Mori Hiroyuki, Shimokawa Naomi, Satoh Yasunari, Ito Koreaki
Institute for Virus Research, Kyoto University, Sakyo-ku, Kyoto 606-8507, Japan.
J Bacteriol. 2004 Jun;186(12):3960-9. doi: 10.1128/JB.186.12.3960-3969.2004.
The SecYEG heterotrimeric membrane protein complex functions as a channel for protein translocation across the Escherichia coli cytoplasmic membrane. SecY is the central subunit of the SecYEG complex and contains 10 transmembrane segments (TM1 to TM10). Previous mutation studies suggested that TM3 and TM4 are particularly important for SecY function. To further characterize TM3 and TM4, we introduced a series of cysteine-scanning mutations into these segments. With one exception (an unstable product), all the mutant proteins complemented the cold-sensitive growth defect of the secY39 mutant. A combination of this secY mutation and the secG deletion resulted in synthetic lethality, and the TM3 and TM4 SecY cysteine substitution mutations were examined for their ability to complement this lethality. Although they were all positive for complementation, some of the complemented cells exhibited significant retardation of protein export. The substitution-sensitive residues in TM3 can be aligned to one side of the alpha-helix, and those in TM4 revealed a tendency for residues closer to the cytosolic side of the membrane to be more severely affected. Disulfide cross-linking experiments identified a specific contact point for TM3 and SecG TM2 as well as for TM4 and SecG TM1. Thus, although TM3 and TM4 do not contain any single residue that is absolutely required, they include functionally important helix surfaces and specific contact points with SecG. These results are discussed in light of the structural information available for the SecY complex.
SecYEG异源三聚体膜蛋白复合物作为蛋白质跨大肠杆菌细胞质膜转运的通道发挥作用。SecY是SecYEG复合物的中心亚基,包含10个跨膜片段(TM1至TM10)。先前的突变研究表明,TM3和TM4对SecY功能尤为重要。为了进一步表征TM3和TM4,我们在这些片段中引入了一系列半胱氨酸扫描突变。除了一个例外(一个不稳定的产物),所有突变蛋白都弥补了secY39突变体的冷敏感生长缺陷。这种secY突变与secG缺失的组合导致合成致死性,我们检测了TM3和TM4的SecY半胱氨酸替代突变弥补这种致死性的能力。尽管它们在互补方面都是阳性的,但一些互补细胞表现出明显的蛋白质输出延迟。TM3中对替代敏感的残基可以排列在α螺旋的一侧,TM4中的残基显示出靠近膜胞质侧的残基受影响更严重的趋势。二硫键交联实验确定了TM3与SecG TM2以及TM4与SecG TM1的特定接触点。因此,尽管TM3和TM4不包含任何绝对必需的单个残基,但它们包括功能上重要的螺旋表面和与SecG的特定接触点。根据SecY复合物可用的结构信息对这些结果进行了讨论。