Submitted to: Postharvest Biology and Technology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: January 28, 1998
Publication Date: N/A
Interpretive Summary: Muskmelons are an important horticultural crop in the United States. The muskmelons produced are primarily for domestic consumption, but significant quantities are exported to Canada. However, the main factor for limiting export is the short shelf-life and development of associated postharvest decays. Some fungi produce symptoms soon after infection while others may stay dormant for several weeks. Dormant or latent infections are not detectable at harvest and fruit are therefore packed and shipped to distant markets. Once the fruit are harvested, the fungus is triggered to become active. Consequently, the fruit may be severely rotted by the time the melons are displayed at the grocery store. Enzymes were obtained from a latent infection pathogen and a wound pathogen to determine and compare their ability to degrade muskmelon fruit tissue. Enzymes of the wound pathogens were able to degrade fruit tissue at all stages of development. However, enzymes of the latent infection pathogen were capable of degrading only tissue of fruit that had been harvested at maturity and stored for 10 days. The results of this study demonstrated that pectolytic enzymes play a major role in the degradation of fruit tissue during the decay process. The ability to degrade fruit tissue, as related to latent infections of muskmelon fruit, may be due to inhibitors in the immature fruit. This information may result in the genetic manipulation to enhance the fungal enzyme inhibitors for effective postharvest disease control without additional pesticide usage.
Partially-purified endo- and exo-polygalacturonases (PG) from two fungal pathogens (Phomopsis cucurbitae and Rhizopus stolonifer) were compared in relation to their ability to macerate cantaloupe tissue at different stages of fruit development. PG extracts from P. cucurbitae, a latent infection pathogen, produced little maceration until fruit were 40 days post-anthesis. In contrast, PGs from R. stolonifer, a wound pathogen, produced high levels of maceration at all stages of fruit development tested from 20 to 50 days post-anthesis. Both pathogens demonstrated highest levels of total PG activity in mesocarp and lowest levels in exocarp (peel) tissues. Isoelectrofocusing-polyacrylamide gel electrophoresis indicated two prominent PG isozymes in R. stolonifer and 9 isozymes in P. cucurbitae. Cell wall carbohydrate analysis showed a 6-fold decrease in galactosyl residue content between 10 and 50 days post-anthesis in uninfected fruit. Infected fruit showed 7- and 8-fold decreases in total non-cellulosic neutral sugar content when infected with P. cucurbitae and R. stolonifer, respectively. Significant decreases in cell wall rhamnosyl and arabinosyl residues occurred during infection of fruit with both pathogens. Our results support a role for cell wall pectin degradation during the infection process and decay of cantaloupe by these pathogens, and that the ability to macerate fruit tissue may be related to the latent infection phenomenon.