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The Scientific World Journal
Volume 2012, Article ID 545784, 12 pages
Research Article

Inactivation of the Catalytic Subunit of cAMP-Dependent Protein Kinase A Causes Delayed Appressorium Formation and Reduced Pathogenicity of Colletotrichum gloeosporioides

1School of Biosciences and Biotechnology, Faculty of Science and Technology, Universiti Kebangsaan Malaysia, Selangor, 43600 Bangi, Malaysia
2Malaysia Genome Institute, Jalan Bangi Lama, Selangor, Kajang 43000, Malaysia

Received 2 November 2011; Accepted 30 November 2011

Academic Editors: S. Kikuchi and S. A. Stephenson

Copyright © 2012 Tri Puji Priyatno et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The cyclic AMP- (cAMP-) dependent protein kinase A signaling pathway is one of the major signaling pathways responsible for regulation of the morphogenesis and pathogenesis of several pathogenic fungi. To evaluate the role of this pathway in the plant pathogenic fungus, Colletotrichum gloeosporioides, the gene encoding the catalytic subunit of cAMP-dependent protein kinase A, CgPKAC, was cloned, inactivated, and the mutant was analyzed. Analysis of the Cgpkac mutant generated via gene replacement showed that the mutants were able to form appressoria; however, their formation was delayed compared to the wild type. In addition, the mutant conidia underwent bipolar germination after appressoria formation, but no appressoria were generated from the second germ tube. The mutants also showed reduced ability to adhere to a hydrophobic surface and to degrade lipids localized in the appressoria. Based on the number of lesions produced during a pathogenicity test, the mutant’s ability to cause disease in healthy mango fruits was reduced, which may be due to failure to penetrate into the fruit. These findings indicate that cAMP-dependent protein kinase A has an important role in regulating morphogenesis and is required for pathogenicity of C. gloeosporioides.