Inhibition of ethylene biosynthesis by antisense ACC oxidase RNA prevents chilling injury in Charentais cantaloupe melons
ABSTRACT Non‐freezing low temperature storage causes injury to melons and most other fruit and vegetables of tropical and subtropical origin. We demonstrate here that ethylene suppression through an antisense ACC oxidase (ACO) gene considerably reduced the sensitivity of Charentais cantaloupe melons...
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Veröffentlicht in: | Plant, cell and environment cell and environment, 1999-12, Vol.22 (12), p.1579-1586 |
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Sprache: | eng |
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Zusammenfassung: | ABSTRACT
Non‐freezing low temperature storage causes injury to melons and most other fruit and vegetables of tropical and subtropical origin. We demonstrate here that ethylene suppression through an antisense ACC oxidase (ACO) gene considerably reduced the sensitivity of Charentais cantaloupe melons to chilling injury. In contrast to wild‐type fruit, antisense ACO melons did not develop the characteristic chilling injury of pitting and browning of the rind neither when stored at low temperature (3 weeks at 2 °C) nor upon rewarming. Treating antisense melons with 10 p.p.m. ethylene for more than 1 d prior to cold storage resulted in the restoration of chilling sensitivity. When the ethylene treatment was performed after cold storage, the chilling injury symptoms did not appear. The tolerance to chilling was associated with a lower accumulation of ethanol and acetaldehyde, reduced membrane deterioration and higher capacity of the fruit to remove active oxygen species. The activities of catalase, superoxide dismutase and peroxidase were markedly increased in antisense ACO fruit in comparison with wild‐type fruit, particulary upon rewarming and post‐storage ethylene treatment. Severe chilling injury symptoms were correlated with a lower activity of activated oxygen scavenging enzymes. These results demonstrate that ethylene acts in conjunction with low temperature to induce metabolic shifts that participate in the development of chilling injury. |
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ISSN: | 0140-7791 1365-3040 |
DOI: | 10.1046/j.1365-3040.1999.00509.x |