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Alterations of the mitochondrial proteome caused by the absence of mitochondrial DNA: A proteomic view
Author(s) -
Chevallet Mireille,
Lescuyer Pierre,
Diemer Hélène,
van Dorsselaer Alain,
LeizeWagner Emmanuelle,
Rabilloud Thierry
Publication year - 2006
Publication title -
electrophoresis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.666
H-Index - 158
eISSN - 1522-2683
pISSN - 0173-0835
DOI - 10.1002/elps.200500704
Subject(s) - mitochondrial dna , mitochondrion , biology , ribosomal protein , mitochondrial carrier , hspa9 , mitochondrial ribosome , proteome , mitochondrial membrane transport protein , dnaja3 , mitochondrial fusion , microbiology and biotechnology , human mitochondrial genetics , inner mitochondrial membrane , biochemistry , bacterial outer membrane , gene , ribosome , rna , peptide sequence , escherichia coli
The proper functioning of mitochondria requires that both the mitochondrial and the nuclear genome are functional. To investigate the importance of the mitochondrial genome, which encodes only 13 subunits of the respiratory complexes, the mitochondrial rRNAs and a few tRNAs, we performed a comparative study on the 143B cell line and on its Rho‐0 counterpart, i.e. , devoid of mitochondrial DNA. Quantitative differences were found, of course in the respiratory complexes subunits, but also in the mitochondrial translation apparatus, mainly mitochondrial ribosomal proteins, and in the ion and protein import system, i.e. , including membrane proteins. Various mitochondrial metabolic processes were also altered, especially electron transfer proteins and some dehydrogenases, but quite often on a few proteins for each pathway. This study also showed variations in some hypothetical or poorly characterized proteins, suggesting a mitochondrial localization for these proteins. Examples include a stomatin‐like protein and a protein sharing homologies with bacterial proteins implicated in tyrosine catabolism. Proteins involved in apoptosis control are also found modulated in Rho‐0 mitochondria.