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Ca(2+)-permeable mechanosensitive channels MCA1 and MCA2 mediate cold-induced cytosolic Ca(2+) increase and cold tolerance in Arabidopsis
Cold shock triggers an immediate rise in the cytosolic free calcium concentration ([Ca(2+)](cyt)) in Arabidopsis thaliana and this cold-induced elevation of [Ca(2+)](cyt) is inhibited by lanthanum or EGTA. It is suggested that intracellular calcium mainly contributes to the cold-induced [Ca(2+)](cyt...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5765038/ https://www.ncbi.nlm.nih.gov/pubmed/29323146 http://dx.doi.org/10.1038/s41598-017-17483-y |
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author | Mori, Kendo Renhu, Na Naito, Maho Nakamura, Aki Shiba, Hayato Yamamoto, Tsuyoshi Suzaki, Takuya Iida, Hidetoshi Miura, Kenji |
author_facet | Mori, Kendo Renhu, Na Naito, Maho Nakamura, Aki Shiba, Hayato Yamamoto, Tsuyoshi Suzaki, Takuya Iida, Hidetoshi Miura, Kenji |
author_sort | Mori, Kendo |
collection | PubMed |
description | Cold shock triggers an immediate rise in the cytosolic free calcium concentration ([Ca(2+)](cyt)) in Arabidopsis thaliana and this cold-induced elevation of [Ca(2+)](cyt) is inhibited by lanthanum or EGTA. It is suggested that intracellular calcium mainly contributes to the cold-induced [Ca(2+)](cyt) response by entering into the cytosol. Two calcium-permeable mechanosensitive channels, MCA1 and MCA2 (mid1-complementing activity), have been identified in Arabidopsis. Here, we demonstrate that MCA1 and MCA2 are involved in a cold-induced increase in [Ca(2+)](cyt). The cold-induced [Ca(2+)](cyt) increase in mca1 and mca2 mutants was markedly lower than that in wild types. The mca1 mca2 double mutant exhibited chilling and freezing sensitivity, compared to wild-type plants. Expression of At5g61820, At3g51660, and At4g15490, which are not regulated by the CBF/DREB1s transcription factor, was down-regulated in mca1 mca2. These results suggest that MCA1 and MCA2 are involved in the cold-induced elevation of [Ca(2+)](cyt), cold tolerance, and CBF/DREB1-independent cold signaling. |
format | Online Article Text |
id | pubmed-5765038 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-57650382018-01-17 Ca(2+)-permeable mechanosensitive channels MCA1 and MCA2 mediate cold-induced cytosolic Ca(2+) increase and cold tolerance in Arabidopsis Mori, Kendo Renhu, Na Naito, Maho Nakamura, Aki Shiba, Hayato Yamamoto, Tsuyoshi Suzaki, Takuya Iida, Hidetoshi Miura, Kenji Sci Rep Article Cold shock triggers an immediate rise in the cytosolic free calcium concentration ([Ca(2+)](cyt)) in Arabidopsis thaliana and this cold-induced elevation of [Ca(2+)](cyt) is inhibited by lanthanum or EGTA. It is suggested that intracellular calcium mainly contributes to the cold-induced [Ca(2+)](cyt) response by entering into the cytosol. Two calcium-permeable mechanosensitive channels, MCA1 and MCA2 (mid1-complementing activity), have been identified in Arabidopsis. Here, we demonstrate that MCA1 and MCA2 are involved in a cold-induced increase in [Ca(2+)](cyt). The cold-induced [Ca(2+)](cyt) increase in mca1 and mca2 mutants was markedly lower than that in wild types. The mca1 mca2 double mutant exhibited chilling and freezing sensitivity, compared to wild-type plants. Expression of At5g61820, At3g51660, and At4g15490, which are not regulated by the CBF/DREB1s transcription factor, was down-regulated in mca1 mca2. These results suggest that MCA1 and MCA2 are involved in the cold-induced elevation of [Ca(2+)](cyt), cold tolerance, and CBF/DREB1-independent cold signaling. Nature Publishing Group UK 2018-01-11 /pmc/articles/PMC5765038/ /pubmed/29323146 http://dx.doi.org/10.1038/s41598-017-17483-y Text en © The Author(s) 2018 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Mori, Kendo Renhu, Na Naito, Maho Nakamura, Aki Shiba, Hayato Yamamoto, Tsuyoshi Suzaki, Takuya Iida, Hidetoshi Miura, Kenji Ca(2+)-permeable mechanosensitive channels MCA1 and MCA2 mediate cold-induced cytosolic Ca(2+) increase and cold tolerance in Arabidopsis |
title | Ca(2+)-permeable mechanosensitive channels MCA1 and MCA2 mediate cold-induced cytosolic Ca(2+) increase and cold tolerance in Arabidopsis |
title_full | Ca(2+)-permeable mechanosensitive channels MCA1 and MCA2 mediate cold-induced cytosolic Ca(2+) increase and cold tolerance in Arabidopsis |
title_fullStr | Ca(2+)-permeable mechanosensitive channels MCA1 and MCA2 mediate cold-induced cytosolic Ca(2+) increase and cold tolerance in Arabidopsis |
title_full_unstemmed | Ca(2+)-permeable mechanosensitive channels MCA1 and MCA2 mediate cold-induced cytosolic Ca(2+) increase and cold tolerance in Arabidopsis |
title_short | Ca(2+)-permeable mechanosensitive channels MCA1 and MCA2 mediate cold-induced cytosolic Ca(2+) increase and cold tolerance in Arabidopsis |
title_sort | ca(2+)-permeable mechanosensitive channels mca1 and mca2 mediate cold-induced cytosolic ca(2+) increase and cold tolerance in arabidopsis |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5765038/ https://www.ncbi.nlm.nih.gov/pubmed/29323146 http://dx.doi.org/10.1038/s41598-017-17483-y |
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