Spatial control of phospholipid flux restricts endoplasmic reticulum sheet formation to allow nuclear envelope breakdown

被引：60

作者：

Bahmanyar, Shirin ^{[1
]}

Biggs, Ronald ^{[1
]}

Schuh, Amber L. ^{[2
]}

Desai, Arshad ^{[1
]}

Mueller-Reichert, Thomas ^{[3
]}

Audhya, Anjon ^{[2
]}

Dixon, Jack E. ^{[4
]}

Oegema, Karen ^{[1
]}

机构：

[1] Univ Calif San Diego, Ludwig Inst Canc Res, Dept Cellular & Mol Med, La Jolla, CA 92093 USA

[2] Univ Wisconsin, Madison Med Sch, Dept Biomol Chem, Madison, WI 53706 USA

[3] Tech Univ Dresden, Med Theoret Ctr, D-01307 Dresden, Germany

[4] Univ Calif San Diego, Dept Pharmacol, La Jolla, CA 92093 USA

来源：

GENES & DEVELOPMENT | 2014年 / 28卷 / 02期

关键词：

lipin; endoplasmic reticulum; phospholipid synthesis; phosphatidylinositol; LIPIN FAMILY; PHOSPHOINOSITIDES; COMPLEX; ROLES;

D O I：

10.1101/gad.230599.113

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

The nuclear envelope is a subdomain of the endoplasmic reticulum (ER). Here we characterize CNEP-1 (CTD [Cterminal domain] nuclear envelope phosphatase-1), a nuclear envelope-enriched activator of the ER-associated phosphatidic acid phosphatase lipin that promotes synthesis of major membrane phospholipids over phosphatidylinositol (PI). CNEP-1 inhibition led to ectopic ER sheets in the vicinity of the nucleus that encased the nuclear envelope and interfered with nuclear envelope breakdown (NEBD) during cell division. Reducing PI synthesis suppressed these phenotypes, indicating that CNEP-1 spatially regulates phospholipid flux, biasing it away from PI production in the vicinity of the nuclear envelope to prevent excess ER sheet formation and NEBD defects.

引用

页码：121 / 126

页数：6

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