RPM2, INDEPENDENTLY OF ITS MITOCHONDRIAL RNASE-P FUNCTION, SUPPRESSESAN ISP42 MUTANT DEFECTIVE IN MITOCHONDRIAL IMPORT AND IS ESSENTIAL FOR NORMAL GROWTH

Citation
Ck. Kassenbrock et al., RPM2, INDEPENDENTLY OF ITS MITOCHONDRIAL RNASE-P FUNCTION, SUPPRESSESAN ISP42 MUTANT DEFECTIVE IN MITOCHONDRIAL IMPORT AND IS ESSENTIAL FOR NORMAL GROWTH, Molecular and cellular biology, 15(9), 1995, pp. 4763-4770
Citations number
30
Categorie Soggetti
Biology
ISSN journal
02707306
Volume
15
Issue
9
Year of publication
1995
Pages
4763 - 4770
Database
ISI
SICI code
0270-7306(1995)15:9<4763:RIOIMR>2.0.ZU;2-O
Abstract
RPM2 is identified here as a high-copy suppressor of isp42-3, a temper ature-sensitive mutant allele of the mitochondrial protein import chan nel component, Isp42p, RPM2 already has an established role as a prote in component of yeast mitochondrial RNase P, a ribonucleoprotein enzym e required for the 5' processing of mitochondrial precursor tRNAs, A r elationship between mitochondrial tRNA processing and protein import i s not readily apparent, and, indeed, the two functions can be separate d, Truncation mutants lacking detectable RNase P activity still suppre ss the isp42-3 growth defect, Moreover, RPM2 is required for normal fe rmentative yeast growth, even though mitochondrial RNase P activity is not, The portion of RPM2 required for normal growth and suppression o f isp42-3 is the same. We conclude that RPM2 is a multifunctional gene . We find Rpm2p to be a soluble protein of the mitochondrial matrix an d discuss models to explain its suppression of isp42-3.