Functional analysis of mTERF5 and mTERF9 contribution to salt tolerance, plastid gene expression and retrograde signalling in Arabidopsis thaliana.

We previously showed that Arabidopsis mda1 and mterf9 mutants, defective in the chloroplast-targeted mitochondrial transcription termination factors mTERF5 and mTERF9, respectively, display altered responses to abiotic stresses and abscisic acid (ABA), as well as perturbed development, likely through abnormal chloroplast biogenesis. To advance the functional analysis of mTERF5 and mTERF9, we obtained and characterized overexpression (OE) lines. Additionally, we studied genetic interactions between sca3-2, affected in the plastid-RNA polymerase RpoTp, and the mda1-1 and mterf9 mutations. We also investigated the role of mTERF5 and mTERF9 in plastid translation and plastid-to-nucleus signalling. We found that mTERF9 OE reduces salt and ABA tolerance, while mTERF5 or mTERF9 OE alter expression of nuclear and plastid genes. We determined that mda1-1 and mterf9 mutations genetically interact with sca3-2. Further, plastid 16S rRNA levels were reduced in mda1-1 and mterf9 mutants, and mterf9 was more sensitive to chemical inhibitors of chloroplast translation. Expression of the photosynthesis gene LHCB1, a retrograde signalling marker, was differentially affected in mda1-1 and/or mterf9 compared to wild-type Col-0, after treatments with inhibitors of carotenoid biosynthesis (norflurazon) or chloroplast translation (lincomycin). Moreover, mterf9, but not mda1-1, synergistically interacts with gun1-1, defective in GUN1, a central integrator of plastid retrograde signals. Our results show that mTERF9, and to a lesser extent mTERF5, are negative regulators of salt tolerance and that both genes are functionally related to RpoTp, and that mTERF9 is likely required for plastid ribosomal stability and/or assembly. Furthermore, our findings support a role for mTERF9 in retrograde signalling.