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H3K4 monomethylation dictates nucleosome dynamics and chromatin remodeling at stress-responsive genes.

Nadal-Ribelles M, Mas G, Millán-Zambrano G, Solé C, Ammerer G, Chávez S, Posas F, de Nadal E - Nucleic Acids Res. (2015)

Bottom Line: Hog1 targets the RSC chromatin remodeling complex to stress-responsive genes and rsc deficient cells display reduced induction of gene expression.Monomethylation of H3K4 is specifically inhibiting RSC-independent chromatin remodeling and thus, it prevents osmostress-induced gene expression.Our findings point to a novel role for H3K4 monomethylation in dictating the specificity of chromatin remodeling, adding an extra layer of regulation to the transcriptional stress response.

View Article: PubMed Central - PubMed

Affiliation: Cell signaling unit, Departament de Ciències Experimentals i de la Salut, Universitat Pompeu Fabra (UPF), Parc de Recerca Biomèdica de Barcelona (PRBB), Barcelona, Spain.

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Set1 prevents chromatin remodeling in the absence of RSC. Set1 mediated methylation of H3K4 inhibits chromatin remodeling in RSC mutants. The indicated strains were grown in YPD at 25ºC until OD660 0.5 and shifted to under non-permissive temperature (37ºC) for 2 h. Nucleosome positioning at chromosomal STL1 was assessed by MNase digestion of chromatin of wild type (wt), set1Δ, rsc9ts or rsc9tsset1Δ cells that were treated (gray triangles) or not (black triangles) with 0.4 M NaCl for 10 min. MNase digested DNA was isolated and analyzed using qPCR with tiled primers spanning the promoter and coding regions (-600 bp upstream and 900 bp downstream of the transcription start site (TSS), respectively). The normalized nucleosome occupancy is shown (x-axis) relative to the TSS. Data represent the mean and standard deviation of three independent experiments.
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Figure 2: Set1 prevents chromatin remodeling in the absence of RSC. Set1 mediated methylation of H3K4 inhibits chromatin remodeling in RSC mutants. The indicated strains were grown in YPD at 25ºC until OD660 0.5 and shifted to under non-permissive temperature (37ºC) for 2 h. Nucleosome positioning at chromosomal STL1 was assessed by MNase digestion of chromatin of wild type (wt), set1Δ, rsc9ts or rsc9tsset1Δ cells that were treated (gray triangles) or not (black triangles) with 0.4 M NaCl for 10 min. MNase digested DNA was isolated and analyzed using qPCR with tiled primers spanning the promoter and coding regions (-600 bp upstream and 900 bp downstream of the transcription start site (TSS), respectively). The normalized nucleosome occupancy is shown (x-axis) relative to the TSS. Data represent the mean and standard deviation of three independent experiments.

Mentions: To analyze the role of histone methylation in nucleosome remodeling following osmostress, we then analyzed the nucleosome positioning at the STL1 locus by Micrococcal Nuclease (MNase) digestion of chromatin before and after stress in wild type, rsc9ts, set1Δ and rsc9tsset1Δ strains. As described, RSC action affects nucleosome position in basal conditions (37,38). We found that, as expected, inactivation of Rsc9 prevented the dramatic changes in chromatin structure observed upon stress in the wild type strain. Nevertheless, deletion of SET1 in the rsc9ts background partially restored such chromatin remodeling (Figure 2). Together, our data suggest that in cells deficient for the RSC complex, methylation by Set1 prevents chromatin reorganization upon stress.


H3K4 monomethylation dictates nucleosome dynamics and chromatin remodeling at stress-responsive genes.

Nadal-Ribelles M, Mas G, Millán-Zambrano G, Solé C, Ammerer G, Chávez S, Posas F, de Nadal E - Nucleic Acids Res. (2015)

Set1 prevents chromatin remodeling in the absence of RSC. Set1 mediated methylation of H3K4 inhibits chromatin remodeling in RSC mutants. The indicated strains were grown in YPD at 25ºC until OD660 0.5 and shifted to under non-permissive temperature (37ºC) for 2 h. Nucleosome positioning at chromosomal STL1 was assessed by MNase digestion of chromatin of wild type (wt), set1Δ, rsc9ts or rsc9tsset1Δ cells that were treated (gray triangles) or not (black triangles) with 0.4 M NaCl for 10 min. MNase digested DNA was isolated and analyzed using qPCR with tiled primers spanning the promoter and coding regions (-600 bp upstream and 900 bp downstream of the transcription start site (TSS), respectively). The normalized nucleosome occupancy is shown (x-axis) relative to the TSS. Data represent the mean and standard deviation of three independent experiments.
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Related In: Results  -  Collection

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Figure 2: Set1 prevents chromatin remodeling in the absence of RSC. Set1 mediated methylation of H3K4 inhibits chromatin remodeling in RSC mutants. The indicated strains were grown in YPD at 25ºC until OD660 0.5 and shifted to under non-permissive temperature (37ºC) for 2 h. Nucleosome positioning at chromosomal STL1 was assessed by MNase digestion of chromatin of wild type (wt), set1Δ, rsc9ts or rsc9tsset1Δ cells that were treated (gray triangles) or not (black triangles) with 0.4 M NaCl for 10 min. MNase digested DNA was isolated and analyzed using qPCR with tiled primers spanning the promoter and coding regions (-600 bp upstream and 900 bp downstream of the transcription start site (TSS), respectively). The normalized nucleosome occupancy is shown (x-axis) relative to the TSS. Data represent the mean and standard deviation of three independent experiments.
Mentions: To analyze the role of histone methylation in nucleosome remodeling following osmostress, we then analyzed the nucleosome positioning at the STL1 locus by Micrococcal Nuclease (MNase) digestion of chromatin before and after stress in wild type, rsc9ts, set1Δ and rsc9tsset1Δ strains. As described, RSC action affects nucleosome position in basal conditions (37,38). We found that, as expected, inactivation of Rsc9 prevented the dramatic changes in chromatin structure observed upon stress in the wild type strain. Nevertheless, deletion of SET1 in the rsc9ts background partially restored such chromatin remodeling (Figure 2). Together, our data suggest that in cells deficient for the RSC complex, methylation by Set1 prevents chromatin reorganization upon stress.

Bottom Line: Hog1 targets the RSC chromatin remodeling complex to stress-responsive genes and rsc deficient cells display reduced induction of gene expression.Monomethylation of H3K4 is specifically inhibiting RSC-independent chromatin remodeling and thus, it prevents osmostress-induced gene expression.Our findings point to a novel role for H3K4 monomethylation in dictating the specificity of chromatin remodeling, adding an extra layer of regulation to the transcriptional stress response.

View Article: PubMed Central - PubMed

Affiliation: Cell signaling unit, Departament de Ciències Experimentals i de la Salut, Universitat Pompeu Fabra (UPF), Parc de Recerca Biomèdica de Barcelona (PRBB), Barcelona, Spain.

Show MeSH
Related in: MedlinePlus