| Magnaporthe oryzae is the pathogen of the devastating blast disease of rice.Carbon catabolite repression(CCR)refers to the preferential use of readily available carbon sources(usually glucose)by microorganisms in the fermentation of mixed carbon sources,while the breakdown of readily available carbon sources inhibits the use of other carbon source components.Our previous results demonstrated that MoCreA,a regulator of CCR pathway,is closely involved in the growth,conidiation and pathogenesis of Magnaporthe oryzae.However,little is known about the detailed regulatory mechanism of MoCreA during the lifecycle of M.oryzae.Therefore,we conduct comparative transcriptomics analysis for the wild type strain and the ΔMocreA mutant to screen candidates under the regulation of MoCreA,and obtain 1506 up-regulated genes and 576 down-regulated genes.Among them,we select three candidates MGG07118,MGG11072 and MGG02155 for functional analysis in this study.So far,we have obtained the deletion mutants of MGG07118,and the overexpression strains of MGG 11072 and MGG02155.Phenotypic analysis results show that,compared with the wild type strain,ΔMGG07118 mutants exhibit obvious defects in vegetative growth and conidiation,and the number of conidiophores is significantly reduced,but the conidial morphogenesis,germination,and pathogenicity on rice and barley show normal.Moreover,the fluorescence microscopy observation results show that MGG07118 is located on the Vacuole membrane.After the overexpression of MGG 02155,the strains show significant defects in conidiophore and conidia production,the overexpression of MGG11072 show no difference in growth rate,morphology,sporulation,spore germination,appressorium formation and pathogenicity compared with the wild type.In conclusion,the phenotypes of MGG07118 knockout mutants and MGG02155 overexpression strains is similar with that of the ΔMocreA mutant,suggesting that the two genes may be regulated by MoCreA and are involved in the regulation of the growth and conidiation of rice blast fungus. |