Yamazaki Katsuhisa, Aso Teijiro, Ohnishi Yoshinori, Ohno Mizuki, Tamura Kenji, Shuin Taro, Kitajima Shigetaka, Nakabeppu Yusaku
Medical Institute of Bioregulation, Kyushu University, and CREST, Japan Science and Technology Corporation, 3-1-1, Maidashi, Higashi-ku, Fukuoka 812-8582, Japan.
J Biol Chem. 2003 Apr 11;278(15):13585-9. doi: 10.1074/jbc.C300047200. Epub 2003 Feb 25.
Elongin A is a transcription elongation factor that increases the overall rate of mRNA chain elongation by RNA polymerase II. To investigate the function of Elongin A in vivo, the two alleles of the Elongin A gene have been disrupted by homologous recombination in murine embryonic stem (ES) cells. The Elongin A-deficient ES cells are viable, but show a slow growth phenotype because they undergo a delayed mitosis. The cDNA microarray and RNase protection assay using the wild-type and Elongin A-deficient ES cells indicate that the expression of only a small subset of genes is affected in the mutant cells. Taken together, our results suggest that Elongin A regulates transcription of a subset but not all of genes and reveal a linkage between Elongin A function and cell cycle progression.
延伸蛋白A是一种转录延伸因子，它可提高RNA聚合酶II介导的mRNA链延伸的总体速率。为了研究延伸蛋白A在体内的功能，延伸蛋白A基因的两个等位基因已通过同源重组在小鼠胚胎干细胞（ES细胞）中被破坏。缺乏延伸蛋白A的ES细胞是有活力的，但表现出生长缓慢的表型，因为它们经历了有丝分裂延迟。使用野生型和缺乏延伸蛋白A的ES细胞进行的cDNA微阵列和核糖核酸酶保护分析表明，突变细胞中只有一小部分基因的表达受到影响。综上所述，我们的结果表明，延伸蛋白A调节一部分而非全部基因的转录，并揭示了延伸蛋白A功能与细胞周期进程之间的联系。
