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Author's Department


Date Submitted

Fall 12-2016

Research Mentor and Department

Elizabeth Haswell, Department of Biology




Plant development requires communication on many levels, including between cells and between organelles in a cell. Due to the sensitivity of metabolic processes they house, organelles such as mitochondria and plastids are often proposed to be sensors of environmental stress. Communication between mitochondria and chloroplasts during plant development may involve three Mechanosensitive channel of Small conductance-Like (MSL) proteins in Arabidopsis thaliana: MSL1, which localizes to the inner mitochondrial membrane, and MSL2 and MSL3, which localize to the inner plastid membrane. MSL proteins are Arabidopsis homologs of the bacterial Mechanosensitive channel of Small conductance (MscS), which relieves cellular osmotic pressure to protect against lysis during hypoosmotic shock. MSL2 and MSL3 are required to maintain plastid osmotic homeostasis during normal growth and development; MSL1 dissipates mitochondrial membrane potential and maintains redox homeostasis in mitochondria. In this study, we characterized the phenotypic effect of a genetic lesion in MSL1, both in wild type and in msl2 msl3 mutant backgrounds. msl1 single mutants appear wild type. While the characteristic leaf rumpling in msl2 msl3 double mutants was exacerbated in the msl1 msl2 msl3 triple mutant, the introduction of the msl1 lesion into the msl2 msl3 mutant background suppressed other msl2 msl3 mutant phenotypes, including ectopic callus formation, accumulation of superoxide and hydrogen peroxide in the shoot apical meristem, decreased root length, and reduced number of lateral roots. All of these phenotypes could be recovered by molecular complementation with a transgene containing a wild type version of MSL1. These results establish that the abnormalities observed in msl2 msl3 double mutants is partially dependent on the presence of functional MSL1, and suggest a possible role for plastid-to-mitochondria communication in seedling development. Future work will determine whether plastid stress signals may at times involve mitochondrial stress signals, and reveal the mechanism behind these seemingly antagonistic interactions.

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