Different respiratory defective phenotypes of Neurospora crassa and Saccharomyces cerevisiae after inactivation of the gene encoding the mitochondrial acyl carrier protein

被引：92

作者：

Schneider, R ^{[1
]}

Massow, M ^{[1
]}

Lisowsky, T ^{[1
]}

Weiss, H ^{[1
]}

机构：

[1] UNIV DUSSELDORF,INST BOT,D-40225 DUSSELDORF,GERMANY

来源：

CURRENT GENETICS | 1995年 / 29卷 / 01期

关键词：

acyl carrier protein; NADH; ubiquinone oxidoreductase; PET gene; fatty acid synthesis;

D O I：

10.1007/BF00313188

中图分类号：

Q3 [遗传学];

学科分类号：

071007 ; 090102 ;

摘要：

The nuclear genes (ncp-1, ACP1) encoding the mitochondrial acyl carrier protein were disrupted in Meurospora crassa and Saccharomyces cerevisiae. In N. crassa acp-1 is a peripheral subunit of the respiratory NADH:ubiquinone oxidoreductase (complex I). S. cerevisiae lacks complex I and its ACP1 appears to be located in the mitochondrial matrix. The loss of acp-1 in N. crassa causes two biochemical lesions. Firstly, the peripheral part of complex I is not assembled, and the membrane part is not properly assembled. The respiratory ubiquinol: cytochrome c oxidoreductase (complex III) and cytochrome c oxidase (complex IV) are normal amounts. Secondly, the lysophospholipid of mitochondrial membranes is increased four-fold. In S. cerevisiae, the loss of ACP1 leads to a pleiotropic respiratory deficient phenotype.

引用

页码：10 / 17

页数：8

共 60 条

[51]

VANGINKEL G, 1994, METHOD ENZYMOL, V233, P273

[52] A NEW ROLE FOR PHOSPHOLIPASE-A2 - PROTECTION OF MEMBRANES FROM LIPID-PEROXIDATION DAMAGE [J].