The mitochondrial protein MTP18 contributes to mitochondrial fission in mammalian cells

被引：185

作者：

Tondera, D ^{[1
]}

Czauderna, F ^{[1
]}

Paulick, K ^{[1
]}

Schwarzer, R ^{[1
]}

Kaufmann, J ^{[1
]}

Santel, A ^{[1
]}

机构：

[1] Atugen AG, D-13125 Berlin, Germany

来源：

JOURNAL OF CELL SCIENCE | 2005年 / 118卷 / 14期

关键词：

mitochondrial morphology; mitofusin; apoptosis; hFis1; Drp1; shRNA;

D O I：

10.1242/jcs.02415

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Mitochondria are dynamic organelles that change morphology by controlled fission and fusion events. Mitochondrial fission is regulated by a conserved protein complex assembled at the outer membrane. Human MTP18 is a novel nuclear-encoded mitochondrial membrane protein, implicated in controlling mitochondrial fission. Upon overexpression of MTP18, mitochondrial morphology was altered from filamentous to punctate structures suggesting excessive mitochondrial fission. Mitochondrial fragmentation was blocked in cells coexpressing either the mitochondrial fusion protein Mfn1 or Drp1(K38A), a dominant negative version of the fission protein Drp1. Also, a loss-of function of endogenous MTP18 by RNA interference (RNAi) resulted in highly fused mitochondria. Moreover, MTP18 appears to be required for mitochondrial fission because it is blocked after overexpression of hFis1 in cells with RNAi-mediated MTP18 knockdown. In conclusion, we propose that MTP18 functions as an essential intramitochondrial component of the mitochondrial division apparatus, contributing to the maintenance of mitochondrial morphology.

引用

页码：3049 / 3059

页数：11

共 47 条

[1] OPA1, encoding a dynamin-related GTPase, is mutated in autosomal dominant optic atrophy linked to chromosome 3q28 [J].