LncRNA MtCIR2 Negatively Regulates Response of Medicago truncatula Seedlings to Salt Stress by Targeting SOS2-Dependent Na Efflux via H2A Ubiquitination.

Increasing evidence indicates that long non-coding RNAs (lncRNAs) play a regulatory role in plant responses to environmental stress. However, the epigenetic mechanisms behind the regulation of salt stress by lncRNAs remain largely elusive. We previously discovered that the lncRNA MtCIR2 of Medicago trnucatula negatively regulated seed germination under salt stress by altering endogenous ABA and GA concentrations via histone ubiquitination. Here we evaluated the roles of MtCIR2 in regulating response of M. truncatula seedlings to salt stress. We found that over-expression and mutation of MtCIR2 reduced and enhanced tolerance to salt stress due to enhanced and suppressed foliar Na accumulation in over-expression and Mtcir2 mutant plants relative to their wild-type counterparts under salt stress. The MtCIR2-depenent Na accumulation was accounted for by the suppression of MtSOS2 that encodes a kinase responsible for Na exclusion from plants. We discovered that MtCIR2 physically interacted with BMI1, a core component of Polycomb Repressive Complex 1 (PRC1), leading to down-regulation of MtSOS2. ChIP assays revealed that MtCIR2 facilitated H2A ubiquitination at the chromatin of MtSOS2, thus repressing its expression, which in turn suppressed the SOS-dependent Na exclusion, and rendered the plants sensitive to salt stress. These results unravel a novel mechanism by which lncRNA epigenetically regulates SOS-mediated Na accumulation via histone ubiquitination in plant response to salt stress.