Calumenin-1 Interacts with Climp63 to Cooperatively Determine the Luminal Width and Distribution of Endoplasmic Reticulum Sheets
Calumenin-1 Interacts with Climp63 to Cooperatively Determine the Luminal Width and Distribution of Endoplasmic Reticulum Sheets
复制标题
Calumenin-1 与 Climp63 相互作用，共同确定内质网片的管腔宽度和分布
DOI：
10.1016/j.isci.2019.10.067
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发表时间：
2019-12-20
期刊：
影响因子：
5.8
通讯作者：
Teng, Junlin
中科院分区：
文献类型：
--
作者：
Shen, Birong;Zheng, Pengli;Teng, Junlin
ER由不同的结构组成，如小管、基质和片层，所有这些结构对其各种功能都很重要。然而，这些不同的ER结构，特别是核周ER片层，是如何形成的仍不清楚。我们在这里报告，ER膜蛋白Climp 63和ER管腔蛋白calumenin-1（Calu 1）合作维持ER片形态。我们发现Climp 63的管腔长度与ER片的管腔宽度呈正相关。此外，Climp 63显性负性的仅内腔突变体使ER片层的内腔变窄，表明Climp 63充当ER内腔桥。我们还发现，Calu 1特异性地与Climp 63相互作用，并在ER片分布和管腔宽度方面拮抗Climp 63。总之，我们的数据提供了深入了解ER片的结构是如何维持和调节的。
The ER is composed of distinct structures like tubules, matrices, and sheets, all of which are important for its various functions. However, how these distinct ER structures, especially the perinuclear ER sheets, are formed remains unclear. We report here that the ER membrane protein Climp63 and the ER luminal protein calumenin-1 (Calu1) collaboratively maintain ER sheet morphology. We show that the luminal length of Climp63 is positively correlated with the luminal width of ER sheets. Moreover, the lumen-only mutant of Climp63 dominant-negatively narrows the lumen of ER sheets, demonstrating that Climp63 acts as an ER luminal bridge. We also reveal that Calu1 specifically interacts with Climp63 and antagonizes Climp63 in terms of both ER sheet distribution and luminal width. Together, our data provide insight into how the structure of ER sheets is maintained and regulated.