A defect in nir1, a nirA-like transcription factor, confers morphological abnormalities and loss of pathogenicity in Colletotrichum acutatum.

摘要: SUMMARY A non-pathogenic mutant of Colletotrichum acutatum, designated Ca5, exhibited epiphytic hyphal growth and did not cause lesions on strawberry plants but grew necrotrophically when inoculated directly onto wounded stolons. In the absence an external nitrogen source, extended germ-tube prior to appressorium formation. The deduced product impaired gene ( nir1 ) is similar NirA, Aspergillus nidulans transcriptional regulator metabolism. Inoculation leaves with wild-type or Ca5 conidia in presence a preferred source resulted massive production, formation rapid symptom development. Expression C. acutatum nitrate reductase nit1 glutamine synthetase gln1 was induced by only expression repressed rich medium. transcription increased during appressorium-production stage, indicating that starvation constitutes cue for regulation transcript various phases infection indicative partial planta . cAMP-dependent protein kinase (PKA) determined be negative immediate post-germination appressoria wildtype. As inhibition PKA activity affect formation, we suggest NIR1 acts either parallel downstream pathway. Our results show pathogenicity determinant preinfection development under nitrogen-starvation conditions availability significant factor prepenetration phase.