Current Genetics

, Volume 29, Issue 1, pp 10–17

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

  • Regina Schneider
  • Michael Massow
  • Thomas Lisowsky
  • Hanns Weiss
Original Paper

DOI: 10.1007/BF00313188

Cite this article as:
Schneider, R., Massow, M., Lisowsky, T. et al. Curr Genet (1995) 29: 10. doi:10.1007/BF00313188

Abstract

The nuclear genes (acp-1, ACP 1) encoding the mitochondrial acyl carrier protein were disrupted in Neurospora 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 oxidose (complex IV) are made in normal amounts. Secondly, the lysophospholipid content of mitochondrial membranes is increased four-fold. In S. cerevisiae, the loss of aCP1 leads to a pleiotropic respiratory deficient phenotype.

Key words

Acyl carrier protein NADH: ubiquinone oxidoreductase PET gene Fatty acid synthesis 

Copyright information

© Springer-Verlag 1995

Authors and Affiliations

  • Regina Schneider
    • 1
  • Michael Massow
    • 1
  • Thomas Lisowsky
    • 2
  • Hanns Weiss
    • 1
  1. 1.Institut für BiochemieHeinrich-Heine-Universität DüsseldorfDüsseldorfGermany
  2. 2.Instrut für BotanikHeinrich-Heine-Universität DüsseldorfDüsseldorfGermany

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