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Transcription Profiling of Rice Panicle in Response to Crude Toxin Extract of Ustilaginoidea virens

Ustilaginoidea virens infects rice, causing rice false smut disease and reduced yields. During its growth, U. virens can also produce some toxins but less is known about the response mechanisms of the plant to U. virens toxins. U. virens toxins can inhibit the accumulation of total sugar in rice pan...

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Autores principales: Fu, Rongtao, Chen, Cheng, Wang, Jian, Liu, Yao, Zhao, Liyu, Lu, Daihua
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9135463/
https://www.ncbi.nlm.nih.gov/pubmed/35633715
http://dx.doi.org/10.3389/fmicb.2022.701489
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author Fu, Rongtao
Chen, Cheng
Wang, Jian
Liu, Yao
Zhao, Liyu
Lu, Daihua
author_facet Fu, Rongtao
Chen, Cheng
Wang, Jian
Liu, Yao
Zhao, Liyu
Lu, Daihua
author_sort Fu, Rongtao
collection PubMed
description Ustilaginoidea virens infects rice, causing rice false smut disease and reduced yields. During its growth, U. virens can also produce some toxins but less is known about the response mechanisms of the plant to U. virens toxins. U. virens toxins can inhibit the accumulation of total sugar in rice panicles. We used RNA sequencing to analyze the differential expression profile induced by infiltrating crude toxins into early growth-stage rice panicles. We compared the transcriptomes of the control and crude toxin-treated rice panicles and determined variable transcriptional responses under the action of the crude toxins. A total of 6,127 differentially expressed genes (DEGs) were identified. Among these genes, 3,150 were upregulated and 2,977 were downregulated. Gene Ontology (GO) and metabolic pathway enrichment analyses indicated that U. virens toxins mainly influenced glycometabolism, amino acid metabolism, and secondary metabolism of rice panicles. DEG analysis showed that the gene expression levels of 10 transcription factor families were significantly changed. Genes involved in phenylpropanoid biosynthesis, flavonoid biosynthesis, sugar transporters, and starch synthesis-related were significantly downregulated, including cytochrome P450, beta-glucosidase, CHS1, sucrose transporters, SWEETs, starch-branching enzymes, and UDP-glucose pyrophosphorylase. However, genes involved in programmed cell death (PCD) were significantly upregulated and contained cytochrome c, metacaspase, and protein kinase genes. The results indicate that U. virens toxins may act as the pathogenic factors to reduce stress resistance, disrupt total sugar accumulation and starch formation, and induce PCD.
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spelling pubmed-91354632022-05-27 Transcription Profiling of Rice Panicle in Response to Crude Toxin Extract of Ustilaginoidea virens Fu, Rongtao Chen, Cheng Wang, Jian Liu, Yao Zhao, Liyu Lu, Daihua Front Microbiol Microbiology Ustilaginoidea virens infects rice, causing rice false smut disease and reduced yields. During its growth, U. virens can also produce some toxins but less is known about the response mechanisms of the plant to U. virens toxins. U. virens toxins can inhibit the accumulation of total sugar in rice panicles. We used RNA sequencing to analyze the differential expression profile induced by infiltrating crude toxins into early growth-stage rice panicles. We compared the transcriptomes of the control and crude toxin-treated rice panicles and determined variable transcriptional responses under the action of the crude toxins. A total of 6,127 differentially expressed genes (DEGs) were identified. Among these genes, 3,150 were upregulated and 2,977 were downregulated. Gene Ontology (GO) and metabolic pathway enrichment analyses indicated that U. virens toxins mainly influenced glycometabolism, amino acid metabolism, and secondary metabolism of rice panicles. DEG analysis showed that the gene expression levels of 10 transcription factor families were significantly changed. Genes involved in phenylpropanoid biosynthesis, flavonoid biosynthesis, sugar transporters, and starch synthesis-related were significantly downregulated, including cytochrome P450, beta-glucosidase, CHS1, sucrose transporters, SWEETs, starch-branching enzymes, and UDP-glucose pyrophosphorylase. However, genes involved in programmed cell death (PCD) were significantly upregulated and contained cytochrome c, metacaspase, and protein kinase genes. The results indicate that U. virens toxins may act as the pathogenic factors to reduce stress resistance, disrupt total sugar accumulation and starch formation, and induce PCD. Frontiers Media S.A. 2022-05-12 /pmc/articles/PMC9135463/ /pubmed/35633715 http://dx.doi.org/10.3389/fmicb.2022.701489 Text en Copyright © 2022 Fu, Chen, Wang, Liu, Zhao and Lu. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Microbiology
Fu, Rongtao
Chen, Cheng
Wang, Jian
Liu, Yao
Zhao, Liyu
Lu, Daihua
Transcription Profiling of Rice Panicle in Response to Crude Toxin Extract of Ustilaginoidea virens
title Transcription Profiling of Rice Panicle in Response to Crude Toxin Extract of Ustilaginoidea virens
title_full Transcription Profiling of Rice Panicle in Response to Crude Toxin Extract of Ustilaginoidea virens
title_fullStr Transcription Profiling of Rice Panicle in Response to Crude Toxin Extract of Ustilaginoidea virens
title_full_unstemmed Transcription Profiling of Rice Panicle in Response to Crude Toxin Extract of Ustilaginoidea virens
title_short Transcription Profiling of Rice Panicle in Response to Crude Toxin Extract of Ustilaginoidea virens
title_sort transcription profiling of rice panicle in response to crude toxin extract of ustilaginoidea virens
topic Microbiology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9135463/
https://www.ncbi.nlm.nih.gov/pubmed/35633715
http://dx.doi.org/10.3389/fmicb.2022.701489
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