tRNA precursors, which are transcribed by RNA polymerase III, undergo end-maturation, splicing, and base modifications. Hypomodified tRNAs, such as tRNA(Val(AAC)), lacking 7-methylguanosine and 5-methylcytidine modifications, are subject to degradation by a rapid tRNA decay pathway. Here we searched for genes which, when overexpressed, restored stability of tRNA(Val(AAC)) molecules in a modification-deficient trm4Δtrm8Δ mutant. We identified TEF1 and VAS1, encoding elongation factor eEF1A and valyl-tRNA synthetase respectively, which likely protect hypomodified tRNA(Val(AAC)) by direct interactions. We also identified MAF1 whose product is a general negative regulator of RNA polymerase III. Expression of a Maf1-7A mutant that constitutively repressed RNA polymerase III transcription resulted in increased stability of hypomodified tRNA(Val(AAC)). Strikingly, inhibition of tRNA transcription in a Maf1-independent manner, either by point mutation in RNA polymerase III subunit Rpc128 or decreased expression of Rpc17 subunit, also suppressed the turnover of the hypomodified tRNA(Val(AAC)). These results support a model where inhibition of tRNA transcription leads to stabilization of hypomodified tRNA(Val(AAC)) due to more efficient protection by tRNA-interacting proteins.

• PMID: 22919049
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Reference Type

Journal Article | Research Support, Non-U.S. Gov't

Authors

Turowski TW, Karkusiewicz I, Kowal J, Boguta M

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