Overexpression of a chromatin architecture-controlling AT-hook protein extends leaf longevity and increases the post-harvest storage life of plants.
Lim, Pyung Ok 1; Kim, Yumi 2; Breeze, Emily 3; Koo, Ja Choon 2,4,+; Woo, Hye Ryun 2,++; Ryu, Jong Sang 4; Park, Don Ha 2; Beynon, Jim 3; Tabrett, Alex 3; Buchanan-Wollaston, Vicky 3; Nam, Hong Gil 2,4,5,*
[Article] Plant Journal. 52(6):1140-1153, December 2007.

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Summary: Leaf senescence is the final stage of leaf development and is finely regulated via a complex genetic regulatory network incorporating both developmental and environmental factors. In an effort to identify negative regulators of leaf senescence, we screened activation-tagged Arabidopsis lines for mutants that exhibit a delayed leaf senescence phenotype. One of the mutants (ore7-1D) showed a highly significant delay of leaf senescence in the heterozygous state, leading to at least a twofold increase in leaf longevity. The activated gene (ORE7/ESC) encoded a protein with an AT-hook DNA-binding motif; such proteins are known to co-regulate transcription of genes through modification of chromatin architecture. We showed that ORE7/ESC, in addition to binding to a plant AT-rich DNA fragment, could also modify the chromatin architecture, as illustrated by an altered distribution of a histone-GFP fusion protein in the nucleus of the mutant. Globally altered gene expression, shown by microarray analysis, also indicated that activation of ORE7/ESC results in a younger condition in the mutant leaves. We propose that ectopically expressed ORE7/ESC is negatively regulating leaf senescence and suggest that the resulting chromatin alteration may have a role in controlling leaf longevity. Interestingly, activation of ORE7/ESC also led to a highly extended post-harvest storage life.

Copyright (C) 2007 Blackwell Publishing Ltd.