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Transcriptomic profiling of Alternaria longipes invasion in tobacco reveals pathogenesis regulated by AlHK1, a group III histidine kinase

Tobacco brown spot, caused by Alternaria species, is a devastating tobacco disease. To explore the role of a group III histidine kinase (AlHK1) on A. longipes pathogenesis, the invasion progress of A. longipes was monitored. We found that the wild-type strain C-00 invaded faster than the AlHK1-disru...

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Autores principales: Yang, Juan, Yin, Zhi-Qun, Kang, Zi-Teng, Liu, Chen-Jian, Yang, Jin-Kui, Yao, Jian-Hua, Luo, Yi-Yong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5700128/
https://www.ncbi.nlm.nih.gov/pubmed/29167535
http://dx.doi.org/10.1038/s41598-017-16401-6
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author Yang, Juan
Yin, Zhi-Qun
Kang, Zi-Teng
Liu, Chen-Jian
Yang, Jin-Kui
Yao, Jian-Hua
Luo, Yi-Yong
author_facet Yang, Juan
Yin, Zhi-Qun
Kang, Zi-Teng
Liu, Chen-Jian
Yang, Jin-Kui
Yao, Jian-Hua
Luo, Yi-Yong
author_sort Yang, Juan
collection PubMed
description Tobacco brown spot, caused by Alternaria species, is a devastating tobacco disease. To explore the role of a group III histidine kinase (AlHK1) on A. longipes pathogenesis, the invasion progress of A. longipes was monitored. We found that the wild-type strain C-00 invaded faster than the AlHK1-disrupted strain HK∆4 in the early and middle infection stages and the reverse trend occurred in the late infection stage. Then, eight invasion transcriptomes were performed using RNA-Seq and 205 shared, 505 C-00 and 222 HK∆4 specific differentially expressed genes (DEGs) were identified. The annotation results showed seven antioxidant activity genes were specifically identified in the HKΔ4 DEGs. A subsequent experiment confirmed that HKΔ4 was more resistant to low concentrations oxidative stress than C-00. In addition, the results from 1) statistics for the number of DEGs, GO enriched terms, DEGs in clusters with rising trends, and 2) analyses of the expression patterns of some DEGs relevant for osmoadaptation and virulence showed that changes in C-00 infection existed mainly in the early and middle stages, while HKΔ4 infection arose mainly in the late stage. Our results reveal firstly the pathogenesis of A. longipes regulated by AlHK1 and provide useful insights into the fungal-plant interactions.
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spelling pubmed-57001282017-11-30 Transcriptomic profiling of Alternaria longipes invasion in tobacco reveals pathogenesis regulated by AlHK1, a group III histidine kinase Yang, Juan Yin, Zhi-Qun Kang, Zi-Teng Liu, Chen-Jian Yang, Jin-Kui Yao, Jian-Hua Luo, Yi-Yong Sci Rep Article Tobacco brown spot, caused by Alternaria species, is a devastating tobacco disease. To explore the role of a group III histidine kinase (AlHK1) on A. longipes pathogenesis, the invasion progress of A. longipes was monitored. We found that the wild-type strain C-00 invaded faster than the AlHK1-disrupted strain HK∆4 in the early and middle infection stages and the reverse trend occurred in the late infection stage. Then, eight invasion transcriptomes were performed using RNA-Seq and 205 shared, 505 C-00 and 222 HK∆4 specific differentially expressed genes (DEGs) were identified. The annotation results showed seven antioxidant activity genes were specifically identified in the HKΔ4 DEGs. A subsequent experiment confirmed that HKΔ4 was more resistant to low concentrations oxidative stress than C-00. In addition, the results from 1) statistics for the number of DEGs, GO enriched terms, DEGs in clusters with rising trends, and 2) analyses of the expression patterns of some DEGs relevant for osmoadaptation and virulence showed that changes in C-00 infection existed mainly in the early and middle stages, while HKΔ4 infection arose mainly in the late stage. Our results reveal firstly the pathogenesis of A. longipes regulated by AlHK1 and provide useful insights into the fungal-plant interactions. Nature Publishing Group UK 2017-11-22 /pmc/articles/PMC5700128/ /pubmed/29167535 http://dx.doi.org/10.1038/s41598-017-16401-6 Text en © The Author(s) 2017 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
Yang, Juan
Yin, Zhi-Qun
Kang, Zi-Teng
Liu, Chen-Jian
Yang, Jin-Kui
Yao, Jian-Hua
Luo, Yi-Yong
Transcriptomic profiling of Alternaria longipes invasion in tobacco reveals pathogenesis regulated by AlHK1, a group III histidine kinase
title Transcriptomic profiling of Alternaria longipes invasion in tobacco reveals pathogenesis regulated by AlHK1, a group III histidine kinase
title_full Transcriptomic profiling of Alternaria longipes invasion in tobacco reveals pathogenesis regulated by AlHK1, a group III histidine kinase
title_fullStr Transcriptomic profiling of Alternaria longipes invasion in tobacco reveals pathogenesis regulated by AlHK1, a group III histidine kinase
title_full_unstemmed Transcriptomic profiling of Alternaria longipes invasion in tobacco reveals pathogenesis regulated by AlHK1, a group III histidine kinase
title_short Transcriptomic profiling of Alternaria longipes invasion in tobacco reveals pathogenesis regulated by AlHK1, a group III histidine kinase
title_sort transcriptomic profiling of alternaria longipes invasion in tobacco reveals pathogenesis regulated by alhk1, a group iii histidine kinase
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5700128/
https://www.ncbi.nlm.nih.gov/pubmed/29167535
http://dx.doi.org/10.1038/s41598-017-16401-6
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