The ubc2 gene of Ustilago maydis encodes a putative novel adaptor protein required for filamentous growth, pheromone response and virulence

The Basidiomycete fungus Ustilago maydis causes corn smut disease and alternates between a budding haploid saprophyte and a filamentous dikaryotic pathogen. Previous work demonstrated that haploid adenylate cyclase (uac1) mutants display a constitutively filamentous phenotype. Suppressor mutants of...

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Published in:Molecular microbiology Vol. 41; no. 6; pp. 1365 - 1379
Main Authors: Mayorga, María E., Gold, Scott E.
Format: Journal Article
Language:English
Published: Oxford, UK Blackwell Science Ltd 01-09-2001
Blackwell Publishing Ltd
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Abstract The Basidiomycete fungus Ustilago maydis causes corn smut disease and alternates between a budding haploid saprophyte and a filamentous dikaryotic pathogen. Previous work demonstrated that haploid adenylate cyclase (uac1) mutants display a constitutively filamentous phenotype. Suppressor mutants of a uac1 disruption strain, named ubc for Ustilagobypass of cyclase, no longer require cAMP for the budding morphology. The ubc2 gene was isolated by complementation and is required for filamentous growth. The deduced amino acid sequence encoded by ubc2 shows localized homology to Sterile Alpha Motif (SAM), Ras Association (RA) and Src homology 3 (SH3) protein–protein interaction domains. A K78E missense mutation within the SAM domain, revealed a genetic interaction between ubc2 and ubc4, a pheromone‐responsive MAP kinase kinase kinase. This indicates involvement of ubc2 in the pheromone‐responsive MAP kinase cascade and ubc2 is required for pheromone‐responsive morphogenesis. The ubc2 gene is a critical virulence factor. Thus, ubc2 encodes a putative novel adaptor protein that may act directly upstream of the pheromone‐responsive MAP kinase cascade in U. maydis.
AbstractList The Basidiomycete fungus Ustilago maydis causes corn smut disease and alternates between a budding haploid saprophyte and a filamentous dikaryotic pathogen. Previous work demonstrated that haploid adenylate cyclase (uac1) mutants display a constitutively filamentous phenotype. Suppressor mutants of a uac1 disruption strain, named ubc for Ustilago bypass of cyclase, no longer require cAMP for the budding morphology. The ubc2 gene was isolated by complementation and is required for filamentous growth. The deduced amino acid sequence encoded by ubc2 shows localized homology to Sterile Alpha Motif (SAM), Ras Association (RA) and Src homology 3 (SH3) protein-protein interaction domains. A K78E missense mutation within the SAM domain, revealed a genetic interaction between ubc2 and ubc4, a pheromone-responsive MAP kinase kinase kinase. This indicates involvement of ubc2 in the pheromone-responsive MAP kinase cascade and ubc2 is required for pheromone-responsive morphogenesis. The ubc2 gene is a critical virulence factor. Thus, ubc2 encodes a putative novel adaptor protein that may act directly upstream of the pheromone-responsive MAP kinase cascade in U. maydis.
The Basidiomycete fungus Ustilago maydis causes corn smut disease and alternates between a budding haploid saprophyte and a filamentous dikaryotic pathogen. Previous work demonstrated that haploid adenylate cyclase (uac1) mutants display a constitutively filamentous phenotype. Suppressor mutants of a uac1 disruption strain, named ubc for Ustilagobypass of cyclase, no longer require cAMP for the budding morphology. The ubc2 gene was isolated by complementation and is required for filamentous growth. The deduced amino acid sequence encoded by ubc2 shows localized homology to Sterile Alpha Motif (SAM), Ras Association (RA) and Src homology 3 (SH3) protein–protein interaction domains. A K78E missense mutation within the SAM domain, revealed a genetic interaction between ubc2 and ubc4, a pheromone‐responsive MAP kinase kinase kinase. This indicates involvement of ubc2 in the pheromone‐responsive MAP kinase cascade and ubc2 is required for pheromone‐responsive morphogenesis. The ubc2 gene is a critical virulence factor. Thus, ubc2 encodes a putative novel adaptor protein that may act directly upstream of the pheromone‐responsive MAP kinase cascade in U. maydis.
