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Mutation of SPOTTED LEAF3 (SPL3) impairs abscisic acid-responsive signaling and delays leaf senescence in rice
- 언어ENG
- URLhttps://db.koreascholar.com/Article/Detail/302509
Lesion mimic mutants commonly display spontaneous cell death in pre-senescent green leaves under normal conditions, without pathogen attack. Despite molecular and phenotypic characterization of several lesion mimic mutants, the mechanisms of the spontaneous formation of cell death lesions remain largely unknown. Here, we examined the rice lesion mimic mutant spotted leaf3 (spl3). In mutants grown under a light/dark cycle, spl3 mutants appeared similar to wild type at early developmental stages, but lesions gradually appeared in the mature leaves close to heading stage. By contrast, in mutants grown under continuous light, severe cell death lesions formed in developing leaves, even at the seedling stage. Histochemical analysis showed that hydrogen peroxide accumulated in the mutants, likely causing the cell death phenotype. By map-based cloning and complementation, we showed that a 1-bp deletion in the first exon of Oryza sativa Mitogen-Activated Protein Kinase Kinase Kinase1 (OsMAPKKK1)/OsEDR1/ OsACDR1 causes the spl3 mutant phenotype. We found that the spl3 mutants were insensitive to abscisic acid (ABA), showing normal root growth in ABA-containing media and delayed leaf yellowing during dark-induced and natural senescence. Expression of ABA signaling-associated genes was also less responsive to ABA treatment in the mutants. Furthermore, the spl3 mutants had lower transcript levels and activities of catalases, which scavenge hydrogen peroxide, probably due to impairment of ABA-responsive signaling. Finally we discuss a possible molecular mechanism of lesion formation in the mature leaves of spl3 mutants.
