Biology subjects

Ishida, J.

Publications and source records attributed to Ishida, J..

3 recordsLinked to original sources

bioRxiv2025

HDA19-mediated deacetylation of histone H3.3 lysine 27 and 36 regulates plant sensitivity to salt stress

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 non-canonical K27/K36 di-acetylation 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 di-acetylation of H3.3 K27/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 H3.3 K27/K36 di-acetylation, modulated by HDA19, drives LEA protein accumulation and enables plants to withstand environmental stress, revealing a previously unknown core mechanism of plant stress resilience. Significance statementHistone acetylation is crucial for regulating chromatin states and transcription, yet the specific histone codes controlled by histone deacetylases and acetyltransferases during plant stress acclimation remain unclear. Arabidopsis mutants lacking histone deacetylase 19 show enhanced tolerance to drought, heat, and salinity. Using acetylome profiling and genetic analyses, we identify a previously unknown di-acetylation of histone H3.3 at lysines 27 and 36 as a key epigenetic switch activating late embryogenesis abundant proteins essential for salt tolerance in seedlings. This discovery reveals a novel mechanism linking histone H3.3 K27/K36 di-acetylation to stress-resilient protein accumulation, offering new insights into epigenetic control of plant stress responses and informing strategies to improve crop resilience under climate change.

plant biology↗

bioRxiv2025

TCP3-mediated regulation of cell expansion in Arabidopsis thaliana

(1) Cell expansion is crucial for organ morphogenesis in multicellular organisms. Apoplast acidification triggers plant cell expansion. Plant hormones and transcription factors such as TEOSINTE BRANCHED, CYCLOIDEA, and PROLIFERATING CELL NUCLEAR ANTIGEN BINDING FACTORs (TCPs) control cell expansion. However, details regarding the regulatory mechanism of cell expansion for organ morphogenesis remain unclear. (2) In this study, we used molecular, biochemical, cellular, genetic, atomic force microscopy, and tensile testing analyses and showed that miR319-targeted TCPs integrated cell expansion with organ morphogenesis in Arabidopsis thaliana. (3) We found that TCPs directly induce the expression of genes encoding cell wall loosening proteins and SMALL AUXIN UP RNAs (SAURs), activators of plasma membrane-localized H+-ATPases. TCP-mediated activation of plasma membrane- localized H+-ATPases stimulates apoplast acidification, reduce cell stiffness, promote cell expansion, and thus exaggerate elongation of the hypocotyl. Ectopic expression of a SAUR gene in sextuple tcp mutant plants substantially recovered the hypocotyl morphology of the tcp mutant, providing genetic evidence of TCP-mediated SAUR regulation. (4) Collectively, our data show that TCPs regulate apoplast acidification for cell expansion.

plant biology↗

bioRxiv2019

Cables2 Is a novel Smad2-regulatory factor essential for early embryonic development in mice

CDK5 and Abl enzyme substrate 2 (Cables2), a member of the Cables family that has a C-terminal cyclin box-like domain, is widely expressed in adult mouse tissues. However, the physiological role of Cables2 in vivo is unknown. We show here that Cables2-deficiency causes post-gastrulation embryonic lethality in mice. The mutant embryos progress to gastrulation, but then arrest, and fail to grow. Analysis of gene expression patterns reveals that formation of the anterior visceral endoderm and the primitive streak is impaired in Cables2-deficient embryos. Tetraploid complementation analyses support the critical requirement of Cables2 in both the epiblast and visceral endoderm for progression of embryogenesis. In addition, we show that Cables2 physically interacts with a key mediator of the canonical Nodal pathway, Smad2, and augments its transcriptional activity. These findings provide novel insights into the essential role of Cables2 in the early embryonic development in mice.

developmental biology↗