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Pathogen‐induced expression of a blight tolerance transgene in American chestnut

American chestnut (Castanea dentata) is a susceptible host of the invasive necrotrophic fungus Cryphonectria parasitica, which causes chestnut blight disease. The fungal pathogen attacks chestnut stems by invading wounded tissue and secreting oxalate. This process leads to the death of infected host...

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Autores principales: Carlson, Erik, Stewart, Kristen, Baier, Kathleen, McGuigan, Linda, Culpepper, Tobi, Powell, William
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8828690/
https://www.ncbi.nlm.nih.gov/pubmed/34841616
http://dx.doi.org/10.1111/mpp.13165
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author Carlson, Erik
Stewart, Kristen
Baier, Kathleen
McGuigan, Linda
Culpepper, Tobi
Powell, William
author_facet Carlson, Erik
Stewart, Kristen
Baier, Kathleen
McGuigan, Linda
Culpepper, Tobi
Powell, William
author_sort Carlson, Erik
collection PubMed
description American chestnut (Castanea dentata) is a susceptible host of the invasive necrotrophic fungus Cryphonectria parasitica, which causes chestnut blight disease. The fungal pathogen attacks chestnut stems by invading wounded tissue and secreting oxalate. This process leads to the death of infected host cells and the formation of cankers, eventually girdling stems and killing the tree above the infections. To reduce damage caused by fungal oxalate, American chestnut has been genetically engineered to express a wheat oxalate oxidase (OxO). This enzyme degrades the oxalate produced by the pathogen and confers elevated tolerance to Cryphonectria parasitica infection. We report new lines of transgenic American chestnut that have been developed with the win3.12 inducible promoter from poplar (Populus deltoides) driving OxO expression. This promoter is responsive to both wounding and pathogen infection, with a low level of baseline expression. Targeted expression of OxO to wounded and infected tissue is sought as an alternative to constitutive expression for potential metabolic resource conservation and transgene stability over the long lifetime of a tree and over successive generations of breeding. Transgenic Castanea dentata lines harbouring the win3.12‐OxO construct were evaluated for transgene expression patterns and tolerance to chestnut blight infection. OxO transcript levels were low in uninfected plants, but robust infection‐induced expression levels were observed, with one transgenic line reaching levels comparable to those of previously characterized CaMV35S‐OxO lines. In chestnut blight infection bioassays, win3.12‐OxO lines showed elevated disease tolerance similar to blight‐resistant Chinese chestnut (Castanea mollissima) controls.
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spelling pubmed-88286902022-02-11 Pathogen‐induced expression of a blight tolerance transgene in American chestnut Carlson, Erik Stewart, Kristen Baier, Kathleen McGuigan, Linda Culpepper, Tobi Powell, William Mol Plant Pathol Original Articles American chestnut (Castanea dentata) is a susceptible host of the invasive necrotrophic fungus Cryphonectria parasitica, which causes chestnut blight disease. The fungal pathogen attacks chestnut stems by invading wounded tissue and secreting oxalate. This process leads to the death of infected host cells and the formation of cankers, eventually girdling stems and killing the tree above the infections. To reduce damage caused by fungal oxalate, American chestnut has been genetically engineered to express a wheat oxalate oxidase (OxO). This enzyme degrades the oxalate produced by the pathogen and confers elevated tolerance to Cryphonectria parasitica infection. We report new lines of transgenic American chestnut that have been developed with the win3.12 inducible promoter from poplar (Populus deltoides) driving OxO expression. This promoter is responsive to both wounding and pathogen infection, with a low level of baseline expression. Targeted expression of OxO to wounded and infected tissue is sought as an alternative to constitutive expression for potential metabolic resource conservation and transgene stability over the long lifetime of a tree and over successive generations of breeding. Transgenic Castanea dentata lines harbouring the win3.12‐OxO construct were evaluated for transgene expression patterns and tolerance to chestnut blight infection. OxO transcript levels were low in uninfected plants, but robust infection‐induced expression levels were observed, with one transgenic line reaching levels comparable to those of previously characterized CaMV35S‐OxO lines. In chestnut blight infection bioassays, win3.12‐OxO lines showed elevated disease tolerance similar to blight‐resistant Chinese chestnut (Castanea mollissima) controls. John Wiley and Sons Inc. 2021-11-28 /pmc/articles/PMC8828690/ /pubmed/34841616 http://dx.doi.org/10.1111/mpp.13165 Text en © 2021 The Authors. Molecular Plant Pathology published by British Society for Plant Pathology and John Wiley & Sons Ltd. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Articles
Carlson, Erik
Stewart, Kristen
Baier, Kathleen
McGuigan, Linda
Culpepper, Tobi
Powell, William
Pathogen‐induced expression of a blight tolerance transgene in American chestnut
title Pathogen‐induced expression of a blight tolerance transgene in American chestnut
title_full Pathogen‐induced expression of a blight tolerance transgene in American chestnut
title_fullStr Pathogen‐induced expression of a blight tolerance transgene in American chestnut
title_full_unstemmed Pathogen‐induced expression of a blight tolerance transgene in American chestnut
title_short Pathogen‐induced expression of a blight tolerance transgene in American chestnut
title_sort pathogen‐induced expression of a blight tolerance transgene in american chestnut
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8828690/
https://www.ncbi.nlm.nih.gov/pubmed/34841616
http://dx.doi.org/10.1111/mpp.13165
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