Garbe David, Doto Jeffrey B, Sundaram Meera V
Department of Genetics, University of Pennsylvania, Philadelphia, Pennsylvania 19104-6100, USA.
Genetics. 2004 Jun;167(2):663-72. doi: 10.1534/genetics.103.026021.
Retinoblastoma (Rb)/E2F complexes repress expression of many genes important for G(1)-to-S transition, but also appear to regulate gene expression at other stages of the cell cycle. In C. elegans, lin-35/Rb and other synthetic Multivulva (SynMuv) group B genes function redundantly with other sets of genes to regulate G(1)/S progression, vulval and pharyngeal differentiation, and other unknown processes required for viability. Here we show that lin-35/Rb, efl-1/E2F, and other SynMuv B genes negatively regulate a component of the anaphase-promoting complex or cyclosome (APC/C). The APC/C is a multisubunit complex that promotes metaphase-to-anaphase progression and G(1) arrest by targeting different substrates for ubiquitination and proteasome-mediated destruction. The C. elegans APC/C gene mat-3/APC8 has been defined by temperature-sensitive embryonic lethal alleles that strongly affect germline meiosis and mitosis but only weakly affect somatic development. We describe severe nonconditional mat-3 alleles and a hypomorphic viable allele (ku233), all of which affect postembryonic cell divisions including those of the vulval lineage. The ku233 lesion is located outside of the mat-3 coding region and reduces mat-3 mRNA expression. Loss-of-function alleles of lin-35/Rb and other SynMuv B genes suppress mat-3(ku233) defects by restoring mat-3 mRNA to wild-type levels. Therefore, Rb/E2F complexes appear to repress mat-3 expression.
视网膜母细胞瘤(Rb)/E2F复合物可抑制许多对G1期到S期转换至关重要的基因的表达,但似乎也在细胞周期的其他阶段调节基因表达。在秀丽隐杆线虫中,lin-35/Rb和其他合成多外阴(SynMuv)B组基因与其他基因集发挥冗余功能,以调节G1/S进程、外阴和咽部分化以及生存所需的其他未知过程。我们在此表明,lin-35/Rb、efl-1/E2F和其他SynMuv B基因对后期促进复合物或细胞周期体(APC/C)的一个组分起负向调节作用。APC/C是一种多亚基复合物,通过靶向不同底物进行泛素化和蛋白酶体介导的破坏来促进中期到后期的进程以及G1期停滞。秀丽隐杆线虫的APC/C基因mat-3/APC8已由温度敏感型胚胎致死等位基因定义,这些等位基因强烈影响生殖系减数分裂和有丝分裂,但对体细胞发育影响较弱。我们描述了严重的非条件性mat-3等位基因和一个功能减退的存活等位基因(ku233),所有这些都影响胚胎后细胞分裂,包括外阴谱系的细胞分裂。ku233损伤位于mat-3编码区之外,并降低mat-3 mRNA表达。lin-35/Rb和其他SynMuv B基因的功能丧失等位基因通过将mat-3 mRNA恢复到野生型水平来抑制mat-3(ku233)缺陷。因此,Rb/E2F复合物似乎抑制mat-3表达。