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The miR164‐GhCUC2‐GhBRC1 module regulates plant architecture through abscisic acid in cotton
Branching determines cotton architecture and production, but the underlying regulatory mechanisms remain unclear. Here, we report that the miR164‐GhCUC2 (CUP‐SHAPED COTYLEDON2) module regulates lateral shoot development in cotton and Arabidopsis. We generated OE‐GhCUC2m (overexpression GhCUC2m) and...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8428825/ https://www.ncbi.nlm.nih.gov/pubmed/33960609 http://dx.doi.org/10.1111/pbi.13599 |
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author | Zhan, Jingjing Chu, Yu Wang, Ye Diao, Yangyang Zhao, Yanyan Liu, Lisen Wei, Xi Meng, Yuan Li, Fuguang Ge, Xiaoyang |
author_facet | Zhan, Jingjing Chu, Yu Wang, Ye Diao, Yangyang Zhao, Yanyan Liu, Lisen Wei, Xi Meng, Yuan Li, Fuguang Ge, Xiaoyang |
author_sort | Zhan, Jingjing |
collection | PubMed |
description | Branching determines cotton architecture and production, but the underlying regulatory mechanisms remain unclear. Here, we report that the miR164‐GhCUC2 (CUP‐SHAPED COTYLEDON2) module regulates lateral shoot development in cotton and Arabidopsis. We generated OE‐GhCUC2m (overexpression GhCUC2m) and STTM164 (short tandem target mimic RNA of miR164) lines in cotton and heterologous expression lines for gh‐miR164, GhCUC2 and GhCUC2m in Arabidopsis to study the mechanisms controlling lateral branching. GhCUC2m overexpression resulted in a short‐branch phenotype similar to STTM164. In addition, heterologous expression of GhCUC2m led to decreased number and length of branches compared with wild type, opposite to the effects of the OE‐gh‐pre164 line in Arabidopsis. GhCUC2 interacted with GhBRC1 and exhibited similar negative regulation of branching. Overexpression of GhBRC1 in the brc1‐2 mutant partially rescued the mutant phenotype and decreased branch number. GhBRC1 directly bound to the NCED1 promoter and activated its transcription, leading to local abscisic acid (ABA) accumulation and response. Mutation of the NCED1 promoter disrupted activation by GhBRC1. This finding demonstrates a direct relationship between BRC1 and ABA signalling and places ABA downstream of BRC1 in the control of branching development. The miR164‐GhCUC2‐GhBRC1‐GhNCED1 module provides a clear regulatory axis for ABA signalling to control plant architecture. |
format | Online Article Text |
id | pubmed-8428825 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-84288252021-09-14 The miR164‐GhCUC2‐GhBRC1 module regulates plant architecture through abscisic acid in cotton Zhan, Jingjing Chu, Yu Wang, Ye Diao, Yangyang Zhao, Yanyan Liu, Lisen Wei, Xi Meng, Yuan Li, Fuguang Ge, Xiaoyang Plant Biotechnol J Research Articles Branching determines cotton architecture and production, but the underlying regulatory mechanisms remain unclear. Here, we report that the miR164‐GhCUC2 (CUP‐SHAPED COTYLEDON2) module regulates lateral shoot development in cotton and Arabidopsis. We generated OE‐GhCUC2m (overexpression GhCUC2m) and STTM164 (short tandem target mimic RNA of miR164) lines in cotton and heterologous expression lines for gh‐miR164, GhCUC2 and GhCUC2m in Arabidopsis to study the mechanisms controlling lateral branching. GhCUC2m overexpression resulted in a short‐branch phenotype similar to STTM164. In addition, heterologous expression of GhCUC2m led to decreased number and length of branches compared with wild type, opposite to the effects of the OE‐gh‐pre164 line in Arabidopsis. GhCUC2 interacted with GhBRC1 and exhibited similar negative regulation of branching. Overexpression of GhBRC1 in the brc1‐2 mutant partially rescued the mutant phenotype and decreased branch number. GhBRC1 directly bound to the NCED1 promoter and activated its transcription, leading to local abscisic acid (ABA) accumulation and response. Mutation of the NCED1 promoter disrupted activation by GhBRC1. This finding demonstrates a direct relationship between BRC1 and ABA signalling and places ABA downstream of BRC1 in the control of branching development. The miR164‐GhCUC2‐GhBRC1‐GhNCED1 module provides a clear regulatory axis for ABA signalling to control plant architecture. John Wiley and Sons Inc. 2021-05-07 2021-09 /pmc/articles/PMC8428825/ /pubmed/33960609 http://dx.doi.org/10.1111/pbi.13599 Text en © 2021 The Authors. Plant Biotechnology Journal published by Society for Experimental Biology and The Association of Applied Biologists and John Wiley & Sons Ltd. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ (https://creativecommons.org/licenses/by-nc-nd/4.0/) License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made. |
spellingShingle | Research Articles Zhan, Jingjing Chu, Yu Wang, Ye Diao, Yangyang Zhao, Yanyan Liu, Lisen Wei, Xi Meng, Yuan Li, Fuguang Ge, Xiaoyang The miR164‐GhCUC2‐GhBRC1 module regulates plant architecture through abscisic acid in cotton |
title | The miR164‐GhCUC2‐GhBRC1 module regulates plant architecture through abscisic acid in cotton |
title_full | The miR164‐GhCUC2‐GhBRC1 module regulates plant architecture through abscisic acid in cotton |
title_fullStr | The miR164‐GhCUC2‐GhBRC1 module regulates plant architecture through abscisic acid in cotton |
title_full_unstemmed | The miR164‐GhCUC2‐GhBRC1 module regulates plant architecture through abscisic acid in cotton |
title_short | The miR164‐GhCUC2‐GhBRC1 module regulates plant architecture through abscisic acid in cotton |
title_sort | mir164‐ghcuc2‐ghbrc1 module regulates plant architecture through abscisic acid in cotton |
topic | Research Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8428825/ https://www.ncbi.nlm.nih.gov/pubmed/33960609 http://dx.doi.org/10.1111/pbi.13599 |
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