Submitted to: Phytochemistry
Publication Type: Peer reviewed journal
Publication Acceptance Date: 12/10/2010
Publication Date: 6/1/2011
Publication URL: hdl.handle.net/10113/49420
Citation: Lafta, A.M., Fugate, K.K. 2011. Metabolic profile of wound-induced changes in primary carbon metabolism in sugarbeet root. Phytochemistry. 72:476-489. Interpretive Summary: Injury to plant products by harvest and storage operations induces respiration and increases consumption of plant storage compounds. The increased consumption of storage compounds is likely to require alterations in plant metabolism, although the nature of these alterations is unknown. To gain insight into how metabolism is altered to support wound-induced increases in respiration, changes in the concentrations of compounds that are involved in the respiratory degradation of sucrose to carbon dioxide were determined in sugarbeet roots in the four days following injury. Changes in respiration rate and metabolite concentrations indicated that metabolism was altered at the wound site and throughout the root in response to injury. The data suggested that in wounded tissue, several enzymes early in the degradative pathway from sucrose to carbon dioxide were limiting, but that these restrictions were overcome by use of metabolic bypasses that allowed compounds to enter the pathway at downstream locations. In the nonwounded tissue of wounded roots, the existing mechanisms for sucrose degradation to carbon dioxide appeared generally capable of supporting the small increase in respiration that occurred in these tissues. Although the mechanism by which respiration is regulated in wounded sugarbeet roots is unknown, changes in respiration were positively associated with indicators of the oxidation:reduction state of the tissue.
Technical Abstract: Injury to plant products induces respiration rate and increases the demand for respiratory substrates. Alterations in primary carbon metabolism are likely to support the elevated demand for respiratory substrates, although the nature of these alterations is unknown. To gain insight into the metabolic changes that occur to provide substrates for wound-induced increases in respiration, changes in the concentrations of compounds that are substrates, intermediates or cofactors in the respiratory pathway were determined in sugarbeet roots in the 4 d following injury. Both wounded and unwounded tissues of wounded roots were analyzed to provide information about localized and systemic changes that occur after wounding. In wounded tissue, respiration increased an average of 186%, fructose, glucose 6-phosphate, ADP and UDP concentrations increased, and fructose 1,6-bisphosphate, triose phosphate, citrate, isocitrate, succinate, ATP, UTP and NAD+ concentrations decreased. In the nonwounded tissue of wounded roots, respiration rate increased an average of 21%, glucose 6-phosphate, fructose 6-phosphate, glucose 1-phosphate and ADP concentrations increased, and isocitrate, UTP, NAD+, NADP+, and NADPH concentrations declined. Changes in respiration rate and metabolite concentrations indicated that localized and systemic changes in primary carbon metabolism occurred in response to injury. In wounded tissue, metabolite concentration changes suggested that activities of the early glycolytic enzymes, fructokinase, phosphofructokinase, phosphoglucose isomerase, and phosphoglucomutase were limiting carbon flow through glycolysis. These restrictions in the respiratory pathway, however, were likely overcome by use of metabolic bypasses that allowed carbon compounds to enter the pathway at glycolytic and tricarboxylic acid (TCA) cycle downstream locations. In nonwounded tissue of wounded roots, metabolic concentration changes suggested that glycolysis and the TCA cycle were generally capable of supporting the small systemic elevation in respiration rate. Although the mechanism by which respiration is regulated in wounded sugarbeet roots is unknown, localized and systemic elevations in respiration were positively associated with one or more indicators of cellular redox status.