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Postharvest Pathology and Mycotoxins

Spread of Aspergillus flavus in Cotton Bolls, Decay of Intercarpellary Membranes, and Production of Fungal Pectinases. R. L. Brown, Southern Regional Research Center, Food and Feed Safety Research Unit, 1100 Robert E. Lee Blvd., New Orleans, LA 70124; T. E. Cleveland, P. J. Cotty, and J. E. Mellon. Southern Regional Research Center, Food and Feed Safety Research Unit, 1100 Robert E. Lee Blvd., New Orleans, LA 70124. Phytopathology 82:462-467. Accepted for publication 12 December 1991. This article is in the public domain and not copyrightable. It may be freely reprinted with customary crediting of the source. The American Phytopathological Society, 1992. DOI: 10.1094/Phyto-82-462.

Developing cotton bolls were wound-inoculated with high- and low-virulence strains of Aspergillus flavus and also with A. nidulans FGSC4 and were examined at maturity for disease symptoms and fungal pectinases. All inoculated bolls showed tight-lock formation (failure of mature locks to expand and fluff out), but specific strain-related differences in intercarpellary membrane decay were observed. A highly significant correlation was found between fungal spread to adjacent locules and decay of intercarpellary membranes in bolls inoculated with A. flavus. The high-virulence strain caused severe deterioration of intercarpellary membranes and produced three polygalacturonase activities in bolls and culture. A pectinesterase also produced by this strain in culture was not detected in inoculated bolls. The low-virulence strain caused less severe deterioration of membranes and was lacking a major A. flavus endopolygalacturonase, P2C. A. nidulans produced pectinases in culture but failed to do so in cotton bolls and caused very little damage to intercarpellary membranes. The endopolygalacturonase, P2C, was the only pectinase produced by the tested strains that was not catabolite-repressed in culture by the simple sugars common in developing cotton bolls. Results support a role for A. flavus pectinases in interlocule fungal spread in bolls and suggest that the lack of catabolite repression of P2C facilitates this role.