Salicylate-Independent Lesion Formation in Arabidopsis lsd Mutants
In many interactions of plants with pathogens, the primary host defense reaction is accompanied by plant cell death at the site of infection. The resulting lesions are correlated with the establishment of an inducible resistance in plants called systemic acquired resistance (SAR), for which salicyli...
| Main Authors: | , , , , , |
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| Format: | Article |
| Language: | English |
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The American Phytopathological Society
1997-07-01
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| Series: | Molecular Plant-Microbe Interactions |
| Subjects: | |
| Online Access: | https://apsjournals.apsnet.org/doi/10.1094/MPMI.1997.10.5.531 |
| _version_ | 1811290176286097408 |
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| author | Michelle D. Hunt Terrence P. Delaney Robert A. Dietrich Kris B. Weymann Jeffery L. Dangl John A. Ryals |
| author_facet | Michelle D. Hunt Terrence P. Delaney Robert A. Dietrich Kris B. Weymann Jeffery L. Dangl John A. Ryals |
| author_sort | Michelle D. Hunt |
| collection | DOAJ |
| description | In many interactions of plants with pathogens, the primary host defense reaction is accompanied by plant cell death at the site of infection. The resulting lesions are correlated with the establishment of an inducible resistance in plants called systemic acquired resistance (SAR), for which salicylic acid (SA) accumulation is a critical signaling event in Arabidopsis and tobacco. In Arabidopsis, the lesions simulating disease (lsd) mutants spontaneously develop lesions in the absence of pathogen infection. Furthermore, lsd mutants express SAR marker genes when lesions are present and are resistant to the same spectrum of pathogens as plants activated for SAR by necrogenic pathogen infection. To assess the epistatic relationship between SA accumulation and cell death, transgenic Arabidopsis unable to accumulate SA due to the expression of the salicylate hydroxylase (nahG) gene were used in crosses with the dominant mutants lsd2 or lsd4. Progeny from the crosses were inhibited for SAR gene expression and disease resistance. However, these progeny retained the spontaneous cell death phenotype similar to siblings not expressing nahG. Because lesions form in the absence of SA accumulation for lsd2 and lsd4, a model is suggested in which lesion formation in these two mutants is determined prior to SA accumulation in SAR signal transduction. By contrast, the loss of SAR gene expression and disease resistance in nahG-expressing lsd mutants indicates that these traits are dependent upon SA accumulation in the SAR signal transduction pathway. |
| first_indexed | 2024-04-13T04:08:17Z |
| format | Article |
| id | doaj.art-eb027461aeba42e684c16f5e39ced2d6 |
| institution | Directory Open Access Journal |
| issn | 0894-0282 1943-7706 |
| language | English |
| last_indexed | 2024-04-13T04:08:17Z |
| publishDate | 1997-07-01 |
| publisher | The American Phytopathological Society |
| record_format | Article |
| series | Molecular Plant-Microbe Interactions |
| spelling | doaj.art-eb027461aeba42e684c16f5e39ced2d62022-12-22T03:03:11ZengThe American Phytopathological SocietyMolecular Plant-Microbe Interactions0894-02821943-77061997-07-0110553153610.1094/MPMI.1997.10.5.531Salicylate-Independent Lesion Formation in Arabidopsis lsd MutantsMichelle D. HuntTerrence P. DelaneyRobert A. DietrichKris B. WeymannJeffery L. DanglJohn A. RyalsIn many interactions of plants with pathogens, the primary host defense reaction is accompanied by plant cell death at the site of infection. The resulting lesions are correlated with the establishment of an inducible resistance in plants called systemic acquired resistance (SAR), for which salicylic acid (SA) accumulation is a critical signaling event in Arabidopsis and tobacco. In Arabidopsis, the lesions simulating disease (lsd) mutants spontaneously develop lesions in the absence of pathogen infection. Furthermore, lsd mutants express SAR marker genes when lesions are present and are resistant to the same spectrum of pathogens as plants activated for SAR by necrogenic pathogen infection. To assess the epistatic relationship between SA accumulation and cell death, transgenic Arabidopsis unable to accumulate SA due to the expression of the salicylate hydroxylase (nahG) gene were used in crosses with the dominant mutants lsd2 or lsd4. Progeny from the crosses were inhibited for SAR gene expression and disease resistance. However, these progeny retained the spontaneous cell death phenotype similar to siblings not expressing nahG. Because lesions form in the absence of SA accumulation for lsd2 and lsd4, a model is suggested in which lesion formation in these two mutants is determined prior to SA accumulation in SAR signal transduction. By contrast, the loss of SAR gene expression and disease resistance in nahG-expressing lsd mutants indicates that these traits are dependent upon SA accumulation in the SAR signal transduction pathway.https://apsjournals.apsnet.org/doi/10.1094/MPMI.1997.10.5.531autofluorescencecallosefeedback amplification loopPeronospora parasitica isolate NocoPR gene expression |
| spellingShingle | Michelle D. Hunt Terrence P. Delaney Robert A. Dietrich Kris B. Weymann Jeffery L. Dangl John A. Ryals Salicylate-Independent Lesion Formation in Arabidopsis lsd Mutants Molecular Plant-Microbe Interactions autofluorescence callose feedback amplification loop Peronospora parasitica isolate Noco PR gene expression |
| title | Salicylate-Independent Lesion Formation in Arabidopsis lsd Mutants |
| title_full | Salicylate-Independent Lesion Formation in Arabidopsis lsd Mutants |
| title_fullStr | Salicylate-Independent Lesion Formation in Arabidopsis lsd Mutants |
| title_full_unstemmed | Salicylate-Independent Lesion Formation in Arabidopsis lsd Mutants |
| title_short | Salicylate-Independent Lesion Formation in Arabidopsis lsd Mutants |
| title_sort | salicylate independent lesion formation in arabidopsis lsd mutants |
| topic | autofluorescence callose feedback amplification loop Peronospora parasitica isolate Noco PR gene expression |
| url | https://apsjournals.apsnet.org/doi/10.1094/MPMI.1997.10.5.531 |
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