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Transcriptome-Based Modeling Reveals that Oxidative Stress Induces Modulation of the AtfA-Dependent Signaling Networks in Aspergillus nidulans
To better understand the molecular functions of the master stress-response regulator AtfA in Aspergillus nidulans, transcriptomic analyses of the atfA null mutant and the appropriate control strains exposed to menadione sodium bisulfite- (MSB-), t-butylhydroperoxide- and diamide-induced oxidative st...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5523550/ https://www.ncbi.nlm.nih.gov/pubmed/28770220 http://dx.doi.org/10.1155/2017/6923849 |
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author | Orosz, Erzsébet Antal, Károly Gazdag, Zoltán Szabó, Zsuzsa Han, Kap-Hoon Yu, Jae-Hyuk Pócsi, István Emri, Tamás |
author_facet | Orosz, Erzsébet Antal, Károly Gazdag, Zoltán Szabó, Zsuzsa Han, Kap-Hoon Yu, Jae-Hyuk Pócsi, István Emri, Tamás |
author_sort | Orosz, Erzsébet |
collection | PubMed |
description | To better understand the molecular functions of the master stress-response regulator AtfA in Aspergillus nidulans, transcriptomic analyses of the atfA null mutant and the appropriate control strains exposed to menadione sodium bisulfite- (MSB-), t-butylhydroperoxide- and diamide-induced oxidative stresses were performed. Several elements of oxidative stress response were differentially expressed. Many of them, including the downregulation of the mitotic cell cycle, as the MSB stress-specific upregulation of FeS cluster assembly and the MSB stress-specific downregulation of nitrate reduction, tricarboxylic acid cycle, and ER to Golgi vesicle-mediated transport, showed AtfA dependence. To elucidate the potential global regulatory role of AtfA governing expression of a high number of genes with very versatile biological functions, we devised a model based on the comprehensive transcriptomic data. Our model suggests that an important function of AtfA is to modulate the transduction of stress signals. Although it may regulate directly only a limited number of genes, these include elements of the signaling network, for example, members of the two-component signal transduction systems. AtfA acts in a stress-specific manner, which may increase further the number and diversity of AtfA-dependent genes. Our model sheds light on the versatility of the physiological functions of AtfA and its orthologs in fungi. |
format | Online Article Text |
id | pubmed-5523550 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Hindawi |
record_format | MEDLINE/PubMed |
spelling | pubmed-55235502017-08-02 Transcriptome-Based Modeling Reveals that Oxidative Stress Induces Modulation of the AtfA-Dependent Signaling Networks in Aspergillus nidulans Orosz, Erzsébet Antal, Károly Gazdag, Zoltán Szabó, Zsuzsa Han, Kap-Hoon Yu, Jae-Hyuk Pócsi, István Emri, Tamás Int J Genomics Research Article To better understand the molecular functions of the master stress-response regulator AtfA in Aspergillus nidulans, transcriptomic analyses of the atfA null mutant and the appropriate control strains exposed to menadione sodium bisulfite- (MSB-), t-butylhydroperoxide- and diamide-induced oxidative stresses were performed. Several elements of oxidative stress response were differentially expressed. Many of them, including the downregulation of the mitotic cell cycle, as the MSB stress-specific upregulation of FeS cluster assembly and the MSB stress-specific downregulation of nitrate reduction, tricarboxylic acid cycle, and ER to Golgi vesicle-mediated transport, showed AtfA dependence. To elucidate the potential global regulatory role of AtfA governing expression of a high number of genes with very versatile biological functions, we devised a model based on the comprehensive transcriptomic data. Our model suggests that an important function of AtfA is to modulate the transduction of stress signals. Although it may regulate directly only a limited number of genes, these include elements of the signaling network, for example, members of the two-component signal transduction systems. AtfA acts in a stress-specific manner, which may increase further the number and diversity of AtfA-dependent genes. Our model sheds light on the versatility of the physiological functions of AtfA and its orthologs in fungi. Hindawi 2017 2017-07-09 /pmc/articles/PMC5523550/ /pubmed/28770220 http://dx.doi.org/10.1155/2017/6923849 Text en Copyright © 2017 Erzsébet Orosz et al. http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Orosz, Erzsébet Antal, Károly Gazdag, Zoltán Szabó, Zsuzsa Han, Kap-Hoon Yu, Jae-Hyuk Pócsi, István Emri, Tamás Transcriptome-Based Modeling Reveals that Oxidative Stress Induces Modulation of the AtfA-Dependent Signaling Networks in Aspergillus nidulans |
title | Transcriptome-Based Modeling Reveals that Oxidative Stress Induces Modulation of the AtfA-Dependent Signaling Networks in Aspergillus nidulans |
title_full | Transcriptome-Based Modeling Reveals that Oxidative Stress Induces Modulation of the AtfA-Dependent Signaling Networks in Aspergillus nidulans |
title_fullStr | Transcriptome-Based Modeling Reveals that Oxidative Stress Induces Modulation of the AtfA-Dependent Signaling Networks in Aspergillus nidulans |
title_full_unstemmed | Transcriptome-Based Modeling Reveals that Oxidative Stress Induces Modulation of the AtfA-Dependent Signaling Networks in Aspergillus nidulans |
title_short | Transcriptome-Based Modeling Reveals that Oxidative Stress Induces Modulation of the AtfA-Dependent Signaling Networks in Aspergillus nidulans |
title_sort | transcriptome-based modeling reveals that oxidative stress induces modulation of the atfa-dependent signaling networks in aspergillus nidulans |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5523550/ https://www.ncbi.nlm.nih.gov/pubmed/28770220 http://dx.doi.org/10.1155/2017/6923849 |
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