Processes underlying the upregulation of Tom proteins in S. cerevisiae mitochondria depleted of the VDAC channel

J Bioenerg Biomembr. 2004 Apr;36(2):187-93. doi: 10.1023/b:jobb.0000023622.66554.a6.

Abstract

It has been shown recently that in Saccharomyces cerevisiae mitochondria depleted of the VDAC channel (delta por1 mitochondria), the TOM complex channel substitutes for the VDAC channel. The additional function of the TOM complex channel is probably facilitated by the upregulation of nuclear-encoded components of the TOM complex as has been shown for Tom40 (a major component of the channel) and Tom70 (one of the surface receptors). Here we report that in S. cerevisiae cells the VDAC channel seems to be an important signal in the expression of the TOM complex components. S. cerevisiae cells depleted of the VDAC channel (delta por1 cells) contain distinctly increased levels of Tom40mRNA, and Tom70mRNA, but their synthesis and translation are affected differentially by the applied inhibitors of transcription and translation. Consequently, it may be concluded that depletion of the VDAC channel might influence differentially the expression of TOM40 and TOM70 genes.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Carrier Proteins / genetics
  • Carrier Proteins / metabolism*
  • Gene Expression Regulation, Fungal / physiology*
  • Mitochondria / genetics
  • Mitochondria / metabolism*
  • Mitochondrial Precursor Protein Import Complex Proteins
  • Porins / deficiency*
  • Saccharomyces cerevisiae / genetics
  • Saccharomyces cerevisiae / metabolism*
  • Saccharomyces cerevisiae Proteins / genetics
  • Saccharomyces cerevisiae Proteins / metabolism
  • Up-Regulation / physiology*
  • Voltage-Dependent Anion Channels

Substances

  • Carrier Proteins
  • Mitochondrial Precursor Protein Import Complex Proteins
  • Porins
  • Saccharomyces cerevisiae Proteins
  • Voltage-Dependent Anion Channels