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Attenuation of radiation toxicity by the phosphine resistance factor dihydrolipoamide dehydrogenase (DLD)
Phosphine gas is an excellent fumigant for disinfesting stored grain of insect pests, but heavy reliance on phosphine has led to resistance in grain pests that threatens its efficacy. Phosphine-resistance was previously reported to be mediated by the enzyme DLD. Here we explore the relationship betw...
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/PMC6478721/ https://www.ncbi.nlm.nih.gov/pubmed/31015501 http://dx.doi.org/10.1038/s41598-019-42678-w |
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author | Alzahrani, Saad M. Ebert, Paul R. |
author_facet | Alzahrani, Saad M. Ebert, Paul R. |
author_sort | Alzahrani, Saad M. |
collection | PubMed |
description | Phosphine gas is an excellent fumigant for disinfesting stored grain of insect pests, but heavy reliance on phosphine has led to resistance in grain pests that threatens its efficacy. Phosphine-resistance was previously reported to be mediated by the enzyme DLD. Here we explore the relationship between phosphine toxicity and genotoxic treatments with the goal of understanding how phosphine works. Specifically, we utilized mutant lines either sensitive or resistant to phosphine, gamma irradiation or UV exposure. The phosphine-resistance mutation in the enzyme of energy metabolism, dihydrolipoamide dehydrogenase exhibited cross-resistance to UV and ionizing radiation. Two radiation-sensitive mutants that are defective in DNA repair as well as a mutant that is defective in the activation of the DAF-16 stress response transcription factor all exhibit sensitivity to phosphine that exceeds the sensitivity of the wild type control. A radiation resistance mutation in cep-1, the p53 orthologue, that is deficient in double strand break repair of DNA and is also deficient in apoptosis causes radiation-resistance results but sensitivity toward phosphine. |
format | Online Article Text |
id | pubmed-6478721 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-64787212019-05-03 Attenuation of radiation toxicity by the phosphine resistance factor dihydrolipoamide dehydrogenase (DLD) Alzahrani, Saad M. Ebert, Paul R. Sci Rep Article Phosphine gas is an excellent fumigant for disinfesting stored grain of insect pests, but heavy reliance on phosphine has led to resistance in grain pests that threatens its efficacy. Phosphine-resistance was previously reported to be mediated by the enzyme DLD. Here we explore the relationship between phosphine toxicity and genotoxic treatments with the goal of understanding how phosphine works. Specifically, we utilized mutant lines either sensitive or resistant to phosphine, gamma irradiation or UV exposure. The phosphine-resistance mutation in the enzyme of energy metabolism, dihydrolipoamide dehydrogenase exhibited cross-resistance to UV and ionizing radiation. Two radiation-sensitive mutants that are defective in DNA repair as well as a mutant that is defective in the activation of the DAF-16 stress response transcription factor all exhibit sensitivity to phosphine that exceeds the sensitivity of the wild type control. A radiation resistance mutation in cep-1, the p53 orthologue, that is deficient in double strand break repair of DNA and is also deficient in apoptosis causes radiation-resistance results but sensitivity toward phosphine. Nature Publishing Group UK 2019-04-23 /pmc/articles/PMC6478721/ /pubmed/31015501 http://dx.doi.org/10.1038/s41598-019-42678-w 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 Alzahrani, Saad M. Ebert, Paul R. Attenuation of radiation toxicity by the phosphine resistance factor dihydrolipoamide dehydrogenase (DLD) |
title | Attenuation of radiation toxicity by the phosphine resistance factor dihydrolipoamide dehydrogenase (DLD) |
title_full | Attenuation of radiation toxicity by the phosphine resistance factor dihydrolipoamide dehydrogenase (DLD) |
title_fullStr | Attenuation of radiation toxicity by the phosphine resistance factor dihydrolipoamide dehydrogenase (DLD) |
title_full_unstemmed | Attenuation of radiation toxicity by the phosphine resistance factor dihydrolipoamide dehydrogenase (DLD) |
title_short | Attenuation of radiation toxicity by the phosphine resistance factor dihydrolipoamide dehydrogenase (DLD) |
title_sort | attenuation of radiation toxicity by the phosphine resistance factor dihydrolipoamide dehydrogenase (dld) |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6478721/ https://www.ncbi.nlm.nih.gov/pubmed/31015501 http://dx.doi.org/10.1038/s41598-019-42678-w |
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