Cargando…
COP1 promotes ABA‐induced stomatal closure by modulating the abundance of ABI/HAB and AHG3 phosphatases
Plant stomata play a crucial role in leaf function, controlling water transpiration in response to environmental stresses and modulating the gas exchange necessary for photosynthesis. The phytohormone abscisic acid (ABA) promotes stomatal closure and inhibits light‐induced stomatal opening. The Arab...
Autores principales: | , , , , , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2020
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7898331/ https://www.ncbi.nlm.nih.gov/pubmed/33048351 http://dx.doi.org/10.1111/nph.17001 |
_version_ | 1783653841722408960 |
---|---|
author | Chen, Qingbin Bai, Ling Wang, Wenjing Shi, Huazhong Ramón Botella, José Zhan, Qidi Liu, Kang Yang, Hong‐Quan Song, Chun‐Peng |
author_facet | Chen, Qingbin Bai, Ling Wang, Wenjing Shi, Huazhong Ramón Botella, José Zhan, Qidi Liu, Kang Yang, Hong‐Quan Song, Chun‐Peng |
author_sort | Chen, Qingbin |
collection | PubMed |
description | Plant stomata play a crucial role in leaf function, controlling water transpiration in response to environmental stresses and modulating the gas exchange necessary for photosynthesis. The phytohormone abscisic acid (ABA) promotes stomatal closure and inhibits light‐induced stomatal opening. The Arabidopsis thaliana E3 ubiquitin ligase COP1 functions in ABA‐mediated stomatal closure. However, the underlying molecular mechanisms are still not fully understood. Yeast two‐hybrid assays were used to identify ABA signaling components that interact with COP1, and biochemical, molecular and genetic studies were carried out to elucidate the regulatory role of COP1 in ABA signaling. The cop1 mutants are hyposensitive to ABA‐triggered stomatal closure under light and dark conditions. COP1 interacts with and ubiquitinates the Arabidopsis clade A type 2C phosphatases (PP2Cs) ABI/HAB group and AHG3, thus triggering their degradation. Abscisic acid enhances the COP1‐mediated degradation of these PP2Cs. Mutations in ABI1 and AHG3 partly rescue the cop1 stomatal phenotype and the phosphorylation level of OST1, a crucial SnRK2‐type kinase in ABA signaling. Our data indicate that COP1 is part of a novel signaling pathway promoting ABA‐mediated stomatal closure by regulating the stability of a subset of the Clade A PP2Cs. These findings provide novel insights into the interplay between ABA and the light signaling component in the modulation of stomatal movement. |
format | Online Article Text |
id | pubmed-7898331 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-78983312021-03-03 COP1 promotes ABA‐induced stomatal closure by modulating the abundance of ABI/HAB and AHG3 phosphatases Chen, Qingbin Bai, Ling Wang, Wenjing Shi, Huazhong Ramón Botella, José Zhan, Qidi Liu, Kang Yang, Hong‐Quan Song, Chun‐Peng New Phytol Research Plant stomata play a crucial role in leaf function, controlling water transpiration in response to environmental stresses and modulating the gas exchange necessary for photosynthesis. The phytohormone abscisic acid (ABA) promotes stomatal closure and inhibits light‐induced stomatal opening. The Arabidopsis thaliana E3 ubiquitin ligase COP1 functions in ABA‐mediated stomatal closure. However, the underlying molecular mechanisms are still not fully understood. Yeast two‐hybrid assays were used to identify ABA signaling components that interact with COP1, and biochemical, molecular and genetic studies were carried out to elucidate the regulatory role of COP1 in ABA signaling. The cop1 mutants are hyposensitive to ABA‐triggered stomatal closure under light and dark conditions. COP1 interacts with and ubiquitinates the Arabidopsis clade A type 2C phosphatases (PP2Cs) ABI/HAB group and AHG3, thus triggering their degradation. Abscisic acid enhances the COP1‐mediated degradation of these PP2Cs. Mutations in ABI1 and AHG3 partly rescue the cop1 stomatal phenotype and the phosphorylation level of OST1, a crucial SnRK2‐type kinase in ABA signaling. Our data indicate that COP1 is part of a novel signaling pathway promoting ABA‐mediated stomatal closure by regulating the stability of a subset of the Clade A PP2Cs. These findings provide novel insights into the interplay between ABA and the light signaling component in the modulation of stomatal movement. John Wiley and Sons Inc. 2020-12-16 2021-02 /pmc/articles/PMC7898331/ /pubmed/33048351 http://dx.doi.org/10.1111/nph.17001 Text en © 2020 The Authors. New Phytologist © 2020 New Phytologist Foundation This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes. |
spellingShingle | Research Chen, Qingbin Bai, Ling Wang, Wenjing Shi, Huazhong Ramón Botella, José Zhan, Qidi Liu, Kang Yang, Hong‐Quan Song, Chun‐Peng COP1 promotes ABA‐induced stomatal closure by modulating the abundance of ABI/HAB and AHG3 phosphatases |
title | COP1 promotes ABA‐induced stomatal closure by modulating the abundance of ABI/HAB and AHG3 phosphatases |
title_full | COP1 promotes ABA‐induced stomatal closure by modulating the abundance of ABI/HAB and AHG3 phosphatases |
title_fullStr | COP1 promotes ABA‐induced stomatal closure by modulating the abundance of ABI/HAB and AHG3 phosphatases |
title_full_unstemmed | COP1 promotes ABA‐induced stomatal closure by modulating the abundance of ABI/HAB and AHG3 phosphatases |
title_short | COP1 promotes ABA‐induced stomatal closure by modulating the abundance of ABI/HAB and AHG3 phosphatases |
title_sort | cop1 promotes aba‐induced stomatal closure by modulating the abundance of abi/hab and ahg3 phosphatases |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7898331/ https://www.ncbi.nlm.nih.gov/pubmed/33048351 http://dx.doi.org/10.1111/nph.17001 |
work_keys_str_mv | AT chenqingbin cop1promotesabainducedstomatalclosurebymodulatingtheabundanceofabihabandahg3phosphatases AT bailing cop1promotesabainducedstomatalclosurebymodulatingtheabundanceofabihabandahg3phosphatases AT wangwenjing cop1promotesabainducedstomatalclosurebymodulatingtheabundanceofabihabandahg3phosphatases AT shihuazhong cop1promotesabainducedstomatalclosurebymodulatingtheabundanceofabihabandahg3phosphatases AT ramonbotellajose cop1promotesabainducedstomatalclosurebymodulatingtheabundanceofabihabandahg3phosphatases AT zhanqidi cop1promotesabainducedstomatalclosurebymodulatingtheabundanceofabihabandahg3phosphatases AT liukang cop1promotesabainducedstomatalclosurebymodulatingtheabundanceofabihabandahg3phosphatases AT yanghongquan cop1promotesabainducedstomatalclosurebymodulatingtheabundanceofabihabandahg3phosphatases AT songchunpeng cop1promotesabainducedstomatalclosurebymodulatingtheabundanceofabihabandahg3phosphatases |