Haynes Cole M, Petrova Kseniya, Benedetti Cristina, Yang Yun, Ron David
Kimmel Center for Biology and Medicine of Skirball Institute and Department of Cell Biology, New York University School of Medicine, New York, NY 10016, USA.
Dev Cell. 2007 Oct;13(4):467-80. doi: 10.1016/j.devcel.2007.07.016.
The cellular response to unfolded and misfolded proteins in the mitochondrial matrix is poorly understood. Here, we report on a genome-wide RNAi-based screen for genes that signal the mitochondrial unfolded protein response (UPR(mt)) in C. elegans. Unfolded protein stress in the mitochondria correlates with complex formation between a homeodomain-containing transcription factor DVE-1 and the small ubiquitin-like protein UBL-5, both of which are encoded by genes required for signaling the UPR(mt). Activation of the UPR(mt) correlates temporally and spatially with nuclear redistribution of DVE-1 and with its enhanced binding to the promoters of mitochondrial chaperone genes. These events and the downstream UPR(mt) are attenuated in animals with reduced activity of clpp-1, which encodes a mitochondrial matrix protease homologous to bacterial ClpP. As ClpP is known to function in the bacterial heat-shock response, our findings suggest that eukaryotes utilize component(s) from the protomitochondrial symbiont to signal the UPR(mt).
线粒体基质中细胞对未折叠和错误折叠蛋白质的反应目前了解甚少。在此,我们报告了一项基于全基因组RNA干扰的筛选,旨在寻找在秀丽隐杆线虫中发出线粒体未折叠蛋白反应(UPR(mt))信号的基因。线粒体中的未折叠蛋白应激与一种含同源结构域的转录因子DVE-1和小泛素样蛋白UBL-5之间的复合物形成相关,这两种蛋白均由发出UPR(mt)信号所需的基因编码。UPR(mt)的激活在时间和空间上与DVE-1的核重新分布及其与线粒体伴侣基因启动子的增强结合相关。在编码与细菌ClpP同源的线粒体基质蛋白酶的clpp-1活性降低的动物中,这些事件以及下游的UPR(mt)会减弱。由于已知ClpP在细菌热休克反应中起作用,我们的研究结果表明,真核生物利用来自原线粒体共生体的成分来发出UPR(mt)信号。