Transcriptomics

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Histone Deacetylase Complex 1 moderates stress responsiveness of germinating seeds via a histone-1-dependent process [RNA-Seq]


ABSTRACT: Plants respond to environmental challenges via a network of signalling pathways. Early responses prevent damage if the stress persists but delay growth in fluctuating conditions. Optimizing these trade-offs requires tunability of plant responsiveness to environmental signals. We have previously shown that Histone Deacetylation Complex 1 (HDC1), which interacts with multiple proteins in histone deacetylation complexes, regulates the sensitivity of Arabidopsis seedlings to salt and ABA, but the underlying mechanism remained elusive. Here we show that knockout of HDC1 enhances transcriptome re-programming prior to growth arrest of salt-treated seedlings and we identify two genes that mediate the effect of salt stress downstream of HDC1. HDC1 attenuates their transcriptional response via a dual mechanism involving H3K9/14 de-acetylation and H3K27 trimethylation. The latter, but not the former, was dependent on the linker histone H1, which interacts with HDC1 via the conserved RXT3 domain. However, a truncated RXT3-like version of HDC1 was not sufficient to recover H3K27me3 deposition in hdc1 suggesting that H1-aided recruitment H3K27 methylation machinery also requires the full-length HDC1-interacting deacetylases. The apparent paradox of repressive marks on stress-induced genes reveals an 'anti-panic' device that employs HDC1 as epigenetic moderator of stress responsiveness offering a leaver to tune stress sensitivity in plants. To identify genes underpinning salt tolerance in Arabidopsis thaliana and regulated by Histone Deacetylation Complex 1 (HDC1) we performed RNA-sequencing on HDC1 fully complemented line (HDC1c), hdc1-1 knock-out mutant (hdc1-1) and hdc1-1 mutant expressing the HDC1 domain RXT3 (RXT3). Seedlings were grown for 3 days on control plates and plates supplemented with 100 mM NaCl.

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE205893 | GEO | 2024/03/27

REPOSITORIES: GEO

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