N-terminal acetylation modulates Bax targeting to mitochondria

被引：13

作者：

Alves, Sara ^{[1
]}

Neiri, Leire ^{[2
]}

Chaves, Susana Rodrigues ^{[1
]}

Vieira, Selma ^{[1
]}

Trindade, Dario ^{[1
]}

Manon, Stephen ^{[3
,4
]}

Dominguez, Veronica ^{[5
]}

Pintado, Belen ^{[5
]}

Jonckheere, Veronique ^{[6
,7
]}

Van Damme, Petra ^{[6
,7
]}

Silva, Rui Duarte ^{[8
,9
]}

Aldabe, Rafael ^{[2
]}

Corte-Real, Manuela ^{[1
]}

机构：

[1] Univ Minho, Dept Biol, Mol & Environm Biol Ctr, Campus Gualtar, P-4710057 Braga, Portugal

[2] Univ Navarra, Ctr Invest Med Aplicada, Gene Therapy & Regulat Gene Express Program, Avda Pio 12 55, Pamplona 31008, Spain

[3] CNRS, UMR5095, 1 Rue Camille St Saens, F-33077 Bordeaux, France

[4] Univ Bordeaux, 146 Rue Leo Saignat, F-33076 Bordeaux, France

[5] CNB, Campus Cantoblanco, Madrid, Spain

[6] VIB, VIB UGent Ctr Med Biotechnol, B-9000 Ghent, Belgium

[7] Univ Ghent, Dept Biochem, B-9000 Ghent, Belgium

[8] Univ Algarve, Dept Ciencias Biomed & Med, Campus Gambelas, Faro, Portugal

[9] Univ Algarve, Ctr Biomed Res, Campus Gambelas, Faro, Portugal

来源：

INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY | 2018年 / 95卷

关键词：

Apoptosis; Bax; N-terminal acetyltransferase; NatB; N-terminal acetylation; Mitochondria; INDUCED CELL-DEATH; ALPHA-ACETYLATION; C-TERMINUS; PROTEIN; YEAST; APOPTOSIS; ACETYLTRANSFERASES; BCL-2; INSERTION; SURVIVAL;

D O I：

10.1016/j.biocel.2017.12.004

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The pro-apoptotic Bax protein is the main effector of mitochondrial permeabilization during apoptosis. Bax is controlled at several levels, including post-translational modifications such as phosphorylation and S-palmitoylation. However, little is known about the contribution of other protein modifications to Bax activity. Here, we used heterologous expression of human Bax in yeast to study the involvement of N-terminal acetylation by yNaa20p (yNatB) on Bax function. We found that human Bax is N-terminal (Nt-)acetylated by yNaa2Op and that Nt-acetylation of Bax is essential to maintain Bax in an inactive conformation in the cytosol of yeast and Mouse Embryonic Fibroblast (MEF) cells. Bax accumulates in the mitochondria of yeast naa20A and Naa25(-/-) MEF cells, but does not promote cytochrome c release, suggesting that an additional step is required for full activation of Bax. Altogether, our results show that Bax N-terminal acetylation by NatB is involved in its mitochondrial targeting.

引用

页码：35 / 42

页数：8

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