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UvKmt6-mediated H3K27 trimethylation is required for development, pathogenicity, and stress response in Ustilaginoidea virens

Polycomb repressive complex 2 (PRC2) is responsible for the trimethylation of lysine 27 of histone H3 (H3K27me3)-mediated transcriptional silencing. At present, its biological roles in the devastating rice pathogenic fungus Ustilaginoidea virens remain unclear. In this study, we analyzed the functio...

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Autores principales: Meng, Shuai, Liu, Zhiquan, Shi, Huanbin, Wu, Zhongling, Qiu, Jiehua, Wen, Hui, Lin, Fucheng, Tao, Zeng, Luo, Chaoxi, Kou, Yanjun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8667953/
https://www.ncbi.nlm.nih.gov/pubmed/34895056
http://dx.doi.org/10.1080/21505594.2021.2008150
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author Meng, Shuai
Liu, Zhiquan
Shi, Huanbin
Wu, Zhongling
Qiu, Jiehua
Wen, Hui
Lin, Fucheng
Tao, Zeng
Luo, Chaoxi
Kou, Yanjun
author_facet Meng, Shuai
Liu, Zhiquan
Shi, Huanbin
Wu, Zhongling
Qiu, Jiehua
Wen, Hui
Lin, Fucheng
Tao, Zeng
Luo, Chaoxi
Kou, Yanjun
author_sort Meng, Shuai
collection PubMed
description Polycomb repressive complex 2 (PRC2) is responsible for the trimethylation of lysine 27 of histone H3 (H3K27me3)-mediated transcriptional silencing. At present, its biological roles in the devastating rice pathogenic fungus Ustilaginoidea virens remain unclear. In this study, we analyzed the function of a putative PRC2 catalytic subunit UvKmt6. The results showed that disruption of UvKMT6 resulted in reduced growth, conidiation and pathogenicity in U. virens. Furthermore, UvKmt6 is essential for establishment of H3K27me3 modification, which covers 321 genes in the genome. Deletion of UvKMT6 led to transcriptional derepression of 629 genes, 140 of which were occupied with H3K27me3 modification. Consistent with RNA-seq and ChIP-seq analysis, UvKmt6 was further confirmed to participate in the transcriptional repression of genes encoding effectors and genes associated with secondary metabolites production, such as PKSs, NRPSs and Cytochrome P450s. Notably, we found that UvKmt6 is involved in transcriptional repression of oxidative, osmotic, cell wall and nutrient starvation stresses response-related genes. From the perspective of gene expression and phenotype, in addition to the relatively conservative role in fungal development, virulence and production of secondary metabolites, we further reported that UvKmt6-mdediated H3K27me3 plays a critical role in the response to various stresses in U. virens.
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spelling pubmed-86679532021-12-14 UvKmt6-mediated H3K27 trimethylation is required for development, pathogenicity, and stress response in Ustilaginoidea virens Meng, Shuai Liu, Zhiquan Shi, Huanbin Wu, Zhongling Qiu, Jiehua Wen, Hui Lin, Fucheng Tao, Zeng Luo, Chaoxi Kou, Yanjun Virulence Research Paper Polycomb repressive complex 2 (PRC2) is responsible for the trimethylation of lysine 27 of histone H3 (H3K27me3)-mediated transcriptional silencing. At present, its biological roles in the devastating rice pathogenic fungus Ustilaginoidea virens remain unclear. In this study, we analyzed the function of a putative PRC2 catalytic subunit UvKmt6. The results showed that disruption of UvKMT6 resulted in reduced growth, conidiation and pathogenicity in U. virens. Furthermore, UvKmt6 is essential for establishment of H3K27me3 modification, which covers 321 genes in the genome. Deletion of UvKMT6 led to transcriptional derepression of 629 genes, 140 of which were occupied with H3K27me3 modification. Consistent with RNA-seq and ChIP-seq analysis, UvKmt6 was further confirmed to participate in the transcriptional repression of genes encoding effectors and genes associated with secondary metabolites production, such as PKSs, NRPSs and Cytochrome P450s. Notably, we found that UvKmt6 is involved in transcriptional repression of oxidative, osmotic, cell wall and nutrient starvation stresses response-related genes. From the perspective of gene expression and phenotype, in addition to the relatively conservative role in fungal development, virulence and production of secondary metabolites, we further reported that UvKmt6-mdediated H3K27me3 plays a critical role in the response to various stresses in U. virens. Taylor & Francis 2021-12-11 /pmc/articles/PMC8667953/ /pubmed/34895056 http://dx.doi.org/10.1080/21505594.2021.2008150 Text en © 2021 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. https://creativecommons.org/licenses/by/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Paper
Meng, Shuai
Liu, Zhiquan
Shi, Huanbin
Wu, Zhongling
Qiu, Jiehua
Wen, Hui
Lin, Fucheng
Tao, Zeng
Luo, Chaoxi
Kou, Yanjun
UvKmt6-mediated H3K27 trimethylation is required for development, pathogenicity, and stress response in Ustilaginoidea virens
title UvKmt6-mediated H3K27 trimethylation is required for development, pathogenicity, and stress response in Ustilaginoidea virens
title_full UvKmt6-mediated H3K27 trimethylation is required for development, pathogenicity, and stress response in Ustilaginoidea virens
title_fullStr UvKmt6-mediated H3K27 trimethylation is required for development, pathogenicity, and stress response in Ustilaginoidea virens
title_full_unstemmed UvKmt6-mediated H3K27 trimethylation is required for development, pathogenicity, and stress response in Ustilaginoidea virens
title_short UvKmt6-mediated H3K27 trimethylation is required for development, pathogenicity, and stress response in Ustilaginoidea virens
title_sort uvkmt6-mediated h3k27 trimethylation is required for development, pathogenicity, and stress response in ustilaginoidea virens
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8667953/
https://www.ncbi.nlm.nih.gov/pubmed/34895056
http://dx.doi.org/10.1080/21505594.2021.2008150
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