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Rho1 is an important member of the Rho family of small G protein , it exists two transformed state : state GDP combined inactivation status and GTP-binding activity . GDP / GTP exchange factor (GEF1) function is to promote Rho1 GDP bound to GTP-binding state conversion . This study, bioinformatics methods MGG 2644 1 theoretical isoelectric point of the genetic , molecular weight , domains and functional prediction analysis , the results show that the gene is a small G protein Rho1 GEF , the gene change is consistent with the evolution of species . Then the gene knockout mutant rice blast fungus as model organisms by homologous recombination , found that the gene deletion mutants slow growth , diaphragm spacing compared with the wild type , however , there was no difference , indicating the gene may be involved in the regulation of the cell division cycle . Mutants in a growth rate is suppressed , indicating the resistance of SDS reduced ability of the starch in the medium of the SDS . In addition , mutants can not produce conidia , mycelium end appressorium differentiation generated , but the appressorium generated number of rare and lost the ability to infect the onion epidermis and rice leaf appressorium , thus making injury and can not be made ??non- injury leaves the formation of the lesion . Phenotype are subject to a Rho1 the regulation , and thus suggesting that related to the function of the gene with Rho1 . Will the promoter MgRhoGEF1 gene transferred to the lack of knockout mutations in the mutant phenotype is restored , the knockout mutant phenotype appear lack of MgRhoGef1 directly or indirectly lead to . The method of using the yeast two-hybrid confirmed MgRhoGef1 its domain can with Rho1 interaction , thus The studies favor of MgRhoGef1 understand Rho1 function of improving the understanding of Rho1 . Lead to The M. grisea loss pathogenic capacity , and thus it is possible to find a suitable drug target through the study of the gene , a new strategy for the prevention and treatment of the rice blast due to MgRhoGef1 absence .
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