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Morphogenetic Alterations of Alternaria alternata Exposed to Dicarboximide Fungicide, Iprodione

Fungicide-resistant Alternaria alternata impede the practical control of the Alternaria diseases in crop fields. This study aimed to investigate cytological fungicide resistance mechanisms of A. alternata against dicarboximide fungicide iprodione. A. alternata isolated from cactus brown spot was cul...

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Autores principales: Kim, Eunji, Lee, Hye Min, Kim, Young Ho
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Korean Society of Plant Pathology 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5291403/
https://www.ncbi.nlm.nih.gov/pubmed/28167893
http://dx.doi.org/10.5423/PPJ.NT.06.2016.0145
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author Kim, Eunji
Lee, Hye Min
Kim, Young Ho
author_facet Kim, Eunji
Lee, Hye Min
Kim, Young Ho
author_sort Kim, Eunji
collection PubMed
description Fungicide-resistant Alternaria alternata impede the practical control of the Alternaria diseases in crop fields. This study aimed to investigate cytological fungicide resistance mechanisms of A. alternata against dicarboximide fungicide iprodione. A. alternata isolated from cactus brown spot was cultured on potato-dextrose agar (PDA) with or without iprodione, and the fungal cultures with different growth characteristics from no, initial and full growth were observed by light and electron microscopy. Mycelia began to grow from one day after incubation (DAI) and continued to be in full growth (control-growth, Con-G) on PDA without fungicide, while on PDA with iprodione, no fungal growth (iprodione-no growth, Ipr-N) occurred for the first 3 DAI, but once the initial growth (iprodione-initial growth, Ipr-I) began at 4–5 DAI, the colonies grew and expanded continuously to be in full growth (iprodione-growth, Ipr-G), suggesting Ipr-I may be a turning moment of the morphogenetic changes resisting fungicidal toxicity. Con-G formed multicellular conidia with cell walls and septa and intact dense cytoplasm. In Ipr-N, fungal sporulation was inhibited by forming mostly undeveloped unicellular conidia with degraded and necrotic cytoplasm. However, in Ipr-I, conspicuous cellular changes occurred during sporulation by forming multicellular conidia with double layered (thickened) cell walls and accumulation of proliferated lipid bodies in the conidial cytoplasm, which may inhibit the penetration of the fungicide into conidial cells, reducing fungicide-associated toxicity, and may be utilized as energy and nutritional sources, respectively, for the further fungal growth to form mature colonies as in Ipr-G that formed multicellular conidia with cell walls and intact cytoplasm with lipid bodies as in Con-G.
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spelling pubmed-52914032017-02-06 Morphogenetic Alterations of Alternaria alternata Exposed to Dicarboximide Fungicide, Iprodione Kim, Eunji Lee, Hye Min Kim, Young Ho Plant Pathol J Note Fungicide-resistant Alternaria alternata impede the practical control of the Alternaria diseases in crop fields. This study aimed to investigate cytological fungicide resistance mechanisms of A. alternata against dicarboximide fungicide iprodione. A. alternata isolated from cactus brown spot was cultured on potato-dextrose agar (PDA) with or without iprodione, and the fungal cultures with different growth characteristics from no, initial and full growth were observed by light and electron microscopy. Mycelia began to grow from one day after incubation (DAI) and continued to be in full growth (control-growth, Con-G) on PDA without fungicide, while on PDA with iprodione, no fungal growth (iprodione-no growth, Ipr-N) occurred for the first 3 DAI, but once the initial growth (iprodione-initial growth, Ipr-I) began at 4–5 DAI, the colonies grew and expanded continuously to be in full growth (iprodione-growth, Ipr-G), suggesting Ipr-I may be a turning moment of the morphogenetic changes resisting fungicidal toxicity. Con-G formed multicellular conidia with cell walls and septa and intact dense cytoplasm. In Ipr-N, fungal sporulation was inhibited by forming mostly undeveloped unicellular conidia with degraded and necrotic cytoplasm. However, in Ipr-I, conspicuous cellular changes occurred during sporulation by forming multicellular conidia with double layered (thickened) cell walls and accumulation of proliferated lipid bodies in the conidial cytoplasm, which may inhibit the penetration of the fungicide into conidial cells, reducing fungicide-associated toxicity, and may be utilized as energy and nutritional sources, respectively, for the further fungal growth to form mature colonies as in Ipr-G that formed multicellular conidia with cell walls and intact cytoplasm with lipid bodies as in Con-G. Korean Society of Plant Pathology 2017-02 2017-02-01 /pmc/articles/PMC5291403/ /pubmed/28167893 http://dx.doi.org/10.5423/PPJ.NT.06.2016.0145 Text en © The Korean Society of Plant Pathology This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Note
Kim, Eunji
Lee, Hye Min
Kim, Young Ho
Morphogenetic Alterations of Alternaria alternata Exposed to Dicarboximide Fungicide, Iprodione
title Morphogenetic Alterations of Alternaria alternata Exposed to Dicarboximide Fungicide, Iprodione
title_full Morphogenetic Alterations of Alternaria alternata Exposed to Dicarboximide Fungicide, Iprodione
title_fullStr Morphogenetic Alterations of Alternaria alternata Exposed to Dicarboximide Fungicide, Iprodione
title_full_unstemmed Morphogenetic Alterations of Alternaria alternata Exposed to Dicarboximide Fungicide, Iprodione
title_short Morphogenetic Alterations of Alternaria alternata Exposed to Dicarboximide Fungicide, Iprodione
title_sort morphogenetic alterations of alternaria alternata exposed to dicarboximide fungicide, iprodione
topic Note
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5291403/
https://www.ncbi.nlm.nih.gov/pubmed/28167893
http://dx.doi.org/10.5423/PPJ.NT.06.2016.0145
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