MOS2 has redundant function with its homolog MOS2H and is required for proper splicing of SNC1

Abstract

Plant immunity is essential for plant survival and resistance (R) proteins serve essential roles in pathogen detection and defense signal initiation. A gain-of-function mutation in SNC1, a TIR-type R gene, results in a characteristic autoimmune phenotype in Arabidopsis. From a forward genetic suppressor screen using snc1, MOS2 (MODIFIER of snc1), which encodes an RNA-binding protein, was identified. When MOS2 function is lost, the autoimmunity caused by snc1 is abolished and basal resistance against virulent pathogens is attenuated. Recently, it was shown that mos2 mutants also have defects in miRNA processing. However, it is not known how the role of MOS2 in miRNA production is related to the suppression of snc1-mediated autoimmunity. Here, we show that MOS2 contributes to proper splicing of SNC1 transcript, agreeing with its potential association with the MOS4-associated complex (MAC). In addition, although mutant plants carrying a mutation in the MOS2 homolog MOS2H are wild-type like, the double mutant mos2 mos2h is lethal. These data suggest that MOS2 and MOS2H have unequally redundant functions. Overall, MOS2 and MOS2H probably have diverse functions in both alternative splicing and miRNA processing. © 2013 Landes Bioscience.