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Arabidopsis HDA6 is required for freezing tolerance

► Arabidopsis histone deacetylase HDA6 is transcriptionally upregulated by cold. ► Cold-treated hda6 mutants show reduced freezing tolerance. ► Cold-treated hda6 mutants show increased freezing-caused electrolyte leakage. ► Several genes showed aberrant expression in the hda6 mutant after cold accli...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 2011-03, Vol.406 (3), p.414-419
Main Authors: To, Taiko Kim, Nakaminami, Kentaro, Kim, Jong-Myong, Morosawa, Taeko, Ishida, Junko, Tanaka, Maho, Yokoyama, Shigeyuki, Shinozaki, Kazuo, Seki, Motoaki
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Language:English
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Summary:► Arabidopsis histone deacetylase HDA6 is transcriptionally upregulated by cold. ► Cold-treated hda6 mutants show reduced freezing tolerance. ► Cold-treated hda6 mutants show increased freezing-caused electrolyte leakage. ► Several genes showed aberrant expression in the hda6 mutant after cold acclimation. ► HDA6 has a crucial role in acquiring freezing tolerance through cold acclimation. Many plants exhibit altered gene expression patterns in response to low nonfreezing temperatures and an increase in freezing tolerance in a phenomenon known as cold acclimation. Here we show, for the first time, that the histone deacetylase gene HDA6 is required for cold acclimation and freezing tolerance in Arabidopsis. HDA6 is transcriptionally upregulated during long-term cold treatment. Cold-treated hda6 mutants showed reduced freezing tolerance compared with the cold-treated wild-type plants. Freezing-caused electrolyte leakage increased in the cold-treated hda6 mutant. In contrast, the non-cold-treated hda6 mutants showed no significant difference in survivability and electrolyte leakage compared to wild-type plants. Transcriptome analysis identified the genes that showed aberrant expression in the hda6 mutant after cold acclimation. We conclude that HDA6 plays a critical role in regulating cold acclimation process that confers freezing resistance on Arabidopsis.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2011.02.058