Mutations in the plant‑conserved uL1m mitochondrial ribosomal protein significantly affect development, growth and abiotic stress tolerance in Arabidopsis thaliana

Abstract

Mitochondria ribosomes, or mitoribosomes, reflect the endosymbiotic origin of this organelle. Mitoribosomes are made up of RNAs and proteins (mitochondrial ribosomal proteins, MRPs). Considering the large amount of MRPs identified in plant mitoribosomes, the number of MRPs for which mutations producing mutant phenotypes have been hitherto reported is rather limited. Moreover, the contribution of plant mitoribosomes, and hence mitochondrial translation, to abiotic stress, is almost completely unknown. To advance knowledge about the role of mitochondrial translation in plant development and stress acclimation, we performed a thorough genetic and phenotypic analysis of the Arabidopsis mrpl1-1 and 3 mutants affected in the MRPL1 (MITOCHONDRIAL RIBOSOMAL PROTEIN L1) gene encoding MRP uL1m. Compared to the wild type, the mrpl1-1 and 3 mutants show delayed growth, small body size and smaller leaf palisade cells, although the morphology of chloroplasts and mitochondria is similar. We identified a novel MRPL1 mutant allele, mrpl1-2, that causes early seedling lethality, which reveals that Arabidopsis MRPL1 is an essential gene. Furthermore, the mrpl1 viable mutants are less responsive than the wild type to increased growth temperature, and are hypersensitive to antibiotics doxycycline and chloramphenicol, and also to salt, osmotic and ABA stress. In summary, impaired MRPL1 function severely hinders plant growth and development, likely by triggering retrograde signaling due to translational perturbation, and it enhances sensitivity to abiotic stress. Besides, our results support a role for mitochondria translation in acclimation to adverse environmental conditions. To our knowledge this is the first work to report an altered abiotic stress sensitivity phenotype due to mutations in a plant MRP gene.