2026-07-16 理化学研究所,ミュンスター大学
HDA19が調節するアセチル化サイトとhda19変異体が耐塩性になるための必須遺伝子を同定
＜関連情報＞
- https://www.riken.jp/press/2026/20260716_2/index.html
- https://www.pnas.org/doi/10.1073/pnas.2534315123
HDA19によるヒストンH3.3のリジン27および36の脱アセチル化は、植物の塩ストレス感受性を調節する HDA19-mediated deacetylation of histone H3.3 at lysines 27 and 36 regulates plant sensitivity to salt stress
Florian Kotnik, Minoru Ueda, Akihiro Ito, +10 , and Iris Finkemeier
Proceedings of the National Academy of Sciences Published:July 13, 2026
DOI:https://doi.org/10.1073/pnas.2534315123
Abstract
Plants survive extreme environments through rapid chromatin reprogramming, yet the epigenetic marks that confer stress resilience remain poorly understood. Histone deacetylase HDA19 is a key epigenetic regulator in Arabidopsis, and hda19-deficient mutants display tolerance to multiple abiotic stresses, including drought, heat, and salinity. Using lysine acetylome profiling, we identified a noncanonical K27/K36 diacetylation mark on histone H3.3, among nine H3 variants, as a specific substrate of HDA19. Under salinity stress, this mark decreased in wild-type plants but increased in hda19 mutants, while other known H3 modifications were similarly affected in both genotypes. Mimicking constitutive diacetylation of H3.3K27/K36 through lysine-to-glutamine substitutions promoted accumulation of stress-responsive late embryogenesis abundant (LEA) proteins and conferred salinity tolerance in seedlings, phenocopying hda19 mutants. Furthermore, generating the lea7-1/lea29-1/rab18-1 triple mutant abolished hda19-dependent salinity tolerance, confirming the LEA proteins’ role downstream of HDA19. Our findings demonstrate that H3.3K27/K36 diacetylation, modulated by HDA19, drives LEA protein accumulation and enables plants to withstand environmental stress, revealing a core mechanism of plant stress resilience.
