Analysis of rho mutability in Saccharomyces cerevisiae

Summary

The Erythromycin induced mutability of the cytoplasmic factor rho in S. cerevisiae does not depend only on the participation of its mitochondrial target (formally a mitochondrial protein synthesis component) to the replication of the mitochondrial DNA.

The relative increase from the spontaneous background in the percentage of RD mutants accumulated in the presence of the drug is the same in mmc and MMC strains whereas the total number of RD mutants accumulated is about tenfold higher in mmc strains. Mutations at the mitochondrial locus that controls the sensitivity to Erythromycin reduce both the Erythromycin induced and the spontaneous mutability of rho in mmc strains indicating that the gene products of nuclear (MMC) and mitochondrial (ERY^s) determinants interact in determining the fidelity of a “replicative complex” for the mitochondrial DNA.

The fact that ERY^R allelesaare able to suppress the pet-ts associated mutability of rho but not the RD conditional trait of these mutants makes evident that the pet-ts gene-products have an additional role beside the enzymatic or the biosynthetic ones.

Since the pet-ts genes are not directly involved in the metabolism of mitochondrial DNA we hypothesize that they provide for some structures that contribute to ensure the proper conformation of a “replicative complex” for mitochondrial DNA.