作者: R. A. Wilson , R. P. Gibson , C. F. Quispe , J. A. Littlechild , N. J. Talbot
关键词:
摘要: To cause rice blast disease, the fungus Magnaporthe oryzae breaches tough outer cuticle of leaf by using specialized infection structures called appressoria. These cells allow to invade host plant and proliferate rapidly within tissue. Here, we show that a unique NADPH-dependent genetic switch regulates in response changing nutritional redox conditions encountered pathogen. The biosynthetic enzyme trehalose-6-phosphate synthase (Tps1) integrates control glucose-6-phosphate metabolism nitrogen source utilization regulating oxidative pentose phosphate pathway, generation NADPH, activity nitrate reductase. We report Tps1 directly binds NADPH and, thereby, set related transcriptional corepressors, comprising three proteins, Nmr1, Nmr2, Nmr3, which can each bind NADP. Targeted deletion any Nmr-encoding genes partially suppresses nonpathogenic phenotype Δtps1 mutant. Tps1-dependent Nmr corepressors expression virulence-associated are derepressed during appressorium-mediated infection. When considered together, these results suggest initiation disease M. requires regulatory mechanism involving an sensor protein, Tps1, NADP-dependent nonconsuming interconversion NADP acting as signal transducer.