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Hydrophobin gene expression in the maize pathogen Cochliobolus heterostrophus
Affiliation:1. Tel-Hai College, Upper Galilee 12210, Israel;2. Molecular Phytopathology Lab, Migal–Galilee Research Institute, Kiryat-Shmona 11016, Israel;3. Department of Biology, Technion–Israel Institute of Technology, Haifa 32000, Israel;1. Department of Chemical Sciences, University of Naples Federico II, via Cintia 4, I-80126 Naples, Italy;2. Department of Life Sciences and Systems Biology, University of Turin, viale P.A. Mattioli 25, I-10125 Turin, Italy;1. The Key Laboratory of Molecular Microbiology and Technology, Ministry of Education, College of Life Sciences, Nankai University, PR China;2. NHC Key Laboratory of Critical Care Medicine, Tianjin First Central Hospital, PR China;3. School of Life Science, Shanxi University, Shanxi, PR China;1. The Key Laboratory of Molecular Microbiology and Technology, Ministry of Education, Nankai University, Tianjin, China;2. Department of Pharmacy, Tianjin Medical University, Tianjin, China;3. Tianjin Neurological Institute, Key Laboratory of Post-Neuroinjury Neuro-repair and Regeneration in Central Nervous System, Ministry of Education and Tianjin City, Tianjin, China
Abstract:Filamentous fungi produce hydrophobins, small proteins localized on the outer surface of their cell walls and involved in growth and development. Hydrophobin gene expression depends on nutrient availability, light, and the activity of conserved signal-transduction pathways. We found four hydrophobins, one class I and three class II family members, in the Cochliobolus heterostrophus genome with high homology to other ascomycete hydrophobins, which present a typical conserved array of cysteines. The expression profile of a selected gene from each class was determined in a series of signaling-deficient mutants. Loss of either of two mitogen-activated protein kinase (MAPK) genes, CHK1 and MPS1, led to decreased hydrophobin class I (CHYD1) gene expression. Mutants in both MAPK genes had easily wettable colonies, but decreased CHYD1 expression was not the sole explanation for this phenotype. A significant elevation of hydrophobin class II (CHYD3) gene expression was measured in the chk1 mutant, suggesting a complex role for MAPK in controlling the expression of these hydrophobins. Similar but less marked tendencies were observed in G-protein α and β subunit loss-of-function mutants; however these showed no alteration in colony hydrophobicity. Overexpression of CHYD1 in the wild-type background caused a change in colony morphology and a small but significant increase in aerial growth. Thus G-protein and MAPK signal transduction influence hydrophobin gene expression and colony hydrophobicity. The connection between colony hydrophobicity and expression of the hydrophobin genes CHYD1 and CHYD3, however, is not one-to-one, indicating that additional factors determine colony-surface properties. The approach of using hydrophobin-overexpression mutants to investigate their role may be generalized to other hydrophobins and small secreted proteins.
Keywords:Hydrophobin  Signal transduction  Maize
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