A protein with an unusually short PPR domain, MEF8, affects editing at over 60 Arabidopsis mitochondrial C targets of RNA editing

作者：Diaz Michael F; Bentolila Stephane^*; Hayes Michael L; Hanson Maureen R; Mulligan R Michael

来源：Plant Journal, 2017, 92(4): 638-649.

DOI：10.1111/tpj.13709

• organelle RNA editing
• mitochondrion
• pentatricopeptide repeat
• DYW domain
• deaminase
• Arabidopsis thaliana

An RNA-seq approach was used to investigate the role of a PLS-subfamily pentatricopeptide repeat protein, Mitochondrial Editing Factor 8 (MEF8), on editing in Arabidopsis mitochondria and plastids. MEF8 has an intact DYW domain, but possesses an unusually short PLS repeat region of only five repeats. The MEF8 T-DNA insertion (mef8) line exhibited reduced editing at 38 mitochondrial editing sites and increased editing at 24 sites; therefore the absence of MEF8 affects 11% of the mitochondrial editome. Notably, 60% of the matR transcripts' sites showed a decrease of editing extent in the mef8 mutant. An E549A substitution in the MEF8 protein replaced the putatively catalytic glutamate of the HXE motif in the DYW domain. Complementation with MEF8-E549A failed to restore editing at the main target sites but was able to restore editing at the matR transcript; it also decreased the editing extent of most of the C targets exhibiting an increase of editing extent in the mef8 mutant plant. Thus, MEF8 has two antagonistic effects on mitochondrial editing: stimulatory, which requires a catalytic glutamate for most of the targets except for the matR transcript, and inhibitory, for which glutamate is dispensable.
Significance Statement MEF8 is a pentatricopeptide repeat protein that is required for C-to-U editing in the mitochondria of Arabidopsis plants. Analysis of mef8 null mutants and of transgenic plants based on next generation sequencing demonstrates that the MEF8 protein plays antagonistic roles in mitochondrial editing for which a glutamate residue is required or not.

• 出版日期2017-11