Document Type
Article
Language
eng
Format of Original
11 p.
Publication Date
2009
Publisher
Oxford University Press
Source Publication
Nucleid Acids Research
Source ISSN
0305-1048
Original Item ID
doi: 10.1093/nar/gkn925; PubMed Central,. PMCID: PMC2615624
Abstract
A synthetic genetic array was used to identify lethal and slow-growth phenotypes produced when a mutation in TRM6, which encodes a tRNA modification enzyme subunit, was combined with the deletion of any non-essential gene in Saccharomyces cerevisiae. We found that deletion of the REX1 gene resulted in a slow-growth phenotype in the trm6-504 strain. Previously, REX1 was shown to be involved in processing the 3′ ends of 5S rRNA and the dimeric tRNAArg-tRNAAsp. In this study, we have discovered a requirement for Rex1p in processing the 3′ end of tRNAiMet precursors and show that precursor tRNAiMet accumulates in a trm6-504 rex1Δ strain. Loss of Rex1p results in polyadenylation of its substrates, including tRNAiMet, suggesting that defects in 3′ end processing can activate the nuclear surveillance pathway. Finally, purified Rex1p displays Mg2+-dependent ribonuclease activity in vitro, and the enzyme is inactivated by mutation of two highly conserved amino acids.
Recommended Citation
Ozanick, Sarah G.; Wang, Xuying; Costanzo, Michael; Brost, Renee L.; Boone, Charles; and Anderson, James T., "Rex1p Deficiency Leads to Accumulation of Precursor Initiator tRNAMet and Polyadenylation of Substrate RNAs in Saccharomyces cerevisiae" (2009). Biological Sciences Faculty Research and Publications. 293.
https://epublications.marquette.edu/bio_fac/293
Comments
Published version. Nucleic Acids Research, Vol. 37, No. 1 (2009): 298-308. DOI. Published under Creative Commons Attribution-NonCommercial 2.0 UK: England & Wales.