The Sesquiterpene Botrydial Produced by Botrytis cinerea Induces the Hypersensitive Response on Plant Tissues and Its Action Is Modulated by Salicylic Acid and Jasmonic Acid Signaling
Botrytis cinerea, as a necrotrophic fungus, kills host tissues and feeds on the remains. This fungus is able to induce the hypersensitive response (HR) on its hosts, thus taking advantage on the host's defense machinery for generating necrotic tissues. However, the identity of HR effectors prod...
| Main Authors: | , , , , , , |
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| Format: | Article |
| Language: | English |
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The American Phytopathological Society
2011-08-01
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| Series: | Molecular Plant-Microbe Interactions |
| Online Access: | https://apsjournals.apsnet.org/doi/10.1094/MPMI-10-10-0248 |
| _version_ | 1811278095867445248 |
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| author | Franco Rubén Rossi Andrés Gárriz María Marina Fernando Matías Romero María Elisa Gonzalez Isidro González Collado Fernando Luis Pieckenstain |
| author_facet | Franco Rubén Rossi Andrés Gárriz María Marina Fernando Matías Romero María Elisa Gonzalez Isidro González Collado Fernando Luis Pieckenstain |
| author_sort | Franco Rubén Rossi |
| collection | DOAJ |
| description | Botrytis cinerea, as a necrotrophic fungus, kills host tissues and feeds on the remains. This fungus is able to induce the hypersensitive response (HR) on its hosts, thus taking advantage on the host's defense machinery for generating necrotic tissues. However, the identity of HR effectors produced by B. cinerea is not clear. The aim of this work was to determine whether botrydial, a phytotoxic sesquiterpene produced by B. cinerea, is able to induce the HR on plant hosts, using Arabidopsis thaliana as a model. Botrydial induced the expression of the HR marker HSR3, callose deposition, and the accumulation of reactive oxygen species and phenolic compounds. Botrydial also induced the expression of PR1 and PDF1.2, two pathogenesis-related proteins involved in defense responses regulated by salicylic acid (SA) and jasmonic acid (JA), respectively. A. thaliana and tobacco plants defective in SA signaling were more resistant to botrydial than wild-type plants, as opposed to A. thaliana plants defective in JA signaling, which were more sensitive. It can be concluded that botrydial induces the HR on its hosts and its effects are modulated by host signaling pathways mediated by SA and JA. |
| first_indexed | 2024-04-13T00:29:43Z |
| format | Article |
| id | doaj.art-1929922088fb4fbba0a31bd179a82f6b |
| institution | Directory Open Access Journal |
| issn | 0894-0282 1943-7706 |
| language | English |
| last_indexed | 2024-04-13T00:29:43Z |
| publishDate | 2011-08-01 |
| publisher | The American Phytopathological Society |
| record_format | Article |
| series | Molecular Plant-Microbe Interactions |
| spelling | doaj.art-1929922088fb4fbba0a31bd179a82f6b2022-12-22T03:10:31ZengThe American Phytopathological SocietyMolecular Plant-Microbe Interactions0894-02821943-77062011-08-0124888889610.1094/MPMI-10-10-0248The Sesquiterpene Botrydial Produced by Botrytis cinerea Induces the Hypersensitive Response on Plant Tissues and Its Action Is Modulated by Salicylic Acid and Jasmonic Acid SignalingFranco Rubén RossiAndrés GárrizMaría MarinaFernando Matías RomeroMaría Elisa GonzalezIsidro González ColladoFernando Luis PieckenstainBotrytis cinerea, as a necrotrophic fungus, kills host tissues and feeds on the remains. This fungus is able to induce the hypersensitive response (HR) on its hosts, thus taking advantage on the host's defense machinery for generating necrotic tissues. However, the identity of HR effectors produced by B. cinerea is not clear. The aim of this work was to determine whether botrydial, a phytotoxic sesquiterpene produced by B. cinerea, is able to induce the HR on plant hosts, using Arabidopsis thaliana as a model. Botrydial induced the expression of the HR marker HSR3, callose deposition, and the accumulation of reactive oxygen species and phenolic compounds. Botrydial also induced the expression of PR1 and PDF1.2, two pathogenesis-related proteins involved in defense responses regulated by salicylic acid (SA) and jasmonic acid (JA), respectively. A. thaliana and tobacco plants defective in SA signaling were more resistant to botrydial than wild-type plants, as opposed to A. thaliana plants defective in JA signaling, which were more sensitive. It can be concluded that botrydial induces the HR on its hosts and its effects are modulated by host signaling pathways mediated by SA and JA.https://apsjournals.apsnet.org/doi/10.1094/MPMI-10-10-0248 |
| spellingShingle | Franco Rubén Rossi Andrés Gárriz María Marina Fernando Matías Romero María Elisa Gonzalez Isidro González Collado Fernando Luis Pieckenstain The Sesquiterpene Botrydial Produced by Botrytis cinerea Induces the Hypersensitive Response on Plant Tissues and Its Action Is Modulated by Salicylic Acid and Jasmonic Acid Signaling Molecular Plant-Microbe Interactions |
| title | The Sesquiterpene Botrydial Produced by Botrytis cinerea Induces the Hypersensitive Response on Plant Tissues and Its Action Is Modulated by Salicylic Acid and Jasmonic Acid Signaling |
| title_full | The Sesquiterpene Botrydial Produced by Botrytis cinerea Induces the Hypersensitive Response on Plant Tissues and Its Action Is Modulated by Salicylic Acid and Jasmonic Acid Signaling |
| title_fullStr | The Sesquiterpene Botrydial Produced by Botrytis cinerea Induces the Hypersensitive Response on Plant Tissues and Its Action Is Modulated by Salicylic Acid and Jasmonic Acid Signaling |
| title_full_unstemmed | The Sesquiterpene Botrydial Produced by Botrytis cinerea Induces the Hypersensitive Response on Plant Tissues and Its Action Is Modulated by Salicylic Acid and Jasmonic Acid Signaling |
| title_short | The Sesquiterpene Botrydial Produced by Botrytis cinerea Induces the Hypersensitive Response on Plant Tissues and Its Action Is Modulated by Salicylic Acid and Jasmonic Acid Signaling |
| title_sort | sesquiterpene botrydial produced by botrytis cinerea induces the hypersensitive response on plant tissues and its action is modulated by salicylic acid and jasmonic acid signaling |
| url | https://apsjournals.apsnet.org/doi/10.1094/MPMI-10-10-0248 |
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