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Analysis of the transcriptomic, metabolomic, and gene regulatory responses to Puccinia sorghi in maize

Common rust, caused by Puccinia sorghi, is a widespread and destructive disease of maize. The Rp1‐D gene confers resistance to the P. sorghi IN2 isolate, mediating a hypersensitive cell death response (HR). To identify differentially expressed genes (DEGs) and metabolites associated with the compati...

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Autores principales: Kim, Saet‐Byul, Van den Broeck, Lisa, Karre, Shailesh, Choi, Hoseong, Christensen, Shawn A., Wang, Guan‐Feng, Jo, Yeonhwa, Cho, Won Kyong, Balint‐Kurti, Peter
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7938627/
https://www.ncbi.nlm.nih.gov/pubmed/33641256
http://dx.doi.org/10.1111/mpp.13040
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author Kim, Saet‐Byul
Van den Broeck, Lisa
Karre, Shailesh
Choi, Hoseong
Christensen, Shawn A.
Wang, Guan‐Feng
Jo, Yeonhwa
Cho, Won Kyong
Balint‐Kurti, Peter
author_facet Kim, Saet‐Byul
Van den Broeck, Lisa
Karre, Shailesh
Choi, Hoseong
Christensen, Shawn A.
Wang, Guan‐Feng
Jo, Yeonhwa
Cho, Won Kyong
Balint‐Kurti, Peter
author_sort Kim, Saet‐Byul
collection PubMed
description Common rust, caused by Puccinia sorghi, is a widespread and destructive disease of maize. The Rp1‐D gene confers resistance to the P. sorghi IN2 isolate, mediating a hypersensitive cell death response (HR). To identify differentially expressed genes (DEGs) and metabolites associated with the compatible (susceptible) interaction and with Rp1‐D‐mediated resistance in maize, we performed transcriptomics and targeted metabolome analyses of P. sorghi IN2‐infected leaves from the near‐isogenic lines H95 and H95:Rp1‐D, which differed for the presence of Rp1‐D. We observed up‐regulation of genes involved in the defence response and secondary metabolism, including the phenylpropanoid, flavonoid, and terpenoid pathways. Metabolome analyses confirmed that intermediates from several transcriptionally up‐regulated pathways accumulated during the defence response. We identified a common response in H95:Rp1‐D and H95 with an additional H95:Rp1‐D‐specific resistance response observed at early time points at both transcriptional and metabolic levels. To better understand the mechanisms underlying Rp1‐D‐mediated resistance, we inferred gene regulatory networks occurring in response to P. sorghi infection. A number of transcription factors including WRKY53, BHLH124, NKD1, BZIP84, and MYB100 were identified as potentially important signalling hubs in the resistance‐specific response. Overall, this study provides a novel and multifaceted understanding of the maize susceptible and resistance‐specific responses to P. sorghi.
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spelling pubmed-79386272021-03-16 Analysis of the transcriptomic, metabolomic, and gene regulatory responses to Puccinia sorghi in maize Kim, Saet‐Byul Van den Broeck, Lisa Karre, Shailesh Choi, Hoseong Christensen, Shawn A. Wang, Guan‐Feng Jo, Yeonhwa Cho, Won Kyong Balint‐Kurti, Peter Mol Plant Pathol Original Articles Common rust, caused by Puccinia sorghi, is a widespread and destructive disease of maize. The Rp1‐D gene confers resistance to the P. sorghi IN2 isolate, mediating a hypersensitive cell death response (HR). To identify differentially expressed genes (DEGs) and metabolites associated with the compatible (susceptible) interaction and with Rp1‐D‐mediated resistance in maize, we performed transcriptomics and targeted metabolome analyses of P. sorghi IN2‐infected leaves from the near‐isogenic lines H95 and H95:Rp1‐D, which differed for the presence of Rp1‐D. We observed up‐regulation of genes involved in the defence response and secondary metabolism, including the phenylpropanoid, flavonoid, and terpenoid pathways. Metabolome analyses confirmed that intermediates from several transcriptionally up‐regulated pathways accumulated during the defence response. We identified a common response in H95:Rp1‐D and H95 with an additional H95:Rp1‐D‐specific resistance response observed at early time points at both transcriptional and metabolic levels. To better understand the mechanisms underlying Rp1‐D‐mediated resistance, we inferred gene regulatory networks occurring in response to P. sorghi infection. A number of transcription factors including WRKY53, BHLH124, NKD1, BZIP84, and MYB100 were identified as potentially important signalling hubs in the resistance‐specific response. Overall, this study provides a novel and multifaceted understanding of the maize susceptible and resistance‐specific responses to P. sorghi. John Wiley and Sons Inc. 2021-02-28 /pmc/articles/PMC7938627/ /pubmed/33641256 http://dx.doi.org/10.1111/mpp.13040 Text en © 2021 The Authors. Molecular Plant Pathology published by British Society for Plant Pathology and John Wiley & Sons Ltd This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Articles
Kim, Saet‐Byul
Van den Broeck, Lisa
Karre, Shailesh
Choi, Hoseong
Christensen, Shawn A.
Wang, Guan‐Feng
Jo, Yeonhwa
Cho, Won Kyong
Balint‐Kurti, Peter
Analysis of the transcriptomic, metabolomic, and gene regulatory responses to Puccinia sorghi in maize
title Analysis of the transcriptomic, metabolomic, and gene regulatory responses to Puccinia sorghi in maize
title_full Analysis of the transcriptomic, metabolomic, and gene regulatory responses to Puccinia sorghi in maize
title_fullStr Analysis of the transcriptomic, metabolomic, and gene regulatory responses to Puccinia sorghi in maize
title_full_unstemmed Analysis of the transcriptomic, metabolomic, and gene regulatory responses to Puccinia sorghi in maize
title_short Analysis of the transcriptomic, metabolomic, and gene regulatory responses to Puccinia sorghi in maize
title_sort analysis of the transcriptomic, metabolomic, and gene regulatory responses to puccinia sorghi in maize
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7938627/
https://www.ncbi.nlm.nih.gov/pubmed/33641256
http://dx.doi.org/10.1111/mpp.13040
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