A novel splice variant of Elp3/Kat9 regulates mitochondrial tRNA modification and function

Sci Rep. 2022 Aug 31;12(1):14804. doi: 10.1038/s41598-022-18114-x.

Abstract

Post-translational modifications, such as lysine acetylation, regulate the activity of diverse proteins across many cellular compartments. Protein deacetylation in mitochondria is catalyzed by the enzymatic activity of the NAD+-dependent deacetylase sirtuin 3 (SIRT3), however it remains unclear whether corresponding mitochondrial acetyltransferases exist. We used a bioinformatics approach to search for mitochondrial proteins with an acetyltransferase catalytic domain, and identified a novel splice variant of ELP3 (mt-ELP3) of the elongator complex, which localizes to the mitochondrial matrix in mammalian cells. Unexpectedly, mt-ELP3 does not mediate mitochondrial protein acetylation but instead induces a post-transcriptional modification of mitochondrial-transfer RNAs (mt-tRNAs). Overexpression of mt-ELP3 leads to the protection of mt-tRNAs against the tRNA-specific RNase angiogenin, increases mitochondrial translation, and furthermore increases expression of OXPHOS complexes. This study thus identifies mt-ELP3 as a non-canonical mt-tRNA modifying enzyme.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Histone Acetyltransferases* / metabolism
  • Mammals / metabolism
  • Mitochondrial Proteins / genetics
  • Mitochondrial Proteins / metabolism
  • Protein Biosynthesis
  • RNA Processing, Post-Transcriptional*
  • RNA, Mitochondrial / metabolism
  • RNA, Transfer / genetics
  • RNA, Transfer / metabolism

Substances

  • Mitochondrial Proteins
  • RNA, Mitochondrial
  • RNA, Transfer
  • Histone Acetyltransferases