The transcriptional regulator MOS1 attenuates salinity stress-induced seed germination inhibition via negative feedback regulation of ABA signaling in Arabidopsis.

Abstract

Seed germination is inhibited by salt stress, and this inhibition is known to be mainly mediated by the plant hormone abscisic acid (ABA). Whether and how this inhibition is fine-tuned is not fully understood. Here, we identified MODIFIER OF snc1-1 (MOS1) as an attenuator of salt-induced inhibition of seed germination. MOS1 expression was induced by salt, and this induction was partly dependent on ABA biosynthesis and signaling. The mos1 mutant showed hypersensitivity to salt stress during seed germination compared with the wild type, accompanied by higher ABA accumulation and stronger salt-induced expression of ABA biosynthesis and signaling genes. Genetic analysis suggested that MOS1 limits both salt-induced ABA biosynthesis and ABA responsiveness. Moreover, ABI5 directly activated MOS1 expression, whereas ABI5 transcripts and protein accumulated to higher levels in mos1 under salt stress. In addition, MOS1 expression was inhibited by the germination-promoting hormone gibberellin (GA), and MOS1 helped maintain GA biosynthesis. Together, these findings suggest that MOS1 attenuates salt-induced inhibition of seed germination, at least in part, through ABI5-linked negative feedback regulation of ABA signaling and modulation of GA biosynthesis.