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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 #253587

Title: The Sprout Inhibitors Chlorpropham and 1, 4-dimethynaphthalene Alter Transcript Levels for KIP1 and KIP2

Author
item GLEICHSNER, ALYSSA - Pennsylvania State University
item HILLDORFER, LINDSAY - Pennsylvania State University
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: Gleichsner, A., Hilldorfer, L., Campbell, M.A., Suttle, J.C. 2010. The Sprout Inhibitors Chlorpropham and 1, 4-dimethynaphthalene Alter Transcript Levels for KIP1 and KIP2 [abstract.] Plant Biology 2010 Abstracts. P08062. Available: http://abstracts.aspb.org/pb2010/public/P08/P08062.html.

Interpretive Summary:

Technical Abstract: Chlorpropham (CIPC) and 1, 4-dimethylnaphthalene (DMN) are two inhibitors used to prevent sprouting in potatoes. CIPC is a synthetic compound which disrupts potato microtubules, preventing spindle formation. DMN is a natural compound isolated from potatoes whose pathway of action is currently unknown. To determine the effect of these treatments on cell division, a selection of genes, which induce or repress the cell cycle, were selected for analysis using Quantitative RealTime PCR (QT-PCR). cDNA was synthesized from RNA isolated from CIPC-treated, DMN-treated, and nondormant potato meristem tissue. QT-PCR tests were run using a StepOneTM Real Time PCR system and results were analyzed with Step One Software v2.0 to determine CT values on a log10 scale using alpha EF1 as a reference. It was found that CIPC treatment resulted in down-regulation of the KIP1 and KIP2 genes which are repressors of cell cycle activity. This is thought to be a response to the build-up of cells in the G2 phase of the cell cycle following treatment with CIPC. Results for DMN were inconclusive but showed up-regulation of both KIP genes, further emphasizing the differences between the two treatments and the manner by which they act to inhibit sprouting.