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Complex general stress response regulation in Sphingomonas melonis Fr1 revealed by transcriptional analyses
The general stress response (GSR) represents an important trait to survive in the environment by leading to multiple stress resistance. In alphaproteobacteria, the GSR is under the transcriptional control of the alternative sigma factor EcfG. Here we performed transcriptome analyses to investigate t...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6599016/ https://www.ncbi.nlm.nih.gov/pubmed/31253827 http://dx.doi.org/10.1038/s41598-019-45788-7 |
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author | Gottschlich, Lisa Geiser, Petra Bortfeld-Miller, Miriam Field, Christopher M. Vorholt, Julia A. |
author_facet | Gottschlich, Lisa Geiser, Petra Bortfeld-Miller, Miriam Field, Christopher M. Vorholt, Julia A. |
author_sort | Gottschlich, Lisa |
collection | PubMed |
description | The general stress response (GSR) represents an important trait to survive in the environment by leading to multiple stress resistance. In alphaproteobacteria, the GSR is under the transcriptional control of the alternative sigma factor EcfG. Here we performed transcriptome analyses to investigate the genes controlled by EcfG of Sphingomonas melonis Fr1 and the plasticity of this regulation under stress conditions. We found that EcfG regulates genes for proteins that are typically associated with stress responses. Moreover, EcfG controls regulatory proteins, which likely fine-tune the GSR. Among these, we identified a novel negative GSR feedback regulator, termed NepR2, on the basis of gene reporter assays, phenotypic analyses, and biochemical assays. Transcriptional profiling of signaling components upstream of EcfG under complex stress conditions showed an overall congruence with EcfG-regulated genes. Interestingly however, we found that the GSR is transcriptionally linked to the regulation of motility and biofilm formation via the single domain response regulator SdrG and GSR-activating histidine kinases. Altogether, our findings indicate that the GSR in S. melonis Fr1 underlies a complex regulation to optimize resource allocation and resilience in stressful and changing environments. |
format | Online Article Text |
id | pubmed-6599016 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-65990162019-07-10 Complex general stress response regulation in Sphingomonas melonis Fr1 revealed by transcriptional analyses Gottschlich, Lisa Geiser, Petra Bortfeld-Miller, Miriam Field, Christopher M. Vorholt, Julia A. Sci Rep Article The general stress response (GSR) represents an important trait to survive in the environment by leading to multiple stress resistance. In alphaproteobacteria, the GSR is under the transcriptional control of the alternative sigma factor EcfG. Here we performed transcriptome analyses to investigate the genes controlled by EcfG of Sphingomonas melonis Fr1 and the plasticity of this regulation under stress conditions. We found that EcfG regulates genes for proteins that are typically associated with stress responses. Moreover, EcfG controls regulatory proteins, which likely fine-tune the GSR. Among these, we identified a novel negative GSR feedback regulator, termed NepR2, on the basis of gene reporter assays, phenotypic analyses, and biochemical assays. Transcriptional profiling of signaling components upstream of EcfG under complex stress conditions showed an overall congruence with EcfG-regulated genes. Interestingly however, we found that the GSR is transcriptionally linked to the regulation of motility and biofilm formation via the single domain response regulator SdrG and GSR-activating histidine kinases. Altogether, our findings indicate that the GSR in S. melonis Fr1 underlies a complex regulation to optimize resource allocation and resilience in stressful and changing environments. Nature Publishing Group UK 2019-06-28 /pmc/articles/PMC6599016/ /pubmed/31253827 http://dx.doi.org/10.1038/s41598-019-45788-7 Text en © The Author(s) 2019 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 Gottschlich, Lisa Geiser, Petra Bortfeld-Miller, Miriam Field, Christopher M. Vorholt, Julia A. Complex general stress response regulation in Sphingomonas melonis Fr1 revealed by transcriptional analyses |
title | Complex general stress response regulation in Sphingomonas melonis Fr1 revealed by transcriptional analyses |
title_full | Complex general stress response regulation in Sphingomonas melonis Fr1 revealed by transcriptional analyses |
title_fullStr | Complex general stress response regulation in Sphingomonas melonis Fr1 revealed by transcriptional analyses |
title_full_unstemmed | Complex general stress response regulation in Sphingomonas melonis Fr1 revealed by transcriptional analyses |
title_short | Complex general stress response regulation in Sphingomonas melonis Fr1 revealed by transcriptional analyses |
title_sort | complex general stress response regulation in sphingomonas melonis fr1 revealed by transcriptional analyses |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6599016/ https://www.ncbi.nlm.nih.gov/pubmed/31253827 http://dx.doi.org/10.1038/s41598-019-45788-7 |
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