BmCREC Is an Endoplasmic Reticulum (ER) Resident Protein and Required for ER/Golgi Morphology*
BmCREC Is an Endoplasmic Reticulum (ER) Resident Protein and Required for ER/Golgi Morphology*
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DOI：
10.1074/jbc.m113.463018
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发表时间：
2013-08
期刊：
影响因子：
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通讯作者：
Qiao Wang;Birong Shen;P. Zheng;H. Feng;Yige Guo;Wenyuan Cao;Liang Chen;Xiao Liu;Guodong Zhao-Guodon
中科院分区：
文献类型：
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作者：
Qiao Wang;Birong Shen;P. Zheng;H. Feng;Yige Guo;Wenyuan Cao;Liang Chen;Xiao Liu;Guodong Zhao-Guodon
背景：BmCREC被认为是在细胞核内超卷DNA。结果：BmCREC通过KDEL受体和COPI介导的转运被回收到内质网。BmCREC内质网检索缺陷导致内质网/高尔基体形态紊乱。结论：BmCREC作为一种内质网腔蛋白，具有维持内质网/高尔基体形态的作用。意义：本研究有助于理解内质网腔蛋白在调节内质网/高尔基体形态中的作用。家蚕后丝腺是研究细胞内转运的模型。在这里，利用这个模型，我们识别了BmKinesin-1的几个潜在的货物蛋白，并集中在一个候选蛋白BmCREC上。BmCREC(又称家蚕DNA超卷曲因子，BmSCF)是先前提出的在细胞核内对DNA进行超卷曲的分子。然而，我们在这里证明了BmCREC定位于内质网管腔。它的C端四肽HDEF被KDEL受体识别，随后被外壳蛋白I(COPI)囊泡逆行转运到内质网。缺乏BmCREC的HDEF四肽或敲除COPI亚基会导致ER保留率下降，同时BmCREC的分泌增加。此外，我们发现BmCREC基因敲除显著破坏了内质网和高尔基体的形态，并导致后丝腺管扩张的缺陷。总之，我们的结果阐明了BmCREC的内质网滞留机制，并揭示了BmCREC对于维持内质网/高尔基体形态是不可或缺的。
Background: BmCREC was supposed to supercoil DNA in the nucleus. Results: BmCREC is retrieved to the ER by KDEL receptor- and COPI-mediated transport. Defects in ER retrieval of BmCREC lead to disrupted ER/Golgi morphology. Conclusion: BmCREC, as an ER luminal protein, functions to maintain ER/Golgi morphology. Significance: This study facilitates the understanding of the roles of ER luminal proteins in regulating ER/Golgi morphology. Silkworm posterior silkgland is a model for studying intracellular trafficking. Here, using this model, we identify several potential cargo proteins of BmKinesin-1 and focus on one candidate, BmCREC. BmCREC (also known as Bombyx mori DNA supercoiling factor, BmSCF) was previously proposed to supercoil DNA in the nucleus. However, we show here that BmCREC is localized in the ER lumen. Its C-terminal tetrapeptide HDEF is recognized by the KDEL receptor, and subsequently it is retrogradely transported by coat protein I (COPI) vesicles to the ER. Lacking the HDEF tetrapeptide of BmCREC or knocking down COPI subunits results in decreased ER retention and simultaneously increased secretion of BmCREC. Furthermore, we find that BmCREC knockdown markedly disrupts the morphology of the ER and Golgi apparatus and leads to a defect of posterior silkgland tube expansion. Together, our results clarify the ER retention mechanism of BmCREC and reveal that BmCREC is indispensable for maintaining ER/Golgi morphology.