Overproduction of OsRACK1A,an effector-targeted scaffold protein promoting OsRBOHB-mediated ROS production,confers rice floral resistance to false smut disease without yield penalty

Grain formation is fundamental for crop yield but is vulnerable to abiotic and biotic stresses.Rice grain production is threatened by the false smut fungus Ustilaginoidea virens,which specifically infects rice floral organs,disrupting fertilization and seed formation.However,little is known about the molecular mechanisms of the U.virens-rice interaction and the genetic basis of floral resistance.Here,we report that U.virens secretes a cytoplasmic effector,UvCBP1,to facilitate infection of rice flowers.Mechanistically,UvCBP1 interacts with the rice scaffold protein OsRACK1A and competes its interaction with the reduced nicotinamide adenine dinucleotide phosphate oxidase OsRBOHB,leading to inhibition of reactive oxygen species(ROS)production.Although the analysis of natural variation revealed no OsRACK1A variants that could avoid being targeted by UvCBP1,expression levels of OsRACK1A are correlated with field resistance against U.virens in rice germplasm.Overproduction of OsRACK1A restores the OsRACK1A-OsRBOHB association and promotes OsRBOHB phosphorylation to enhance ROS production,conferring rice floral resistance to U.virens without yield penalty.Taken together,our findings reveal a new pathogenic mechanism mediated by an essential effector from a flower-specific pathogen and provide a valuable genetic resource for balancing disease resistance and crop yield.

Osa-miR167d facilitates infection of Magnaporthe oryzae in rice

MicroRNAs(miRNAs)play important roles in rice response to Magnaporthe oryzae,the causative agent of rice blast disease.Studying the roles of rice miRNAs is of great significance for the disease control.Osa-miR167d belongs to a conserved miRNA family targeting auxin responsive factor(ARF)genes that act in developmental and stress-induced responses.Here,we show that OsamiR167d plays a negative role in rice immunity against M.oryzae by suppressing its target gene.The expression of Osa-miR167d was significantly suppressed in a resistant accession at and after 24 h post inoculation(hpi),however,its expression was significantly increased at 24 hpi in the susceptible accession upon M.oryzae infection.Transgenic rice lines over-expressing Osa-miR167d were highly susceptible to multiple blast fungal strains.By contrast,transgenic lines expressing a target mimicry to block OsamiR167d enhanced resistance to rice blast disease.In addition,knocking out the target gene ARF12 led to hypersusceptibility to multiple blast fungal strains.Taken together,our results indicate that Osa-miR167d negatively regulate rice immunity to facilitate the infection of M.oryzae by downregulating ARF12.Thus,Osa-miR167d-ARF12 regulatory module could be valuable in improvement of blast-disease resistance.

ANNEXIN 8 negatively regulates RPW8.1-mediated cell death and disease resistance in Arabidopsis

Study on the regulation of broad-spectrum resistance is an active area in plant biology. RESISTANCE TO POWDERY MILDEW 8.1(RPW8.1)is one of a few broad-spectrum resistance genes triggering the hypersensitive response(HR) to restrict multiple pathogenic infections. To address the question how RPW8.1 signaling is regulated,we performed a genetic screen and tried to identify mutations enhancing RPW8.1-mediated HR.Here, we provided evidence to connect an annexin protein with RPW8.1-mediated resistance in Arabidopsis against powdery mildew. We isolated and characterized Arabidopsis b7-6 mutant.A point mutation in b7-6 at the At5 g12380 locus resulted in an amino acid substitution in ANNEXIN8(AtANN8). Loss-of-function or RNA-silencing of AtANN8 led to enhanced expression of RPW8.1,RPW8.1-dependent necrotic lesions in leaves, and defense against powdery mildew. Conversely,over-expression of AtANN8 compromised RPW8.1-mediated disease resistance and cell death. Interestingly, the mutation in AtANN8 enhanced RPW8.1-triggered H2O2. In addition, mutation in AtANN8 led to hypersensitivity to salt stress. Together, our data indicate that AtANN8 is involved in multiple stress signaling pathways and negatively regulates RPW8.1-mediated resistance against powdery mildew and cell death, thus linking ANNEXIN’s function with plant immunity.