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AtGAP1 Promotes the Resistance to Pseudomonas syringae pv. tomato DC3000 by Regulating Cell-Wall Thickness and Stomatal Aperture in Arabidopsis
GTP is an important signaling molecule involved in the growth, development, and stress adaptability of plants. The functions are mediated via binding to GTPases which are in turn regulated by GTPase-activating proteins (GAPs). Satellite reports have suggested the positive roles of GAPs in regulating...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9323218/ https://www.ncbi.nlm.nih.gov/pubmed/35886893 http://dx.doi.org/10.3390/ijms23147540 |
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author | Cheng, Sau-Shan Ku, Yee-Shan Cheung, Ming-Yan Lam, Hon-Ming |
author_facet | Cheng, Sau-Shan Ku, Yee-Shan Cheung, Ming-Yan Lam, Hon-Ming |
author_sort | Cheng, Sau-Shan |
collection | PubMed |
description | GTP is an important signaling molecule involved in the growth, development, and stress adaptability of plants. The functions are mediated via binding to GTPases which are in turn regulated by GTPase-activating proteins (GAPs). Satellite reports have suggested the positive roles of GAPs in regulating ABA signaling and pathogen resistance in plants. However, the molecular mechanisms that bring forth the pathogen resistance have remained unclear. In this study, we demonstrated that the expression of AtGAP1 was inducible by Pseudomonas syringae pv. tomato DC3000 (Pst DC3000). The overexpression of AtGAP1 in Arabidopsis promoted the expression of PR1 and the resistance to Pst DC3000. Proteomic analyses revealed the enhanced accumulation of cell-wall-modifying proteins as a result of AtGAP1 overexpression. By microscopic analyses, we showed that the overexpression of AtGAP1 resulted in increased thickness of the mesophyll cell wall and reduced stomatal aperture, which are effective strategies for restricting the entry of foliar pathogens. Altogether, we demonstrated that AtGAP1 increases the resistance to Pst DC3000 in Arabidopsis by promoting cellular strategies that restrict the entry of pathogens into the cells. These results point to a future direction for studying the modes of action of GAPs in regulating plant cell structures and disease resistance. |
format | Online Article Text |
id | pubmed-9323218 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-93232182022-07-27 AtGAP1 Promotes the Resistance to Pseudomonas syringae pv. tomato DC3000 by Regulating Cell-Wall Thickness and Stomatal Aperture in Arabidopsis Cheng, Sau-Shan Ku, Yee-Shan Cheung, Ming-Yan Lam, Hon-Ming Int J Mol Sci Article GTP is an important signaling molecule involved in the growth, development, and stress adaptability of plants. The functions are mediated via binding to GTPases which are in turn regulated by GTPase-activating proteins (GAPs). Satellite reports have suggested the positive roles of GAPs in regulating ABA signaling and pathogen resistance in plants. However, the molecular mechanisms that bring forth the pathogen resistance have remained unclear. In this study, we demonstrated that the expression of AtGAP1 was inducible by Pseudomonas syringae pv. tomato DC3000 (Pst DC3000). The overexpression of AtGAP1 in Arabidopsis promoted the expression of PR1 and the resistance to Pst DC3000. Proteomic analyses revealed the enhanced accumulation of cell-wall-modifying proteins as a result of AtGAP1 overexpression. By microscopic analyses, we showed that the overexpression of AtGAP1 resulted in increased thickness of the mesophyll cell wall and reduced stomatal aperture, which are effective strategies for restricting the entry of foliar pathogens. Altogether, we demonstrated that AtGAP1 increases the resistance to Pst DC3000 in Arabidopsis by promoting cellular strategies that restrict the entry of pathogens into the cells. These results point to a future direction for studying the modes of action of GAPs in regulating plant cell structures and disease resistance. MDPI 2022-07-07 /pmc/articles/PMC9323218/ /pubmed/35886893 http://dx.doi.org/10.3390/ijms23147540 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Cheng, Sau-Shan Ku, Yee-Shan Cheung, Ming-Yan Lam, Hon-Ming AtGAP1 Promotes the Resistance to Pseudomonas syringae pv. tomato DC3000 by Regulating Cell-Wall Thickness and Stomatal Aperture in Arabidopsis |
title | AtGAP1 Promotes the Resistance to Pseudomonas syringae pv. tomato DC3000 by Regulating Cell-Wall Thickness and Stomatal Aperture in Arabidopsis |
title_full | AtGAP1 Promotes the Resistance to Pseudomonas syringae pv. tomato DC3000 by Regulating Cell-Wall Thickness and Stomatal Aperture in Arabidopsis |
title_fullStr | AtGAP1 Promotes the Resistance to Pseudomonas syringae pv. tomato DC3000 by Regulating Cell-Wall Thickness and Stomatal Aperture in Arabidopsis |
title_full_unstemmed | AtGAP1 Promotes the Resistance to Pseudomonas syringae pv. tomato DC3000 by Regulating Cell-Wall Thickness and Stomatal Aperture in Arabidopsis |
title_short | AtGAP1 Promotes the Resistance to Pseudomonas syringae pv. tomato DC3000 by Regulating Cell-Wall Thickness and Stomatal Aperture in Arabidopsis |
title_sort | atgap1 promotes the resistance to pseudomonas syringae pv. tomato dc3000 by regulating cell-wall thickness and stomatal aperture in arabidopsis |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9323218/ https://www.ncbi.nlm.nih.gov/pubmed/35886893 http://dx.doi.org/10.3390/ijms23147540 |
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