Rice blast disease, caused by the filamentous fungus Magnaporthe grisea, is one of the most devastating diseases to global rice production. To understand the regulation mechanism of conidiation in M. grisea, a morphological mutant, acr1, has been studied. Acr1 is a functional homolog of MedA, a conidiophore-developmental regulator in Aspergillus nidulans. The acr1 mutants produce chains of elongated conidia in a head-to-tail array, while the wild type conidia are produced in a sympodial array. In acr1, appressoria production is greatly reduced and the appressoria are defective in plant penetration. The reductions in the appressorium formation and penetration rates in the mutant are not complemented by the addition of exogenous cAMP. To investigate the genes upregulated by Acr1, an oligo DNA microarray, and nylon membranes arrayed with subtraction libraries constructed from conidial mRNA of acr1 and its isogenic wild-type strain Guy11 were used. Results from these analyses were further confirmed by RT-PCR. The expression level of Saccharomyces cerevisiae PCL1 - like G1 cyclin was reduced in acr1. Expression of several genes related to secondary metabolism were also controlled by Acr1. Recent progress on analysis of these genes will be presented.
Full conference title:
23rd Fungal Genetics Conference
- Fungal Genetics Conference 23rd (2002)