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The Plasmid pEX18Gm Indirectly Increases Caenorhabditis elegans Fecundity by Accelerating Bacterial Methionine Synthesis

Plasmids are mostly found in bacteria as extrachromosomal genetic elements and are widely used in genetic engineering. Exploring the mechanisms of plasmid–host interaction can provide crucial information for the application of plasmids in genetic engineering. However, many studies have generally foc...

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Autores principales: Guo, Rui, Li, Gen, Lu, Leilei, Sun, Shan, Liu, Ting, Li, Mengsha, Zheng, Yong, Walhout, Albertha J. M., Wu, Jun, Li, Huixin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9102816/
https://www.ncbi.nlm.nih.gov/pubmed/35563392
http://dx.doi.org/10.3390/ijms23095003
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author Guo, Rui
Li, Gen
Lu, Leilei
Sun, Shan
Liu, Ting
Li, Mengsha
Zheng, Yong
Walhout, Albertha J. M.
Wu, Jun
Li, Huixin
author_facet Guo, Rui
Li, Gen
Lu, Leilei
Sun, Shan
Liu, Ting
Li, Mengsha
Zheng, Yong
Walhout, Albertha J. M.
Wu, Jun
Li, Huixin
author_sort Guo, Rui
collection PubMed
description Plasmids are mostly found in bacteria as extrachromosomal genetic elements and are widely used in genetic engineering. Exploring the mechanisms of plasmid–host interaction can provide crucial information for the application of plasmids in genetic engineering. However, many studies have generally focused on the influence of plasmids on their bacterial hosts, and the effects of plasmids on bacteria-feeding animals have not been explored in detail. Here, we use a “plasmid–bacteria–Caenorhabditis elegans” model to explore the impact of plasmids on their host bacteria and bacterivorous nematodes. First, the phenotypic responses of C. elegans were observed by feeding Escherichia coli OP50 harboring different types of plasmids. We found that E. coli OP50 harboring plasmid pEX18Gm unexpectedly increases the fecundity of C. elegans. Subsequently, we found that the plasmid pEX18Gm indirectly affects C. elegans fecundity via bacterial metabolism. To explore the underlying regulatory mechanism, we performed bacterial RNA sequencing and performed in-depth analysis. We demonstrated that the plasmid pEX18Gm upregulates the transcription of methionine synthase gene metH in the bacteria, which results in an increase in methionine that supports C. elegans fecundity. Additionally, we found that a pEX18Gm-induced increase in C. elegans can occur in different bacterial species. Our findings highlight the plasmid–bacteria–C. elegans model to reveal the mechanism of plasmids’ effects on their host and provide a new pattern for systematically studying the interaction between plasmids and multi-species.
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spelling pubmed-91028162022-05-14 The Plasmid pEX18Gm Indirectly Increases Caenorhabditis elegans Fecundity by Accelerating Bacterial Methionine Synthesis Guo, Rui Li, Gen Lu, Leilei Sun, Shan Liu, Ting Li, Mengsha Zheng, Yong Walhout, Albertha J. M. Wu, Jun Li, Huixin Int J Mol Sci Article Plasmids are mostly found in bacteria as extrachromosomal genetic elements and are widely used in genetic engineering. Exploring the mechanisms of plasmid–host interaction can provide crucial information for the application of plasmids in genetic engineering. However, many studies have generally focused on the influence of plasmids on their bacterial hosts, and the effects of plasmids on bacteria-feeding animals have not been explored in detail. Here, we use a “plasmid–bacteria–Caenorhabditis elegans” model to explore the impact of plasmids on their host bacteria and bacterivorous nematodes. First, the phenotypic responses of C. elegans were observed by feeding Escherichia coli OP50 harboring different types of plasmids. We found that E. coli OP50 harboring plasmid pEX18Gm unexpectedly increases the fecundity of C. elegans. Subsequently, we found that the plasmid pEX18Gm indirectly affects C. elegans fecundity via bacterial metabolism. To explore the underlying regulatory mechanism, we performed bacterial RNA sequencing and performed in-depth analysis. We demonstrated that the plasmid pEX18Gm upregulates the transcription of methionine synthase gene metH in the bacteria, which results in an increase in methionine that supports C. elegans fecundity. Additionally, we found that a pEX18Gm-induced increase in C. elegans can occur in different bacterial species. Our findings highlight the plasmid–bacteria–C. elegans model to reveal the mechanism of plasmids’ effects on their host and provide a new pattern for systematically studying the interaction between plasmids and multi-species. MDPI 2022-04-30 /pmc/articles/PMC9102816/ /pubmed/35563392 http://dx.doi.org/10.3390/ijms23095003 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Guo, Rui
Li, Gen
Lu, Leilei
Sun, Shan
Liu, Ting
Li, Mengsha
Zheng, Yong
Walhout, Albertha J. M.
Wu, Jun
Li, Huixin
The Plasmid pEX18Gm Indirectly Increases Caenorhabditis elegans Fecundity by Accelerating Bacterial Methionine Synthesis
title The Plasmid pEX18Gm Indirectly Increases Caenorhabditis elegans Fecundity by Accelerating Bacterial Methionine Synthesis
title_full The Plasmid pEX18Gm Indirectly Increases Caenorhabditis elegans Fecundity by Accelerating Bacterial Methionine Synthesis
title_fullStr The Plasmid pEX18Gm Indirectly Increases Caenorhabditis elegans Fecundity by Accelerating Bacterial Methionine Synthesis
title_full_unstemmed The Plasmid pEX18Gm Indirectly Increases Caenorhabditis elegans Fecundity by Accelerating Bacterial Methionine Synthesis
title_short The Plasmid pEX18Gm Indirectly Increases Caenorhabditis elegans Fecundity by Accelerating Bacterial Methionine Synthesis
title_sort plasmid pex18gm indirectly increases caenorhabditis elegans fecundity by accelerating bacterial methionine synthesis
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9102816/
https://www.ncbi.nlm.nih.gov/pubmed/35563392
http://dx.doi.org/10.3390/ijms23095003
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