Frome the Department of Cell Biology, Nanobiology Institute, Yale School of Medicine, Yale West Campus, West Haven, Connecticut, USA.
Frome the Department of Cell Biology, Nanobiology Institute, Yale School of Medicine, Yale West Campus, West Haven, Connecticut, USA.
J Biol Chem. 2020 Nov 13;295(46):15498-15510. doi: 10.1074/jbc.RA120.012992. Epub 2020 Sep 2.
A large number of newly synthesized membrane proteins in the endoplasmic reticulum (ER) are assembled into multiprotein complexes, but little is known about the mechanisms required for assembly membrane proteins. It has been suggested that membrane chaperones might exist, akin to the molecular chaperones that stabilize and direct the assembly of soluble protein complexes, but the mechanisms by which these proteins would bring together membrane protein components is unclear. Here, we have identified that the tail length of the C-terminal transmembrane domains (C-TMDs) determines efficient insertion and assembly of membrane proteins in the ER. We found that membrane proteins with C-TMD tails shorter than ∼60 amino acids are poorly inserted into the ER membrane, which suggests that translation is terminated before they are recognized by the Sec61 translocon for insertion. These C-TMDs with insufficient hydrophobicity are post-translationally recognized and retained by the Sec61 translocon complex, providing a time window for efficient assembly with TMDs from partner proteins. Retained TMDs that fail to assemble with their cognate TMDs are slowly translocated into the ER lumen and are recognized by the ER-associated degradation (ERAD) pathway for removal. In contrast, C-TMDs with sufficient hydrophobicity or tails longer than ∼80 residues are quickly released from the Sec61 translocon into the membrane or the ER lumen, resulting in inefficient assembly with partner TMDs. Thus, our data suggest that C-terminal tails harbor crucial signals for both the insertion and assembly of membrane proteins.
内质网(ER)中大量新合成的膜蛋白组装成多蛋白复合物,但对于组装膜蛋白所需的机制知之甚少。有人认为可能存在膜伴侣蛋白,类似于稳定和指导可溶性蛋白复合物组装的分子伴侣,但这些蛋白将膜蛋白成分聚集在一起的机制尚不清楚。在这里,我们已经确定 C 端跨膜结构域(C-TMD)的尾部长度决定了 ER 中膜蛋白的有效插入和组装。我们发现,C-TMD 尾部短于约 60 个氨基酸的膜蛋白插入 ER 膜的效率较低,这表明在它们被 Sec61 易位子识别进行插入之前,翻译就已经终止。这些疏水性不足的 C-TMD 被 Sec61 易位子复合物识别并保留,为与伴侣蛋白的 TMD 进行有效组装提供了一个时间窗口。未能与同源 TMD 组装的保留 TMD 会缓慢易位到 ER 腔中,并被 ER 相关降解(ERAD)途径识别以去除。相比之下,具有足够疏水性或尾部长度超过约 80 个残基的 C-TMD 会从 Sec61 易位子迅速释放到膜或 ER 腔中,导致与伴侣 TMD 组装效率低下。因此,我们的数据表明 C 端尾部对于膜蛋白的插入和组装都具有关键信号。