Molecular Mechanisms Of Plant Disease Resistance Mediated By BAK1-ATG18a Interaction And RppK-AvrRppK Interaction

Plant diseases have always been an important factor threatening national food security,which can not only reduce the yield of crops,but also reduce the quality and safety of agricultural products.Gray mold and southern corn rust(SCR)are one of the important diseases in current agricultural production.Utilizing resistance genes to cultivate resistance varieties is the most efficient way to control Botrytis cinerea and SCR.Validation of molecular mechanism of disease resistance is the premise and foundation of using resistance genes to cultivate disease-resistance varieties.However,the molecular mechanism of plant resistance to B.cinerea and SCR is still unclear.Previous studies have shown that ATG18 a,a key protein in the autophagy pathway and positively regulates plant resistance against B.cinerea.But how plant regulates ATG18 a in autophagy pathway and resistance against necrotrophs remains poorly understood.In this study,five amino acids on ATG18a(Thr241,Ser328,Ser344,Ser361,Thr387)were found to be phosphorylated by mass spectrometry.Phosphorylation of ATG18 a inhibited B.cinerea-induced autophagy and plant resistance to B.cinerea.While dephosphorylation of ATG18 a protein can effectively promote B.cinereainduced autophagy and plant resistance to B.cinerea.Moreover,BAK1 interacts with ATG18 a and is directly responsible for the phosphorylation of four sites(Thr241,Ser328,Ser361,Thr387)of ATG18 a protein.Mutant BAK1 gene enhanced plant autophagy signaling and plant resistance to B.cinerea.In conclusion,this study revealed that plants utilized BAK1 to phosphorylate ATG18 a to achieve fine regulation of autophagy levels and disease resistance.It explored important molecular mechanisms for plant resistance against necrotrophs,and also provides a theoretical support for the use of gene editing to improve the ATG18 a gene to cultivate diseaseresistant varieties.Previous studies have cloned the broad-spectrum resistance against SCR NLR gene Rpp K in maize,but the molecular mechanism of its broad-spectrum resistance to SCR remains poorly understood.In this study,the effector Avr Rpp K recognized by Rpp K was identified from the pathogenic fungus Puccinia polysora by large-scale protoplast experiments screening.Based on sequencing analysis,it was found that Avr Rpp K gene exists in all isolates P.polysora strains and is 100% conserved.In addition,the expression of the Avr Rpp K gene in maize could effectively inhibit the chitin-activated PTI response.Thus,Avr Rpp K protein is a core effector of P.polysora.Because of the broad-spectrum disease resistance function of Rpp K gene against SCR and the core effector protein properties of Avr Rpp K gene.We concluded that a single NLR gene recognizing a core effector is sufficient to confer broad resistance against a particular pathogen.In summary,the analysis of the molecular mechanism of plant disease resistance not only improves our understanding of plant-pathogen interactions,but also provides new genes,new materials and new theoretical support for the genetic improvement of disease resistance.