Prophage protein RacR activates lysozyme LysN, causing the growth defect of E. coli JM83

Prophage enriched the prokaryotic genome, and their transcriptional factors improved the protein expression network of the host. In this study, we uncovered a new prophage-prophage interaction in E. coli JM83. The Rac prophage protein RacR (GenBank accession no. AVI55875.1) directly activated the tr...

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Autores principales: Tang, Qiongwei, Feng, Meilin, Hou, Bingbing, Ye, Jiang, Wu, Haizhen, Zhang, Huizhan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2019
Materias:
Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6715736/
https://www.ncbi.nlm.nih.gov/pubmed/31467306
http://dx.doi.org/10.1038/s41598-019-48690-4
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author Tang, Qiongwei
Feng, Meilin
Hou, Bingbing
Ye, Jiang
Wu, Haizhen
Zhang, Huizhan
author_facet Tang, Qiongwei
Feng, Meilin
Hou, Bingbing
Ye, Jiang
Wu, Haizhen
Zhang, Huizhan
author_sort Tang, Qiongwei
collection PubMed
description Prophage enriched the prokaryotic genome, and their transcriptional factors improved the protein expression network of the host. In this study, we uncovered a new prophage-prophage interaction in E. coli JM83. The Rac prophage protein RacR (GenBank accession no. AVI55875.1) directly activated the transcription of φ80dlacZΔM15 prophage lysozyme encoding gene 19 (GenBank accession no. ACB02445.1, renamed it lysN, lysozyme nineteen), resulting in the growth defect of JM83. This phenomenon also occurred in DH5α, but not in BL21(DE3) and MG1655 due to the genotype differences. However, deletion of lysN could not completely rescued JM83 from the growth arrest, indicating that RacR may regulate other related targets. In addition, passivation of RacR regulation was found in the late period of growth of JM83, and it was transmissible to daughter cells. Altogether, our study revealed part of RacR regulatory network, which suggested some advanced genetic strategies in bacteria.
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spelling pubmed-67157362019-09-13 Prophage protein RacR activates lysozyme LysN, causing the growth defect of E. coli JM83 Tang, Qiongwei Feng, Meilin Hou, Bingbing Ye, Jiang Wu, Haizhen Zhang, Huizhan Sci Rep Article Prophage enriched the prokaryotic genome, and their transcriptional factors improved the protein expression network of the host. In this study, we uncovered a new prophage-prophage interaction in E. coli JM83. The Rac prophage protein RacR (GenBank accession no. AVI55875.1) directly activated the transcription of φ80dlacZΔM15 prophage lysozyme encoding gene 19 (GenBank accession no. ACB02445.1, renamed it lysN, lysozyme nineteen), resulting in the growth defect of JM83. This phenomenon also occurred in DH5α, but not in BL21(DE3) and MG1655 due to the genotype differences. However, deletion of lysN could not completely rescued JM83 from the growth arrest, indicating that RacR may regulate other related targets. In addition, passivation of RacR regulation was found in the late period of growth of JM83, and it was transmissible to daughter cells. Altogether, our study revealed part of RacR regulatory network, which suggested some advanced genetic strategies in bacteria. Nature Publishing Group UK 2019-08-29 /pmc/articles/PMC6715736/ /pubmed/31467306 http://dx.doi.org/10.1038/s41598-019-48690-4 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
Tang, Qiongwei
Feng, Meilin
Hou, Bingbing
Ye, Jiang
Wu, Haizhen
Zhang, Huizhan
Prophage protein RacR activates lysozyme LysN, causing the growth defect of E. coli JM83
title Prophage protein RacR activates lysozyme LysN, causing the growth defect of E. coli JM83
title_full Prophage protein RacR activates lysozyme LysN, causing the growth defect of E. coli JM83
title_fullStr Prophage protein RacR activates lysozyme LysN, causing the growth defect of E. coli JM83
title_full_unstemmed Prophage protein RacR activates lysozyme LysN, causing the growth defect of E. coli JM83
title_short Prophage protein RacR activates lysozyme LysN, causing the growth defect of E. coli JM83
title_sort prophage protein racr activates lysozyme lysn, causing the growth defect of e. coli jm83
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6715736/
https://www.ncbi.nlm.nih.gov/pubmed/31467306
http://dx.doi.org/10.1038/s41598-019-48690-4
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