ABSTRACT
The plant hormone ethylene regulates developmental processes as well as responses to abiotic stress and pathogens. Ethylene influences interactions between the gray mold pathogen, Botrytis cinerea, and its hosts. The primary objective of this study was to determine the effect of ethylene on gray mold susceptibility of pear fruits. B. cinerea induced ethylene emission from infected pear fruits. As expected, ethylene production and softening of pear fruits were accelerated by propylene and inhibited by 1-methylcyclopropene (1-MCP), but these chemical treatments had a relatively small effect on the rate of lesion expansion after wound inoculation with B. cinerea. Cotreatment of pear fruits with 1-MCP and aminoethoxyvinylglycine (AVG) delayed the onset of ethylene emission well beyond the onset of lesion expansion. The trace amount of ethylene produced after inhibition with AVG and 1-MCP was at least partially produced via 1-aminocyclopropane-1-carboxylic acid. Gray mold susceptibility was cultivar-dependent; d'Anjou pears were more susceptible than Bartlett fruits. Storage enhanced the susceptibility of pear fruits. Virulence of the B. cinerea strain B05.10 on pear fruits was dependent on the polygalacturonase gene Bcpg1, but not on the pectin methylesterase gene Bcpme1. Thus, we conclude that, unlike exogenous manipulation of ethylene and associated changes in fruit softening, pectin catabolism plays a major role in gray mold susceptibility of pear.
Additional keywords:cell wall, host--microbe association, pathogenesis, phytohormone