The Basidiomycete fungus Ustilago maydis causes corn smut disease and alternates between a budding haploid saprophyte and a filamentous dikaryotic pathogen. Previous work demonstrated that haploid adenylate cyclase (uac1) mutants display a constitutively filamentous phenotype. Suppressor mutants of a uac1 disruption strain, named ubc for stilago ypass of yclase, no longer require cAMP for the budding morphology. The ubc2 gene was isolated by complementation and is required for filamentous growth. The deduced amino acid sequence encoded by ubc2 shows localized homology to Sterile Alpha Motif (SAM), Ras Association (RA) and Src homology 3 (SH3) protein-protein interaction domains. A K78E missense mutation within the SAM domain, revealed a genetic interaction between ubc2 and ubc4, a pheromone-responsive MAP kinase kinase kinase. This indicates involvement of ubc2 in the pheromone-responsive MAP kinase cascade and ubc2 is required for pheromone-responsive morphogenesis. The ubc2 gene is a critical virulence factor. Thus, ubc2 encodes a putative novel adaptor protein that may act directly upstream of the pheromone-responsive MAP kinase cascade in U. maydis.
The Basidiomycete fungus Ustilago maydis causes corn smut disease and alternates between a budding haploid saprophyte and a filamentous dikaryotic pathogen. Previous work demonstrated that haploid adenylate cyclase ( uac1 ) mutants display a constitutively filamentous phenotype. Suppressor mutants of a uac1 disruption strain, named ubc for U stilago b ypass of c yclase, no longer require cAMP for the budding morphology. The ubc2 gene was isolated by complementation and is required for filamentous growth. The deduced amino acid sequence encoded by ubc2 shows localized homology to Sterile Alpha Motif (SAM), Ras Association (RA) and Src homology 3 (SH3) protein–protein interaction domains. A K78E missense mutation within the SAM domain, revealed a genetic interaction between ubc2 and ubc4 , a pheromone‐responsive MAP kinase kinase kinase. This indicates involvement of ubc2 in the pheromone‐responsive MAP kinase cascade and ubc2 is required for pheromone‐responsive morphogenesis. The ubc2 gene is a critical virulence factor. Thus, ubc2 encodes a putative novel adaptor protein that may act directly upstream of the pheromone‐responsive MAP kinase cascade in U. maydis .
Author Gold, Scott E.
Mayorga, María E.
Author_xml – sequence: 1
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/11580841$$D View this record in MEDLINE/PubMed
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Snippet The Basidiomycete fungus Ustilago maydis causes corn smut disease and alternates between a budding haploid saprophyte and a filamentous dikaryotic pathogen....
The Basidiomycete fungus Ustilago maydis causes corn smut disease and alternates between a budding haploid saprophyte and a filamentous dikaryotic pathogen....
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SubjectTerms adaptor protein
Adaptor Proteins, Signal Transducing
Amino Acid Sequence
Base Sequence
Cloning, Molecular
DNA Primers - genetics
Fungal Proteins - chemistry
Fungal Proteins - genetics
Fungal Proteins - physiology
Gene Deletion
Genes, Fungal
Genetic Complementation Test
Mitogen-Activated Protein Kinases - genetics
Molecular Sequence Data
Mutation, Missense
Phenotype
Pheromones - pharmacology
Plant Diseases - microbiology
Protein Structure, Tertiary
Sequence Homology, Amino Acid
Temperature
ubc2 gene
Ustilago - genetics
Ustilago - growth & development
Ustilago - pathogenicity
Ustilago - physiology
Ustilago maydis
Virulence - genetics
Zea mays - microbiology
Title The ubc2 gene of Ustilago maydis encodes a putative novel adaptor protein required for filamentous growth, pheromone response and virulence
URI https://onlinelibrary.wiley.com/doi/abs/10.1046%2Fj.1365-2958.2001.02606.x
https://www.ncbi.nlm.nih.gov/pubmed/11580841
https://www.proquest.com/docview/196501088
https://search.proquest.com/docview/18120812
https://search.proquest.com/docview/71215851
Volume 41
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