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Physiological role of isocitrate lyase in dibenzo-p-dioxin and dibenzofuran metabolism by Sphingomonas wittichii RW1

BACKGROUND: Sphingomonas wittichii RW1 is one out of three strains capable of metabolizing dioxin as a sole source for carbon and energy. Under laboratory conditions the degradation rates for these aromatics are relatively high (5 and 8 h for dibenzofuran (DBF) and dibenzo-p-dioxin (DD), respectivel...

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Autores principales: Faisal, Rayan M., Rasol, Aveen H.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer Berlin Heidelberg 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8967917/
https://www.ncbi.nlm.nih.gov/pubmed/35353212
http://dx.doi.org/10.1186/s43141-022-00334-3
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author Faisal, Rayan M.
Rasol, Aveen H.
author_facet Faisal, Rayan M.
Rasol, Aveen H.
author_sort Faisal, Rayan M.
collection PubMed
description BACKGROUND: Sphingomonas wittichii RW1 is one out of three strains capable of metabolizing dioxin as a sole source for carbon and energy. Under laboratory conditions the degradation rates for these aromatics are relatively high (5 and 8 h for dibenzofuran (DBF) and dibenzo-p-dioxin (DD), respectively). However, their degradation rates are much lower in the environment due to several factors. One of these factors is the availability of other carbon sources. Acetate is a metabolized carbon source by S. wittichii RW1 and its presence in the environment would have a negative impact on DBF and DD degradation. In addition, expression of most of the genes for DBF and DD degradation were downregulated when grown on acetate compared to their growth on DBF and DD. We hypothesized that blocking the acetate utilization pathway in S. wittichii RW1 would prevent it from using acetate when present along with DD and DBF in contaminated sites. RESULTS: Blocking the glyoxylate shunt by deleting isocitrate lyase gene (icl) prevented the mutant strain (RW1Δicl) from using acetate as a sole carbon source thus depending on available DBF and DD in polluted sites. Our results showed that deletion of icl did not affect growth of S. wittichii RW1 on DBF and DD but blocked it from growing on acetate. CONCLUSION: Our results introduces an engineered strain that can be used as a new candidate to clean dioxin-contaminated sites which are rich with acetate.
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spelling pubmed-89679172022-04-14 Physiological role of isocitrate lyase in dibenzo-p-dioxin and dibenzofuran metabolism by Sphingomonas wittichii RW1 Faisal, Rayan M. Rasol, Aveen H. J Genet Eng Biotechnol Research BACKGROUND: Sphingomonas wittichii RW1 is one out of three strains capable of metabolizing dioxin as a sole source for carbon and energy. Under laboratory conditions the degradation rates for these aromatics are relatively high (5 and 8 h for dibenzofuran (DBF) and dibenzo-p-dioxin (DD), respectively). However, their degradation rates are much lower in the environment due to several factors. One of these factors is the availability of other carbon sources. Acetate is a metabolized carbon source by S. wittichii RW1 and its presence in the environment would have a negative impact on DBF and DD degradation. In addition, expression of most of the genes for DBF and DD degradation were downregulated when grown on acetate compared to their growth on DBF and DD. We hypothesized that blocking the acetate utilization pathway in S. wittichii RW1 would prevent it from using acetate when present along with DD and DBF in contaminated sites. RESULTS: Blocking the glyoxylate shunt by deleting isocitrate lyase gene (icl) prevented the mutant strain (RW1Δicl) from using acetate as a sole carbon source thus depending on available DBF and DD in polluted sites. Our results showed that deletion of icl did not affect growth of S. wittichii RW1 on DBF and DD but blocked it from growing on acetate. CONCLUSION: Our results introduces an engineered strain that can be used as a new candidate to clean dioxin-contaminated sites which are rich with acetate. Springer Berlin Heidelberg 2022-03-30 /pmc/articles/PMC8967917/ /pubmed/35353212 http://dx.doi.org/10.1186/s43141-022-00334-3 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Research
Faisal, Rayan M.
Rasol, Aveen H.
Physiological role of isocitrate lyase in dibenzo-p-dioxin and dibenzofuran metabolism by Sphingomonas wittichii RW1
title Physiological role of isocitrate lyase in dibenzo-p-dioxin and dibenzofuran metabolism by Sphingomonas wittichii RW1
title_full Physiological role of isocitrate lyase in dibenzo-p-dioxin and dibenzofuran metabolism by Sphingomonas wittichii RW1
title_fullStr Physiological role of isocitrate lyase in dibenzo-p-dioxin and dibenzofuran metabolism by Sphingomonas wittichii RW1
title_full_unstemmed Physiological role of isocitrate lyase in dibenzo-p-dioxin and dibenzofuran metabolism by Sphingomonas wittichii RW1
title_short Physiological role of isocitrate lyase in dibenzo-p-dioxin and dibenzofuran metabolism by Sphingomonas wittichii RW1
title_sort physiological role of isocitrate lyase in dibenzo-p-dioxin and dibenzofuran metabolism by sphingomonas wittichii rw1
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8967917/
https://www.ncbi.nlm.nih.gov/pubmed/35353212
http://dx.doi.org/10.1186/s43141-022-00334-3
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