The Magnaporthe grisea class VII chitin synthase is required for normal appressorial development and function

SUMMARY The plant pathogenic fungus Magnaporthe grisea is able to enter its host via appressorium‐mediated penetration. Earlier investigations have shown that these infection structures are rich in the cell wall polysaccharide chitin. Previously, we have described how the transcription of a class VII chitin synthase‐encoding gene CHS7 is completely dependent on the putative transcription factor Con7p during the germination of conidia, and how con7 − mutants are unable to form appressoria under any conditions tested. Because of the pleiotropic effects of the con7 − mutation, we examined the consequences of the targeted deletion of CHS7 . The chs7 − mutants generated were unable to form appressoria on artificial surfaces, except following the application of the exogenous inducers 1,16‐hexadecanediol and cyclic adenosine monophosphate. The appressoria formed had a reduced chitin content and were often found to be smaller and misshapen compared with the wild‐type. chs7 − mutants were significantly reduced in their ability to enter rice plants, but growth in planta was not affected. Reverse transcriptase‐polymerase chain reaction analysis demonstrated that CHS7 transcription was strongly induced on germination of spores, and a green fluorescent protein‐tagged Chs7p protein was found to be produced abundantly during infection‐related morphogenesis. Together, these data suggest that the class VII chitin synthase Chs7p of M. grisea is required for normal appressorium formation and function.