Submitted to: American Journal of Potato Research
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 6/26/2003
Publication Date: 11/3/2003
Citation: SUTTLE, J.C. AUXIN-INDUCED SPROUT GROWTH INHIBITION: ROLE OF ENDOGENOUS ETHYLENE. AMERICAN JOURNAL OF POTATO RESEARCH. 2003. v. 80. p. 303-309.
Interpretive Summary: For an indeterminate period of time following harvest, potatoes will not sprout and are physiologically dormant. Dormancy is gradually lost during postharvest storage and the resultant sprouting is detrimental to the nutritional and processing qualities of potatoes. Because of this, sprouting results in severe financial loss to producers. Currently sprouting is controlled through the use of synthetic sprout inhibitors. The research being conducted in this lab is directed towards 1) identifying key physiological processes that naturally regulate tuber dormancy and, ultimately 2) modifying these processes genetically or chemically with naturally occurring sprout inhibitors thereby eliminated the need for artificial sprout suppression. Much of our current research concerns the roles of plant hormones in tuber dormancy regulation. Previous reports have demonstrated that both synthetic and naturally occurring auxin-like compounds inhibit sprout growth but their mechanism of action was unknown. In this paper, the role of the plant hormone ethylene (itself a powerful sprout inhibitor) in auxin-induced sprout growth inhibition was determined. The results show that although auxin treatment stimulated ethylene production by tubers, it played no role in auxin-induced sprout growth inhibition. These results also indicated that various auxins have potential as sprout control agents in stored potatoes.
Technical Abstract: The role of endogenous ethylene in auxin-mediated tuber sprout growth inhibition was determined in potato (Solanum tuberosum L. cv. Russet Burbank) minitubers. Treatment of tubers with biologically active auxins resulted in transient, dose-dependent increase in ethylene production and inhibition of sprout growth. Biologically inactive auxin analogs elicited neither response. Continuous exposure to >0.001 uL L-1 exogenous ethylene inhibited sprout growth in a dose-dependent manner with complete inhibition occurring at ethylene concentrations >u 1 uL L-1. In further studies with the active auxin alpha-naphthalene acetic acid (NAA), the role of ethylene in auxin-induced sprout growth inhibition was determined using ethylene biosynthesis and action inhibitors. The ethylene biosynthesis inhibitor aminoethoxyvinylglycine reduced NAA-induced ethylene biosynthesis by over 80% but had no effect on sprout growth inhibition. The non-competitive ethylene action inhibitor silver thiosulfate had no effect on NAA-induced sprout growth inhibition. Similarly, both the competitive ethylene action inhibitor 2,5-norbornadiene and the irreversible action inhibitor 1-methylcyclopropene were ineffective in reducing NAA-mediated sprout growth inhibition. Taken together, these results demonstrate that although ethylene is a potent growth inhibitor in potato whose synthesis is dramatically stimulated by auxin treatment, it does not play a role in auxin-mediated sprout growth inhibition.