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HvCEBiP, a gene homologous to rice chitin receptor CEBiP, contributes to basal resistance of barley to Magnaporthe oryzae
BACKGROUND: Rice CEBiP recognizes chitin oligosaccharides on the fungal cell surface or released into the plant apoplast, leading to the expression of plant disease resistance against fungal infection. However, it has not yet been reported whether CEBiP is actually required for restricting the growt...
Autores principales: | , , , , , , , , , |
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Formato: | Texto |
Lenguaje: | English |
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BioMed Central
2010
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3020183/ https://www.ncbi.nlm.nih.gov/pubmed/21190588 http://dx.doi.org/10.1186/1471-2229-10-288 |
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author | Tanaka, Shigeyuki Ichikawa, Akari Yamada, Kaori Tsuji, Gento Nishiuchi, Takumi Mori, Masashi Koga, Hironori Nishizawa, Yoko O'Connell, Richard Kubo, Yasuyuki |
author_facet | Tanaka, Shigeyuki Ichikawa, Akari Yamada, Kaori Tsuji, Gento Nishiuchi, Takumi Mori, Masashi Koga, Hironori Nishizawa, Yoko O'Connell, Richard Kubo, Yasuyuki |
author_sort | Tanaka, Shigeyuki |
collection | PubMed |
description | BACKGROUND: Rice CEBiP recognizes chitin oligosaccharides on the fungal cell surface or released into the plant apoplast, leading to the expression of plant disease resistance against fungal infection. However, it has not yet been reported whether CEBiP is actually required for restricting the growth of fungal pathogens. Here we evaluated the involvement of a putative chitin receptor gene in the basal resistance of barley to the ssd1 mutant of Magnaporthe oryzae, which induces multiple host defense responses. RESULTS: The mossd1 mutant showed attenuated pathogenicity on barley and appressorial penetration was restricted by the formation of callose papillae at attempted entry sites. When conidial suspensions of mossd1 mutant were spotted onto the leaves of HvCEBiP-silenced plants, small brown necrotic flecks or blast lesions were produced but these lesions did not expand beyond the inoculation site. Wild-type M. oryzae also produced slightly more severe symptoms on the leaves of HvCEBiP-silenced plants. Cytological observation revealed that these lesions resulted from appressorium-mediated penetration into plant epidermal cells. CONCLUSIONS: These results suggest that HvCEBiP is involved in basal resistance against appressorium-mediated infection and that basal resistance might be triggered by the recognition of chitin oligosaccharides derived from M. oryzae. |
format | Text |
id | pubmed-3020183 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2010 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-30201832011-01-13 HvCEBiP, a gene homologous to rice chitin receptor CEBiP, contributes to basal resistance of barley to Magnaporthe oryzae Tanaka, Shigeyuki Ichikawa, Akari Yamada, Kaori Tsuji, Gento Nishiuchi, Takumi Mori, Masashi Koga, Hironori Nishizawa, Yoko O'Connell, Richard Kubo, Yasuyuki BMC Plant Biol Research Article BACKGROUND: Rice CEBiP recognizes chitin oligosaccharides on the fungal cell surface or released into the plant apoplast, leading to the expression of plant disease resistance against fungal infection. However, it has not yet been reported whether CEBiP is actually required for restricting the growth of fungal pathogens. Here we evaluated the involvement of a putative chitin receptor gene in the basal resistance of barley to the ssd1 mutant of Magnaporthe oryzae, which induces multiple host defense responses. RESULTS: The mossd1 mutant showed attenuated pathogenicity on barley and appressorial penetration was restricted by the formation of callose papillae at attempted entry sites. When conidial suspensions of mossd1 mutant were spotted onto the leaves of HvCEBiP-silenced plants, small brown necrotic flecks or blast lesions were produced but these lesions did not expand beyond the inoculation site. Wild-type M. oryzae also produced slightly more severe symptoms on the leaves of HvCEBiP-silenced plants. Cytological observation revealed that these lesions resulted from appressorium-mediated penetration into plant epidermal cells. CONCLUSIONS: These results suggest that HvCEBiP is involved in basal resistance against appressorium-mediated infection and that basal resistance might be triggered by the recognition of chitin oligosaccharides derived from M. oryzae. BioMed Central 2010-12-30 /pmc/articles/PMC3020183/ /pubmed/21190588 http://dx.doi.org/10.1186/1471-2229-10-288 Text en Copyright ©2010 Tanaka et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (<url>http://creativecommons.org/licenses/by/2.0</url>), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Tanaka, Shigeyuki Ichikawa, Akari Yamada, Kaori Tsuji, Gento Nishiuchi, Takumi Mori, Masashi Koga, Hironori Nishizawa, Yoko O'Connell, Richard Kubo, Yasuyuki HvCEBiP, a gene homologous to rice chitin receptor CEBiP, contributes to basal resistance of barley to Magnaporthe oryzae |
title | HvCEBiP, a gene homologous to rice chitin receptor CEBiP, contributes to basal resistance of barley to Magnaporthe oryzae |
title_full | HvCEBiP, a gene homologous to rice chitin receptor CEBiP, contributes to basal resistance of barley to Magnaporthe oryzae |
title_fullStr | HvCEBiP, a gene homologous to rice chitin receptor CEBiP, contributes to basal resistance of barley to Magnaporthe oryzae |
title_full_unstemmed | HvCEBiP, a gene homologous to rice chitin receptor CEBiP, contributes to basal resistance of barley to Magnaporthe oryzae |
title_short | HvCEBiP, a gene homologous to rice chitin receptor CEBiP, contributes to basal resistance of barley to Magnaporthe oryzae |
title_sort | hvcebip, a gene homologous to rice chitin receptor cebip, contributes to basal resistance of barley to magnaporthe oryzae |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3020183/ https://www.ncbi.nlm.nih.gov/pubmed/21190588 http://dx.doi.org/10.1186/1471-2229-10-288 |
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