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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Impact of a mutation in the mitochondrial LSU rRNA gene from Chlamydomonas reinhardtii on the activity and the assembly of respiratory-chain complexes.

Two substitutions A1090G and A1098C (together called the m mutation) located in the conserved GTPase domain of the mitochondrial LSU rRNA gene were recently shown to weakly compensate for the phenotypical effect of a -1T frameshift mutation in the mitochondrial cox1 gene of C. reinhardtii. In order to analyze the impact of the m mutation on the mitochondrial translational machinery, a strain carrying the m mutation but wild-type for the cox1 gene was isolated. We found that the growth and the respiratory rate of the m mutant were affected and that the activities of complexes I, III, and IV, all containing mitochondria-encoded subunits, were lowered. In contrast the activities of complex II and of the alternative oxidase, both encoded exclusively by the nuclear genome, were not modified. The steady-state levels of complex I enzyme and of several components of the respiratory complexes I, III, and IV were also reduced in the mutant. We moreover showed that m did not suppress other frameshift or UGA stop mutations which affect mitochondrial genes.[1]

References

  1. Impact of a mutation in the mitochondrial LSU rRNA gene from Chlamydomonas reinhardtii on the activity and the assembly of respiratory-chain complexes. Remacle, C., Gloire, G., Cardol, P., Matagne, R.F. Curr. Genet. (2004) [Pubmed]
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