Gangula Narmadha Reddy, Maddika Subbareddy
From the Laboratory of Cell Death and Cell Survival, Centre for DNA Fingerprinting and Diagnostics, Nampally, Hyderabad 500001, India.
From the Laboratory of Cell Death and Cell Survival, Centre for DNA Fingerprinting and Diagnostics, Nampally, Hyderabad 500001, India.
J Biol Chem. 2017 Aug 25;292(34):13947-13958. doi: 10.1074/jbc.M117.782896. Epub 2017 Jul 10.
Kinetochores link chromosomes to spindle microtubules and are essential for accurate chromosome segregation during cell division. Kinetochores assemble at the centromeric region of chromosomes as a multiprotein complex. However, the molecular mechanisms of kinetochore assembly have not yet been fully elucidated. In this study, we identified pleckstrin homology domain and leucine-rich repeat protein phosphatase 1 (PHLPP1) as a regulatory phosphatase that facilitates proper kinetochore assembly. We found that PHLPP1 interacted with the essential outer-kinetochore protein SGT1 and stabilized its protein levels. Loss of PHLPP1 from cells led to SGT1 degradation and thereby caused defective kinetochore assembly. We also found that the ring finger protein 41 (RNF41) as an E3 ligase ubiquitinated and degraded SGT1 in a phosphorylation-dependent manner. PHLPP1 dephosphorylated SGT1 at four conserved residues (Ser-17, Ser-249, Ser-289, and Thr-233) and thereby prevented SGT1 from associating with RNF41, in turn, countering SGT1 degradation. Importantly, depletion of RNF41 or expression of a non-phosphorylatable SGT1 mutant rescued the kinetochore defects caused by the loss of PHLPP1. Taken together, our results suggest that PHLPP1 plays an important role in the assembly of kinetochores by counteracting RNF41-mediated SGT1 degradation.
动粒将染色体与纺锤体微管相连,对于细胞分裂过程中染色体的准确分离至关重要。动粒作为一种多蛋白复合体在染色体的着丝粒区域组装。然而,动粒组装的分子机制尚未完全阐明。在本研究中,我们鉴定出普列克底物蛋白同源结构域和富含亮氨酸重复序列蛋白磷酸酶1(PHLPP1)作为一种调节性磷酸酶,它有助于动粒的正确组装。我们发现PHLPP1与外动粒必需蛋白SGT1相互作用,并稳定其蛋白水平。细胞中PHLPP1的缺失导致SGT1降解,从而引起动粒组装缺陷。我们还发现,泛素连接酶指环蛋白41(RNF41)以磷酸化依赖的方式使SGT1泛素化并降解。PHLPP1使SGT1的四个保守残基(Ser-17、Ser-249、Ser-289和Thr-233)去磷酸化,从而阻止SGT1与RNF41结合,进而对抗SGT1的降解。重要的是,RNF41的缺失或不可磷酸化的SGT1突变体的表达挽救了因PHLPP1缺失导致的动粒缺陷。综上所述,我们的结果表明,PHLPP1通过对抗RNF41介导的SGT1降解在动粒组装中发挥重要作用。