Screen Of The Potential Drug Targets Of Protein Kinases In Magnaporthe Oryzae

Rice blast, caused by Magnaporthe oryzae, is one of the destructive rice diseases which threaten global cultured crop production. Its representative life cycle and infection process make it a suitable model of filamentous fungal pathogenesis and a model for host-fungal pathogen interactions. Further research on the mechanism of pathogenic process provides insights into the prevention of this pathogen. Protein kinases are a major class of signaling molecules that catalyze reversible phosphorylation of a large proportion of cellular proteins, thereby modulating protein activity and gene expression. The coordinated action of multiple PK pathways in fungal plant pathogens integrates a variety of external and internal cues to orchestrate key processes of the fungal life cycle, such as the cell cycle, gene transcription and metabolism. Protein kinases as key factors of pathogenic development and disease make themselves potential drug targets to control diseases. In this study, we analyzed the functions of the protein kinases during the development of M. oryzae to find some potential drug targets to control the rice blast.We identified 113 protein kinase genes and got 38 gene-deletion mutants in M. oryzae. Then we analyzed the phenotypes of these mutants including mycelial growth, conidiogenesis, infection-related development, pathogenicity and sensitivity to stresses. Colony morphology analyses showed that the deletion of 18 protein kinase genes led to reduced mycelial growth more than 10% incomparison with the wild-type strain, and the growth rates of the three mutants ΔMo02656,ΔMo02757,Δ reduced more than 30%. Twenty five genes were involved in conidiation and 12 of them showed reduced conidiation more than 40% in comparison with the wild-type stain Guyll. Three mutants of them (ΔMo05074, Δ,Δ) almost lost the ability to produce conidia. In sexual reproduction assays,12 mutants produced fewer perithecia compared to Guyll.ΔMo07012 and ΔMo13931 were more sensitive to CFW, SDS and Congo red compared to Guyl 1. AMo07012 and ΔMo13931 mutants lost pathogenicity on barley leaves. In addition, the Δ4o05074 mutants howed reduced pathogenicity on barley leaves with its disability to produce conidium. The defects on conidiation and pathogenicity could be rescued by re-introducing the full length gene to the ΔMo07012 and ΔMo13931 mutants respectively. So we confirm that Mo07012 and Mo13931 played key roles in pathogenoicity in M. oryzae. In conclusion, all these genes involved in growth, conidiation, cell wall integrity, and pathogenicity are the candidate drug targets.