Abstract.
Trichoderma atroviride parasitizes a large variety of phytopathogenic fungi. This characteristic has allowed its use as a biological control agent. The production of hydrolytic enzymes appears to be a key element in the parasitic process. Among the enzymes released by Trichoderma, the proteinase Prb1 plays a major role. We show here that the corresponding gene (prb1) is subject to nitrogen catabolite repression. Accordingly, induction of prb1 transcription by Rhizoctonia solani cell walls and by osmotic stress requires release from a repressed condition, which is determined by nitrogen availability. Furthermore, the transcription pattern of the prb1 gene was not affected when an inhibitor of p38-Hog1, a regulator of the response to osmotic shock, was used. In contrast, a MEK1/2 (MAPK/ERK) inhibitor blocked prb1 transcription in response to nitrogen limitation, indicating that the pathway employed in the nitrogen response involves proteins similar to p42-p44. Fusion of the prb1 promoter to the gfp reporter gene allowed the detection of a novel regulatory element, providing an initial insight into the nature of the sites that control prb1 expression.
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Olmedo-Monfil, .V., Mendoza-Mendoza, .A., Gómez, .I. et al. Multiple environmental signals determine the transcriptional activation of the mycoparasitism related gene prb1 in Trichoderma atroviride . Mol Gen Genomics 267, 703–712 (2002). https://doi.org/10.1007/s00438-002-0703-4
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DOI: https://doi.org/10.1007/s00438-002-0703-4