TaHDA1-mediated histone and non-histone deacetylation orchestrates drought tolerance in wheat.
TL;DR
A dual mechanism by which TaHDA1 integrates non-histone and histone deacetylation to balance growth and stress adaptation is uncovered, providing a promising target for breeding drought-resilient and nutritionally enhanced wheat varieties.
Abstract
Drought stress severely constrains wheat (Triticum aestivum L.) growth and productivity. Here, we identify the histone deacetylase TaHDA1 as a negative regulator of drought tolerance in wheat. We demonstrate that TaHDA1 interacts with and deacetylates the L-glutamate decarboxylase TaGAD1 at lysine 493, promoting its ubiquitination-dependent degradation and thereby suppressing γ-aminobutyric acid (GABA) accumulation. Loss of TaHDA1 function enhances TaGAD1 stability, increases GABA levels, and confers markedly improved drought tolerance, along with elevated grain GABA content. Integrated multi-omics analyses further reveal that TaHDA1 globally modulates H3K9 acetylation to orchestrate drought-responsive transcriptional programs. Notably, tahda1-ko mutants show a slight reduction in grain size under normal conditions, but maintain stable yield under drought stress. Our findings uncover a dual mechanism by which TaHDA1 integrates non-histone and histone deacetylation to balance growth and stress adaptation, providing a promising target for breeding drought-resilient and nutritionally enhanced wheat varieties.