MTF1, encoding the yeast mitochondrial RNA polymerase specificity factor, is located on chromosome XIII.

MTF1 is a nuclear gene that encodes the promoter recognition factor of the yeast mitochondrial RNA polymerase. The MTF1 gene was physically mapped to chromosome XIII. Genetic mapping data indicate that the gene is closely linked to RNA1.

Glucose repression of yeast mitochondrial transcription: kinetics of derepression and role of nuclear genes.

Yeast mitochondrial transcript and gene product abundance has been observed to increase upon release from glucose repression, but the mechanism of regulation of this process has not been determined. We report a kinetic analysis of this phenomenon, which demonstrates that the abundance of all classes of mitochondrial RNA changes slowly relative to changes observed for glucose-repressed nuclear genes. Several cell doublings are required to achieve the 2- to 20-fold-higher steady-state levels observed after a shift to a nonrepressing carbon source. Although we observed that in some yeast strains the mitochondrial DNA copy number also increases upon derepression, this does not seem to play the major role in increased RNA abundance. Instead we found that three- to sevenfold increases in RNA synthesis rates, measured by in vivo pulse-labelling experiments, do correlate with increased transcript abundance. We found that mutations in the SNF1 and REG1 genes, which are known to affect the expression of many nuclear genes subject to glucose repression, affect derepression of mitochondrial transcript abundance. These genes do not appear to regulate mitochondrial transcript levels via regulation of the nuclear genes RPO41 and MTF1, which encode the subunits of the mitochondrial RNA polymerase. We conclude that a nuclear gene-controlled factor(s) in addition to the two RNA polymerase subunits must be involved in glucose repression of mitochondrial transcript abundance.

The yeast IMP1 gene is allelic to GAL2.

We have found that many laboratory strains of yeast are defective in galactose metabolism owing to a recessive mutation in the previously characterized nuclear gene, IMP1. This defect leads to a requirement for mitochondrial function for growth on, and metabolism of, galactose. Genetic background affects the degree to which cells are defective. In particular, alleles of GAL3 affect the ability to score the Imp phenotype. We have found that in imp1 strains, transcriptional induction of the galactose inducible genes (GAL1, 2, 7 + 10, MEL1) is normal, but galactose transport is reduced in both rho+ and rho0 cells. This phenotype is normally associated with mutations in GAL2, the galactose permease. Although the growth phenotypes of gal2 and imp1 mutants are distinct, we found that the transformation of imp1 rho0 strains with a plasmid containing the GAL2 gene allows these strains to grow on galactose. Initial genetic analyses did not demonstrate linkage between the GAL2 and IMP1 genes owing to the effects of an unlinked gene on the Imp phenotype. By disrupting the GAL2 gene in an Imp+ background, we have shown that IMP1 and GAL2 segregate as tightly linked genes. Based on these data, we believe that imp1 is a partially defective allele of the GAL2 gene.