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ARS Home » Plains Area » Fargo, North Dakota » Edward T. Schafer Agricultural Research Center » Sugarbeet and Potato Research » Research » Publications at this Location » Publication #191475

Title: CHEMICALLY FORCED DORMANCY TERMINATION MIMICS NATURAL DORMANCY PROGRESSION IN POTATO TUBER MERISTEMS BY REDUCING ABA LEVELS AND MODIFYING EXPRESSION OF GENES INVOLVED IN REGULATING ABA CONTENT.

Author
item Destefano Beltran, Luis
item Knauber, Donna
item Young, Linda
item Suttle, Jeffrey

Submitted to: Journal of Experimental Botany
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 5/11/2006
Publication Date: 8/1/2006
Citation: Destefano Beltran, L.J., Knauber, D.C., Huckle, L.L., Suttle, J.C. 2006. Chemically forced dormancy termination mimics natural dormancy progression in potato tuber meristems by reducing ABA content and modifying expression of genes involved in regulating ABA synthesis and metabolism. Journal of Experimental Botany. 57(11):2879-2886.

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 thereby eliminating the need for artificial sprout suppression. The plant hormone abscisic acid (ABA) is the principal regulator of tuber dormancy initiation and maintenance. The internal processes controlling ABA content in tubers are unknown. In this paper, the effects of chemically forced dormancy termination on the contents and metabolism of ABA and the expression of each of these genes have been determined. Following BE treatment ABA levels rose briefly then declined dramatically. The decline in ABA content was accompanied by an increased rate of ABA metabolism. In general, levels of ABA biosynthetic genes were highest immediately after treatment when ABA content was highest. As ABA levels fell, expression of early biosynthetic genes declined while levels of genes encoding enzymes of ABA destruction increased. These results suggest that ABA content during tuber dormancy exit is controlled by a balance of synthesis and destruction.

Technical Abstract: The length of potato tuber dormancy depends on both the genotype and environmental conditions during growth and storage. Abscisic acid (ABA) has been shown to play a critical role in tuber dormancy control but the mechanisms regulating ABA content during dormancy as well as the sites of ABA synthesis and catabolism are unknown. Recently, a temporal correlation between changes in ABA content and certain ABA biosynthetic and catabolic genes has been reported in stored field tubers during physiological dormancy progression. However, the protracted length of natural dormancy progression complicated interpretation of these data. To address this issue, in this study the synthetic dormancy-terminating agent bromoethane (BE) was used to induce rapid and highly synchronous sprouting of dormant tubers. The endogenous ABA content of tuber meristems increased 2-fold 24 hours after BE treatment and then declined dramatically. By 7 days post-treatment, meristem ABA content had declined by >80%. Exogenous [3H]-ABA was readily metabolized by isolated meristems to phaseic and dihydro-phaseic acids. BE treatment resulted in nearly a 2-fold increase in the rate of ABA metabolism. A differential expression of both the StNCED and StCYP707A gene family members in meristems of BE-treated is consistent with a regulatory role for StNCED2 and the StCYP707A1 and StCYP707A2 genes. Our results show that the changes in ABA content observed during tuber dormancy progression are the result of a dynamic equilibrium of ABA biosynthesis and degradation that increasingly favors catabolism as dormancy progresses.