Loss of the SIN3 transcriptional corepressor results in aberrant mitochondrial function
1 Department of Biological Sciences, Wayne State University, 5047 Gullen Mall, Detroit, Michigan 48202, USA
2 Center for Molecular Medicine and Genetics, Wayne State University School of Medicine, 540 E. Canfield, Detroit, Michigan 48201, USA
3 Chemical Biology, University of Michigan, 930 N. University Ave. Rm. 4250, Ann Arbor, Michigan 48109, USA
BMC Biochemistry 2010, 11:26 doi:10.1186/1471-2091-11-26Published: 9 July 2010
SIN3 is a transcriptional repressor protein known to regulate many genes, including a number of those that encode mitochondrial components.
By monitoring RNA levels, we find that loss of SIN3 in Drosophila cultured cells results in up-regulation of not only nuclear encoded mitochondrial genes, but also those encoded by the mitochondrial genome. The up-regulation of gene expression is accompanied by a perturbation in ATP levels in SIN3-deficient cells, suggesting that the changes in mitochondrial gene expression result in altered mitochondrial activity. In support of the hypothesis that SIN3 is necessary for normal mitochondrial function, yeast sin3 null mutants exhibit very poor growth on non-fermentable carbon sources and show lower levels of ATP and reduced respiration rates.
The findings that both yeast and Drosophila SIN3 affect mitochondrial activity suggest an evolutionarily conserved role for SIN3 in the control of cellular energy production.