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Exploring the cAMP/PKA pathway in the corn smut pathogen Ustilago maydis through serial analysis of gene expression Jabeen, Mehnaz
Abstract
Ustilago maydis is the causative agent of corn smut disease. The ability of the fungus to switch from budding to filamentous growth is required for pathogenesis. Mating type genes and signaling pathways (cAMP and MAPK) regulate morphogenesis and pathogenesis in U. maydis. A novel protein Hgll appears to be a downstream component of the cAMP pathway that influences cell morphology and sporulation during infection. The focus of this work was to further explore the role of the hgll gene in U. maydis through the construction of Serial Analysis of Gene Expression (SAGE) libraries to compare the transcriptomes of wild type and hgll mutant strains. The SAGE approach provides a quantitative gene expression profile and identifies differentially expressed genes. A key result of the SAGE work was the identification of a number of differentially expressed genes for putative zinc finger proteins in the transcriptome. A hypothetical protein encoded by the cthl (Cystine 3-histidine) gene had similarity to a zinc finger protein. This gene was disrupted to investigate its role in the morphology of U. maydis and in disease progression. Phenotypic characterization of the cthl mutant lead to the conclusion that the gene is required for normal morphology and completion of the life cycle in U. maydis, and that it might also be involved in the regulation of cell division. Overall, this work makes a contribution to our understanding of the cAMP signaling pathway in U. maydis and provides a wealth of expression data for future analysis.
Item Metadata
Title |
Exploring the cAMP/PKA pathway in the corn smut pathogen Ustilago maydis through serial analysis of gene expression
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Creator | |
Publisher |
University of British Columbia
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Date Issued |
2007
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Description |
Ustilago maydis is the causative agent of corn smut disease. The ability of the
fungus to switch from budding to filamentous growth is required for pathogenesis.
Mating type genes and signaling pathways (cAMP and MAPK) regulate morphogenesis
and pathogenesis in U. maydis. A novel protein Hgll appears to be a downstream
component of the cAMP pathway that influences cell morphology and sporulation during
infection. The focus of this work was to further explore the role of the hgll gene in U.
maydis through the construction of Serial Analysis of Gene Expression (SAGE) libraries
to compare the transcriptomes of wild type and hgll mutant strains. The SAGE approach
provides a quantitative gene expression profile and identifies differentially expressed
genes. A key result of the SAGE work was the identification of a number of
differentially expressed genes for putative zinc finger proteins in the transcriptome. A
hypothetical protein encoded by the cthl (Cystine 3-histidine) gene had similarity to a
zinc finger protein. This gene was disrupted to investigate its role in the morphology of
U. maydis and in disease progression. Phenotypic characterization of the cthl mutant
lead to the conclusion that the gene is required for normal morphology and completion of
the life cycle in U. maydis, and that it might also be involved in the regulation of cell
division. Overall, this work makes a contribution to our understanding of the cAMP
signaling pathway in U. maydis and provides a wealth of expression data for future
analysis.
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Genre | |
Type | |
Language |
eng
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Date Available |
2011-02-16
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Provider |
Vancouver : University of British Columbia Library
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Rights |
For non-commercial purposes only, such as research, private study and education. Additional conditions apply, see Terms of Use https://open.library.ubc.ca/terms_of_use.
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DOI |
10.14288/1.0100639
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URI | |
Degree | |
Program | |
Affiliation | |
Degree Grantor |
University of British Columbia
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Campus | |
Scholarly Level |
Graduate
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Aggregated Source Repository |
DSpace
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Rights
For non-commercial purposes only, such as research, private study and education. Additional conditions apply, see Terms of Use https://open.library.ubc.ca/terms_of_use.