Multiple environmental signals determine the transcriptional activation of the mycoparasitism related gene prb1 in Trichoderma atroviride

• Published in: Molecular genetics and genomics : MGG Vol. 267; no. 6; pp. 703 - 712
• Main Authors: Olmedo Monfil, V, Mendoza Mendoza, A, Gomez, I, Cortes, C, Herrera Estrella, A
• Format: Journal Article
• Language: English
• Published: Germany Springer Nature B.V 01.08.2002
• Subjects: Blotting, Northern; Cell Wall - metabolism; Crop diseases; Enzymes; Fungal Proteins; Fungi; Gene Expression Regulation, Enzymologic; Gene Expression Regulation, Fungal; Genes; Genetic engineering; Genomics; Kinases; MAP Kinase Signaling System - physiology; Metabolism; Nitrogen; Nitrogen Compounds - metabolism; Organisms, Genetically Modified; Osmotic Pressure; Plasmids; Promoter Regions, Genetic; Serine Endopeptidases - genetics; Signal transduction; Transcription, Genetic; Trichoderma - enzymology; Trichoderma - genetics; United States > US; Detroit Michigan
• DOI: 10.1007/s00438-002-0703-4
• ISSN: 1617-4615

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.