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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 #253586

Title: Chlorpropham and 1,4-dimethylnaphthalene Control Sprout Growth in Potato Tubers Through Different Mechanisms and not Through Prolongation of Dormancy

Author
item CAMPBELL, MICHAEL - Pennsylvania State University
item Suttle, Jeffrey

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 5/3/2010
Publication Date: 8/9/2010
Citation: Campbell, M.A., Suttle, J.C. 2010. Chlorpropham and 1,4-dimethylnaphthalene Control Sprout Growth in Potato Tubers Through Different Mechanisms and not Through Prolongation of Dormancy [abstract.] Plant Biology 2010 Abstracts. P04049. Available: http://abstracts.aspb.org/pb2010/public/P04/P04049.html

Interpretive Summary:

Technical Abstract: Application of Chlorpropham (CIPC) and 1,4-dimethylnaphthalene (DMN) to potato tubers prevents sprouting. CIPC prevents growth and suppresses sprouting by disruption of microtubules. DMN is a natural product originally isolated from potato skins suppresses sprout growth via an unknown mechanism. Because DMN is a natural compound associated with potato tubers there has been speculation that is prevents sprouting by extending the dormant state of treated tubers. We examined hormone levels and transcript profiles of potato tubers as they progressed through the natural dormancy cycle and after exposure to CIPC and DMN to ascertain whether theses sprout inhibitors function through a common mechanism or if they can be correlated to an extension of the dormant state. Abscisic acid (ABA) levels are elevated in dormant potato tissues but exposure to DMN or CIPC does not result in maintenance of this hormone. DMN and CIPC treatments altered transcript profiles for oxygen-related metabolism. DMN alone resulted in changes in transcripts in gene linked to osmotic regulation. There were significant differences in transcript profiles of CIPC and DMN suggesting that they prevent sprouting via different mechanisms. A comparison of transcript profiles induced by both sprout inhibitors and from tubers allowed to terminate dormancy naturally demonstrates that neither CIPC nor DMN prolong the dormant state but function through suppressive mechanisms of sprout growth.