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Histone Deacetylase Activity and Phytotoxic Effects Following Exposure of Duckweed (Lemna pausicostata L.) to Apicidin and HC-Toxin

December 2001 , Volume 91 , Number  12
Pages  1,141 - 1,148

Hamed K. Abbas , John W. Gronwald , Kathryn L. Plaisance , Rex N. Paul , and Yin W. Lee

First and fourth authors: U.S. Department of Agriculture-Agricultural Research Service, Southern Weed Science Research Unit, Stoneville, MS 38776; second author: U.S. Department of Agriculture-Agricultural Research Service, Plant Science Research Unit, St. Paul, MN 55108; third author: Department of Agronomy and Plant Genetics, University of Minnesota, St. Paul, MN 55108; and fifth author: School of Agricultural Biotechnology and Research Center for New Bio-materials in Agriculture, Seoul National University, Suwon 441-744, Korea

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Accepted for publication 23 August 2001.

The effects of two cyclic tetrapeptide fungal toxins, apicidin (from Fusarium spp.) and HC-toxin (from Cochliobolus carbonum), on duckweed (Lemna pausicostata L.) were examined. Both toxins inhibited histone deacetylase (HD) activity from duckweed plantlets; the effective concentration (EC50) for inhibition of HD was 5.6 and 1.1 μM for apicidin and HC-toxin, respectively. Approximately 65 and 85% of in vitro HD activity was inhibited by 50 μM apicidin or HC-toxin, respectively. Exposing duckweed for 72 h to apicidin or HC-toxin (25 or 50 μM) enhanced cellular leakage, impaired chlorophyll synthesis, and inhibited growth (cell division). At equivalent concentrations, the effects of HC-toxin were more pronounced than those of apicidin. In fronds, 72 h of exposure to 50 μM apicidin resulted in chloroplast deterioration indicated by loss of orientation and excess starch accumulation. In roots, a 72-h treatment with 50 μM apicidin resulted in the loss of the root cap and increased vacuolization and starch accumulation in plastids.

The American Phytopathological Society, 2001