p38betaMAPK, FRAP/TOR and JAK/STAT). In addition, by simultaneously analysing several phenotypes, we identify a translational regulator, eIF-3p66, that specifically affects the Cyclin/Cdk pathway activity.
许多针对真核细胞周期的高通量功能丧失分析都依赖于单细胞酵母物种酿酒酵母和裂殖酵母。然而,在多细胞生物中,还有其他控制机制来调节细胞周期,以确定生物体及其组成器官的大小。为了鉴定此类基因,我们在此使用流式细胞术分析了果蝇70%的基因(包括90%在人类中保守的基因)功能丧失对S2细胞周期进程的影响。为了解决冗余问题,我们还同时靶向了参与蛋白质磷酸化的基因及其同源物。我们鉴定出了控制细胞大小、胞质分裂、细胞死亡和/或凋亡以及细胞周期的G1期和G2/M期的基因。基于这些表型通过无监督层次聚类将基因分类到不同途径中,结果表明,除了诸如Myc/Max、细胞周期蛋白/细胞周期蛋白依赖性激酶(Cyclin/Cdk)和E2F等经典调控机制外,S2细胞中的细胞周期进程还受囊泡和核转运蛋白、COP9信号体活性以及四条细胞外信号调节途径(Wnt、p38β丝裂原活化蛋白激酶(p38betaMAPK)、FKBP12-雷帕霉素相关蛋白/雷帕霉素靶蛋白(FRAP/TOR)和Janus激酶/信号转导子和转录激活子(JAK/STAT))的控制。此外,通过同时分析多种表型,我们鉴定出一种翻译调节因子,即真核起始因子3 p66(eIF-3p66),它特异性地影响细胞周期蛋白/细胞周期蛋白依赖性激酶途径的活性。