Iwasa Shingo, Sato Naoko, Wang Chao-Wen, Cheng Yun-Hsin, Irokawa Hayato, Hwang Gi-Wook, Naganuma Akira, Kuge Shusuke
Department of Microbiology, Faculty of Pharmaceutical Sciences, Tohoku Medical and Pharmaceutical University, Sendai, Miyagi, 981-8558, Japan.
Laboratory of Molecular and Biochemical Toxicology, Graduate School of Pharmaceutical Sciences, Tohoku University, Sendai, Miyagi, 980-8578, Japan.
PLoS One. 2016 Jul 26;11(7):e0159324. doi: 10.1371/journal.pone.0159324. eCollection 2016.
Chronic infection with the hepatitis C virus frequently induces steatosis, which is a significant risk factor for liver pathogenesis. Steatosis is characterized by the accumulation of lipid droplets in hepatocytes. The structural protein core of the virus induces lipid droplet formation and localizes on the surface of the lipid droplets. However, the precise molecular mechanisms for the core-induced formation of lipid droplets remain elusive. Recently, we showed that the expression of the core protein in yeast as a model system could induce lipid droplet formation. In this study, we probed the cellular factors responsible for the formation of core-induced lipid-droplets in yeast cells. We demonstrated that one of the enzymes responsible for triglyceride synthesis, a phospholipid:diacylglycerol acyltransferase (Lro1), is required for the core-induced lipid droplet formation. While core proteins inhibit Lro1 degradation and alter Lro1 localization, the characteristic localization of Lro1 adjacent to the lipid droplets appeared to be responsible for the core-induced lipid droplet formation. RNA virus genomes have evolved using high mutation rates to maintain their ability to replicate. Our observations suggest a functional relationship between the core protein with hepatocytes and yeast cells. The possible interactions between core proteins and the endoplasmic reticulum membrane affect the mobilization of specific proteins.
丙型肝炎病毒的慢性感染常常会诱发脂肪变性,而脂肪变性是肝脏发病的一个重要风险因素。脂肪变性的特征是肝细胞内脂质小滴的积累。该病毒的结构蛋白核心可诱导脂质小滴的形成,并定位于脂质小滴的表面。然而,核心蛋白诱导脂质小滴形成的确切分子机制仍不清楚。最近,我们发现,在作为模型系统的酵母中表达核心蛋白可诱导脂质小滴的形成。在本研究中,我们探究了酵母细胞中负责核心蛋白诱导脂质小滴形成的细胞因子。我们证明,甘油三酯合成所必需的一种酶,即磷脂:二酰甘油酰基转移酶(Lro1),是核心蛋白诱导脂质小滴形成所必需的。虽然核心蛋白可抑制Lro1的降解并改变Lro1的定位,但Lro1在脂质小滴附近的特征性定位似乎是核心蛋白诱导脂质小滴形成的原因。RNA病毒基因组通过高突变率进化,以维持其复制能力。我们的观察结果表明,核心蛋白在肝细胞和酵母细胞之间存在功能关系。核心蛋白与内质网膜之间可能的相互作用会影响特定蛋白质的动员。