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Auxin decreases chromatin accessibility through the TIR1/AFBs auxin signaling pathway in proliferative cells

Chromatin accessibility is closely associated with chromatin functions such as gene expression, DNA replication, and maintenance of DNA integrity. However, the relationship between chromatin accessibility and plant hormone signaling has remained elusive. Here, based on the correlation between chroma...

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Autores principales: Hasegawa, Junko, Sakamoto, Takuya, Fujimoto, Satoru, Yamashita, Tomoe, Suzuki, Takamasa, Matsunaga, Sachihiro
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5958073/
https://www.ncbi.nlm.nih.gov/pubmed/29773913
http://dx.doi.org/10.1038/s41598-018-25963-y
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author Hasegawa, Junko
Sakamoto, Takuya
Fujimoto, Satoru
Yamashita, Tomoe
Suzuki, Takamasa
Matsunaga, Sachihiro
author_facet Hasegawa, Junko
Sakamoto, Takuya
Fujimoto, Satoru
Yamashita, Tomoe
Suzuki, Takamasa
Matsunaga, Sachihiro
author_sort Hasegawa, Junko
collection PubMed
description Chromatin accessibility is closely associated with chromatin functions such as gene expression, DNA replication, and maintenance of DNA integrity. However, the relationship between chromatin accessibility and plant hormone signaling has remained elusive. Here, based on the correlation between chromatin accessibility and DNA damage, we used the sensitivity to DNA double strand breaks (DSBs) as an indicator of chromatin accessibility and demonstrated that auxin regulates chromatin accessibility through the TIR1/AFBs signaling pathway in proliferative cells. Treatment of proliferating plant cells with an inhibitor of the TIR1/AFBs auxin signaling pathway, PEO-IAA, caused chromatin loosening, indicating that auxin signaling functions to decrease chromatin accessibility. In addition, a transcriptome analysis revealed that several histone H4 genes and a histone chaperone gene, FAS1, are positively regulated through the TIR1/AFBs signaling pathway, suggesting that auxin plays a role in promoting nucleosome assembly. Analysis of the fas1 mutant of Arabidopsis thaliana confirmed that FAS1 is required for the auxin-dependent decrease in chromatin accessibility. These results suggest that the positive regulation of chromatin-related genes mediated by the TIR1/AFBs auxin signaling pathway enhances nucleosome assembly, resulting in decreased chromatin accessibility in proliferative cells.
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spelling pubmed-59580732018-05-21 Auxin decreases chromatin accessibility through the TIR1/AFBs auxin signaling pathway in proliferative cells Hasegawa, Junko Sakamoto, Takuya Fujimoto, Satoru Yamashita, Tomoe Suzuki, Takamasa Matsunaga, Sachihiro Sci Rep Article Chromatin accessibility is closely associated with chromatin functions such as gene expression, DNA replication, and maintenance of DNA integrity. However, the relationship between chromatin accessibility and plant hormone signaling has remained elusive. Here, based on the correlation between chromatin accessibility and DNA damage, we used the sensitivity to DNA double strand breaks (DSBs) as an indicator of chromatin accessibility and demonstrated that auxin regulates chromatin accessibility through the TIR1/AFBs signaling pathway in proliferative cells. Treatment of proliferating plant cells with an inhibitor of the TIR1/AFBs auxin signaling pathway, PEO-IAA, caused chromatin loosening, indicating that auxin signaling functions to decrease chromatin accessibility. In addition, a transcriptome analysis revealed that several histone H4 genes and a histone chaperone gene, FAS1, are positively regulated through the TIR1/AFBs signaling pathway, suggesting that auxin plays a role in promoting nucleosome assembly. Analysis of the fas1 mutant of Arabidopsis thaliana confirmed that FAS1 is required for the auxin-dependent decrease in chromatin accessibility. These results suggest that the positive regulation of chromatin-related genes mediated by the TIR1/AFBs auxin signaling pathway enhances nucleosome assembly, resulting in decreased chromatin accessibility in proliferative cells. Nature Publishing Group UK 2018-05-17 /pmc/articles/PMC5958073/ /pubmed/29773913 http://dx.doi.org/10.1038/s41598-018-25963-y Text en © The Author(s) 2018 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Hasegawa, Junko
Sakamoto, Takuya
Fujimoto, Satoru
Yamashita, Tomoe
Suzuki, Takamasa
Matsunaga, Sachihiro
Auxin decreases chromatin accessibility through the TIR1/AFBs auxin signaling pathway in proliferative cells
title Auxin decreases chromatin accessibility through the TIR1/AFBs auxin signaling pathway in proliferative cells
title_full Auxin decreases chromatin accessibility through the TIR1/AFBs auxin signaling pathway in proliferative cells
title_fullStr Auxin decreases chromatin accessibility through the TIR1/AFBs auxin signaling pathway in proliferative cells
title_full_unstemmed Auxin decreases chromatin accessibility through the TIR1/AFBs auxin signaling pathway in proliferative cells
title_short Auxin decreases chromatin accessibility through the TIR1/AFBs auxin signaling pathway in proliferative cells
title_sort auxin decreases chromatin accessibility through the tir1/afbs auxin signaling pathway in proliferative cells
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5958073/
https://www.ncbi.nlm.nih.gov/pubmed/29773913
http://dx.doi.org/10.1038/s41598-018-25963-y
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