Magnaporthe grisea has emerged as a model system for the elucidation of mechanisms of fungal pathogenesis in crops. During the leaf infection process, the hyphal tip of a germinated conidium swells to form a melanised penetration structure known as an appressorium. Subsequently, M. grisea penetrates the leaf epidermis and develops a pseudohyphal and filamentous-like growth to colonise the first infected cell. We plan to use a multidisciplinary approach which includes transcriptomics, cell biology, biochemistry and bioinformatics to elucidate the genetic components required for pathogenesis-related development in M. grisea. The programme of work will be achieved through the functional characterisation of M581 mutant defective in bulbous growth on PS-PHIL. Although several mutants defective in IH growth have been identified in our laboratory, M581 constitutes one of the most interesting mutants for functional characterisation for several reasons. First, its hyperbranching phenotype which has, in other pathogenic filamentous fungi, been associated with reduced host virulence. Second, M581 is tagged in the putative transcription factor MgRFEG, which, due to the nature of the screen, suggests that MgRFEG is regulated by the MAPK PMK1 pathway. We plan to investigate the role of this new putative transcriptional regulator by adressing the following questions: i) What is the function of MgRFEG during plant colonisation and when is it required by the fungus to colonise plant cells? ii) Which genes are differentially expressed during the dimorphic transition of M. grisea on PS-PHIL surfaces and which are regulated by MgRFEG? iii) What are the target genes of MgRFEG and what is the sequence identified by MgRFEG in the promoter regions of these genes?
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