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Preliminary study on the effect of catabolite repression gene knockout on p-nitrophenol degradation in Pseudomonas putida DLL-E4
P-nitrophenol (PNP) is a carcinogenic, teratogenic, and mutagenic compound that can cause serious harm to the environment. A strain of Pseudomonas putida DLL-E4, can efficiently degrade PNP in a complex process that is influenced by many factors. Previous studies showed that the expression level of...
Autores principales: | , , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9718395/ https://www.ncbi.nlm.nih.gov/pubmed/36459525 http://dx.doi.org/10.1371/journal.pone.0278503 |
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author | Li, Shuang Tang, Yichao Tang, Lingran Yan, Xuanyu Xiao, Jiali Xiang, Huijun Wu, Qing Yu, Ruqi Jin, Yushi Yu, Jingyu Xu, Nuo Wu, Chu Wang, Shengqin Wang, Chuanhua Chen, Qiongzhen |
author_facet | Li, Shuang Tang, Yichao Tang, Lingran Yan, Xuanyu Xiao, Jiali Xiang, Huijun Wu, Qing Yu, Ruqi Jin, Yushi Yu, Jingyu Xu, Nuo Wu, Chu Wang, Shengqin Wang, Chuanhua Chen, Qiongzhen |
author_sort | Li, Shuang |
collection | PubMed |
description | P-nitrophenol (PNP) is a carcinogenic, teratogenic, and mutagenic compound that can cause serious harm to the environment. A strain of Pseudomonas putida DLL-E4, can efficiently degrade PNP in a complex process that is influenced by many factors. Previous studies showed that the expression level of pnpA, a key gene involved in PNP degradation, was upregulated significantly and the degradation of PNP was obviously accelerated in the presence of glucose. In addition, the expression of crc, crcY, and crcZ, key genes involved in catabolite repression, was downregulated, upregulated, and upregulated, respectively. To investigate the effect of the carbon catabolite repression (CCR) system on PNP degradation, the crc, crcY, and crcZ genes were successfully knocked out by conjugation experiments. Our results showed that the knockout of crc accelerated PNP degradation but slowed down the cell growth. However, the knockout of crcY or crcZ alone accelerated PNP degradation when PNP as the sole carbon source, but that knockout slowed down PNP degradation when glucose was added. The results indicate that the CCR system is involved in the regulation of PNP degradation, and further work is required to determine the details of the specific regulatory mechanism. |
format | Online Article Text |
id | pubmed-9718395 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-97183952022-12-03 Preliminary study on the effect of catabolite repression gene knockout on p-nitrophenol degradation in Pseudomonas putida DLL-E4 Li, Shuang Tang, Yichao Tang, Lingran Yan, Xuanyu Xiao, Jiali Xiang, Huijun Wu, Qing Yu, Ruqi Jin, Yushi Yu, Jingyu Xu, Nuo Wu, Chu Wang, Shengqin Wang, Chuanhua Chen, Qiongzhen PLoS One Research Article P-nitrophenol (PNP) is a carcinogenic, teratogenic, and mutagenic compound that can cause serious harm to the environment. A strain of Pseudomonas putida DLL-E4, can efficiently degrade PNP in a complex process that is influenced by many factors. Previous studies showed that the expression level of pnpA, a key gene involved in PNP degradation, was upregulated significantly and the degradation of PNP was obviously accelerated in the presence of glucose. In addition, the expression of crc, crcY, and crcZ, key genes involved in catabolite repression, was downregulated, upregulated, and upregulated, respectively. To investigate the effect of the carbon catabolite repression (CCR) system on PNP degradation, the crc, crcY, and crcZ genes were successfully knocked out by conjugation experiments. Our results showed that the knockout of crc accelerated PNP degradation but slowed down the cell growth. However, the knockout of crcY or crcZ alone accelerated PNP degradation when PNP as the sole carbon source, but that knockout slowed down PNP degradation when glucose was added. The results indicate that the CCR system is involved in the regulation of PNP degradation, and further work is required to determine the details of the specific regulatory mechanism. Public Library of Science 2022-12-02 /pmc/articles/PMC9718395/ /pubmed/36459525 http://dx.doi.org/10.1371/journal.pone.0278503 Text en © 2022 Li et al https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Research Article Li, Shuang Tang, Yichao Tang, Lingran Yan, Xuanyu Xiao, Jiali Xiang, Huijun Wu, Qing Yu, Ruqi Jin, Yushi Yu, Jingyu Xu, Nuo Wu, Chu Wang, Shengqin Wang, Chuanhua Chen, Qiongzhen Preliminary study on the effect of catabolite repression gene knockout on p-nitrophenol degradation in Pseudomonas putida DLL-E4 |
title | Preliminary study on the effect of catabolite repression gene knockout on p-nitrophenol degradation in Pseudomonas putida DLL-E4 |
title_full | Preliminary study on the effect of catabolite repression gene knockout on p-nitrophenol degradation in Pseudomonas putida DLL-E4 |
title_fullStr | Preliminary study on the effect of catabolite repression gene knockout on p-nitrophenol degradation in Pseudomonas putida DLL-E4 |
title_full_unstemmed | Preliminary study on the effect of catabolite repression gene knockout on p-nitrophenol degradation in Pseudomonas putida DLL-E4 |
title_short | Preliminary study on the effect of catabolite repression gene knockout on p-nitrophenol degradation in Pseudomonas putida DLL-E4 |
title_sort | preliminary study on the effect of catabolite repression gene knockout on p-nitrophenol degradation in pseudomonas putida dll-e4 |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9718395/ https://www.ncbi.nlm.nih.gov/pubmed/36459525 http://dx.doi.org/10.1371/journal.pone.0278503 |
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