Highlights
•Rice sheath blight is caused by necrotrophic dreadful fungus Rhizoctonia solani.
•Forward genetics tools identified RSS1 (IMPA2; IMPORTIN ALPHA 2) as a NHR gene.
•Mutation in RSS1 at P65S in first exon compromise the immunity to R. solani.
•rss1 shows enhanced cell death, ROS, callose deposition and developmental defect.•RSS1 activates early salicylic acid mediated defense response against R. solani.
Abstract
There is neither resistant rice cultivar nor any control measure against Rhizoctonia solani AG-1 IA (RS), causal of sheath blight and a major threat to global rice production. Rice is a host and Arabidopsis is a nonhost with underlying nonhost resistance (NHR) gene which is largely untested. Using approaches of forward genetics and tools, cytology, and molecular biology, we identified homozygous mutants in Arabidopsis, mapped the NHR gene, and functionally characterized it in response to RS. Rss1 was mapped on Ch 4 between JAERI18 and Ch4_9.18 (844.6 Kb) and identified IMPORTIN ALPHA 2 as the candidate RSS1 gene. We found that breach of immunity in rss1 by RS activates defense responses whereas photosynthetic pigment biosynthesis and developmental processes are negatively regulated. In addition, a gradual decrease in PR1 by 3 dpi revealed that RSS1 positively regulated early SA-mediated resistance. Whereas increased expression of PDF1.2 by 3 dpi supported switching to necrotrophy, SA-mediated defense in Col-0 leading to immune response. Enhanced expression of ATG8a in rss1 supported autophagic cell death. IMPA2, IMPA1, and RAN1 function together to provide NHR against RS. These findings demonstrate that IMPA2 provides NHR against RS in Col-0 that evoke SA-mediated early immunity with boulevard for potential biotechnological application. Free article. Read more at: https://www.sciencedirect.com/science/article/pii/S2666517422000062
