Submitted to: American Society of Sugarbeet Technologists
Publication Type: Abstract Only
Publication Acceptance Date: 2/3/2003
Publication Date: 2/14/2003
Citation: KLOTZ, K.L., ANDERSON, M.D. CONTRIBUTION OF CYTOCHROME C AND ALTERNATIVE OXIDASE PATHWAYS TO RESPIRATORY SUCROSE LOSS IN POSTHARVEST SUGARBEET (BETA VULGARIS L.) ROOTS. ABSTRACTS OF JOINT MEETING OF INTERNATIONAL INSTITUTE FOR BEET RESEARCH AND THE AMERICAN SOCIETY OF SUGARBEET TECHNOLOGISTS. 2003. ABSTRACT p. 60. Interpretive Summary:
Technical Abstract: It is estimated that cellular respiration is responsible for 50 to 70% of the sucrose loss that occurs during postharvest storage of sugarbeet roots. Respiration occurs to provide the metabolic energy and carbon substrates needed to maintain healthy tissue during storage, heal wounds acquired during harvest and defend against pathogens. Two respiratory pathways, the cytochrome c oxidase pathway and the alternative oxidase pathway, contribute to total respiration. In sugarbeet, little information is available on the role of these two pathways in sucrose utilization and postharvest sucrose loss. This information, however, may prove useful to not only improve our understanding of this physiological process but may potentially provide insight into methods to reduce postharvest respiratory sucrose loss. Analyses of the changes in total respiration and the contribution of the two pathways in sugarbeet roots subjected to different storage conditions and durations, and in response to typical harvest stresses are in progress. Initial results indicate that the cytochrome c respiratory pathway predominates in healthy, nonstressed sugarbeet roots, as has been observed in most other plant species. Respiration is also greatest at the root surface. Oxygen utilization by epidermal tissue was approximately 3- to 4-fold higher than by internal cortical tissue, consistent with the idea that a higher level of energy is needed at the surface of the sugarbeet root for repair of mechanical damage and defense against pathogen attack.