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| Status |
Public on Mar 27, 2024 |
| Title |
Histone Deacetylase Complex 1 moderates stress responsiveness of germinating seeds via a histone-1-dependent process [ChIP-Seq] |
| Organism |
Arabidopsis thaliana |
| Experiment type |
Genome binding/occupancy profiling by high throughput sequencing
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| Summary |
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 potential direct targets of HDC1 we isolated nuclei from control and salt-treated HDC1c and hdc1-1 seedlings and performed chromatin immunoprecipitation (ChIP) with an antibody against acetylated lysines 9 and 14 in histone 3 (anti-H3K9K14Ac).
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| Overall design |
To pinpoint possible candidates for a causal link between HDC1 function and salt sensitivity we combined the obtained ChIP-Seq profiles with RNAseq data and extracted genes that showed both stronger transcriptional activation and stronger H3K9K14 hyperacetylation upon salt in hdc1-1 compared to HDC1c.
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| Contributor(s) |
Perella G, Herzyk P, Amtmann A |
| Citation(s) |
37565540 |
| |
| Submission date |
Jun 13, 2022 |
| Last update date |
Mar 28, 2024 |
| Contact name |
Pawel Herzyk |
| E-mail(s) |
pawel.herzyk@glasgow.ac.uk
|
| Phone |
00441413303180
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| Organization name |
University of Glasgow
|
| Department |
College of Medical, Veterinary and Life Sciences
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| Lab |
Glasgow Polyomics
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| Street address |
Wolfson Wohl Cancer Research Centre, Garscube Estate
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| City |
Bearsden |
| ZIP/Postal code |
G61 1QH |
| Country |
United Kingdom |
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| Platforms (1) |
| GPL19580 |
Illumina NextSeq 500 (Arabidopsis thaliana) |
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| Samples (4)
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| GSM6241061 |
H3K9K14Ac, HDC1 KO mutant, control medium |
| GSM6241062 |
H3K9K14Ac, HDC1 KO mutant, 100 mM NaCl |
| GSM6241063 |
H3K9K14Ac, HDC1 KO mutant complemented with full length HDC1 gene sequence, control media |
| GSM6241064 |
H3K9K14Ac, HDC1 KO mutant complemented with full length HDC1 gene sequence, 100 mM NaCl |
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| This SubSeries is part of SuperSeries: |
| GSE206055 |
Histone Deacetylase Complex 1 moderates stress responsiveness of germinating seeds via a histone-1-dependent process |
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| Relations |
| BioProject |
PRJNA848923 |
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