Dubey Rudra Narayan, Nakwal Nandni, Bisht Kamlesh Kumar, Saini Ashok, Haldar Swati, Singh Jagmohan
Institute of Microbial Technology, Sector 39A, Chandigarh-160036, India.
J Biol Chem. 2009 Mar 13;284(11):7165-76. doi: 10.1074/jbc.M806461200. Epub 2008 Dec 30.
Heterochromatin assembly in fission yeast is initiated by binding of Swi6/HP1 to the Lys-9-dimethylated H3 followed by spreading via cooperative recruitment of Swi6/HP1. Recruitment of Cohesin by Swi6/HP1 further stabilizes the heterochromatin structure and integrity. Subsequently, polyubiquitylation of Cut2 by anaphase-promoting complex-cyclosome (APC/C)-ubiquitin-protein isopeptide ligase (E3 ligase) followed by degradation of Cut2 releases Cut1, which cleaves the Rad21 subunit of Cohesin, facilitating sister chromatid separation during mitosis. Here, we demonstrate a surprising role of APC/C in assembly of heterochromatin and silencing at mating type, centromere, and ribosomal DNA loci. Coincidentally with the loss of silencing, recruitment of Swi6, H3-Lys-9-Me2, and Clr4 at dg-dh repeats at cen1 and the K region of mat locus is abrogated in mutants cut4, cut9, and nuc2. Surprisingly, both Cut4 and Cut9 are also highly enriched at these regions in wild type and depleted in swi6Delta mutant. Cut4 and Cut9 interact directly with Swi6/HP1 and Clr4, whereas the mutant Cut4 does not, suggesting that a direct physical interaction of APC subunits Cut4 and Cut9 with Swi6 and Clr4 is instrumental in heterochromatin assembly. The silencing defect in APC mutants is causally related to ubiquitylation activity of APC-E3 ligase. Like swi6 mutant, APC mutants are also defective in Cohesin recruitment and exhibit defects like lagging chromosomes, chromosome loss, and aberrant recombination in the mat region. In addition, APC mutants exhibit a bidirectional expression of dh repeats, suggesting a role in the RNA interference pathway. Thus, APC and heterochromatin proteins Swi6 and Clr4 play a mutually cooperative role in heterochromatin assembly, thereby ensuring chromosomal integrity, inheritance, and segregation during mitosis and meiosis.
裂殖酵母中的异染色质组装是由Swi6/HP1与赖氨酸-9-二甲基化的H3结合启动的,随后通过Swi6/HP1的协同募集进行扩展。Swi6/HP1对黏连蛋白的募集进一步稳定了异染色质结构和完整性。随后,后期促进复合物-细胞周期体(APC/C)-泛素-蛋白质异肽连接酶(E3连接酶)对Cut2进行多聚泛素化,随后Cut2降解释放出Cut1,Cut1切割黏连蛋白的Rad21亚基,促进有丝分裂期间姐妹染色单体的分离。在此,我们证明了APC/C在异染色质组装以及在交配型、着丝粒和核糖体DNA位点的沉默中具有惊人的作用。与沉默丧失同时发生的是,在cut4、cut9和nuc2突变体中,cen1的dg-dh重复序列以及mat位点的K区域处Swi6、H3-赖氨酸-9-二甲基化(H3-Lys-9-Me2)和Clr4的募集被消除。令人惊讶的是,Cut4和Cut9在野生型中也在这些区域高度富集,而在swi6Delta突变体中则减少。Cut4和Cut9直接与Swi6/HP1和Clr4相互作用,而突变型Cut4则不然,这表明APC亚基Cut4和Cut9与Swi6和Clr4的直接物理相互作用在异染色质组装中起作用。APC突变体中的沉默缺陷与APC-E3连接酶的泛素化活性因果相关。与swi6突变体一样,APC突变体在黏连蛋白募集方面也存在缺陷,并表现出如滞后染色体、染色体丢失以及mat区域异常重组等缺陷。此外,APC突变体表现出dh重复序列的双向表达,表明其在RNA干扰途径中发挥作用。因此,APC与异染色质蛋白Swi6和Clr4在异染色质组装中发挥相互协作的作用,从而确保有丝分裂和减数分裂期间的染色体完整性、遗传和分离。