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Type-B ARRs Control Carpel Regeneration Through Mediating AGAMOUS Expression in Arabidopsis
Plants are known for their capacity to regenerate organs, such as shoot, root and floral organs. Recently, a number of studies contributed to understanding the mechanisms of shoot and root regeneration. However, the mechanisms underlying floral organ regeneration are largely unknown. In this study,...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Oxford University Press
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6018948/ https://www.ncbi.nlm.nih.gov/pubmed/29186581 http://dx.doi.org/10.1093/pcp/pcx187 |
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author | Rong, Xiao Fei Sang, Ya Lin Wang, Liang Meng, Wen Jing Zou, Chun Hao Dong, Yu Xiu Bie, Xiao Min Cheng, Zhi Juan Zhang, Xian Sheng |
author_facet | Rong, Xiao Fei Sang, Ya Lin Wang, Liang Meng, Wen Jing Zou, Chun Hao Dong, Yu Xiu Bie, Xiao Min Cheng, Zhi Juan Zhang, Xian Sheng |
author_sort | Rong, Xiao Fei |
collection | PubMed |
description | Plants are known for their capacity to regenerate organs, such as shoot, root and floral organs. Recently, a number of studies contributed to understanding the mechanisms of shoot and root regeneration. However, the mechanisms underlying floral organ regeneration are largely unknown. In this study, we established a carpel regeneration system in which two types of carpels were induced by exogenous cytokinin. For type I, all the floral organs in the regenerated inflorescence were transformed into carpels. For type II, carpels were generated directly from callus. The transcript level of AGAMOUS (AG), the carpel identity gene, was up-regulated during carpel induction. The expression signals of AG were detected in the initiating carpel primordia and regenerating carpels, and co-localized with those of two Type-B ARABIDOPSIS RESPONSE REGULATORs (ARRs), ARR1 and ARR10. Repression of either AG or type-B ARRs reduced carpel regeneration. Binding analyses showed that ARR1 and ARR10 directly bound to transcriptional regulatory regions of AG and positively regulated its expression. In addition, the expression of type-B ARRs overlapped with that of AG in the floral primordia in planta. Defects in type-B ARRs reduced the number of carpels. The results indicate that type-B ARRs control carpel regeneration through activating AG expression. Our results provide new information for understanding the mechanism of carpel formation. |
format | Online Article Text |
id | pubmed-6018948 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Oxford University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-60189482018-07-10 Type-B ARRs Control Carpel Regeneration Through Mediating AGAMOUS Expression in Arabidopsis Rong, Xiao Fei Sang, Ya Lin Wang, Liang Meng, Wen Jing Zou, Chun Hao Dong, Yu Xiu Bie, Xiao Min Cheng, Zhi Juan Zhang, Xian Sheng Plant Cell Physiol Special Issue – Regular Papers Plants are known for their capacity to regenerate organs, such as shoot, root and floral organs. Recently, a number of studies contributed to understanding the mechanisms of shoot and root regeneration. However, the mechanisms underlying floral organ regeneration are largely unknown. In this study, we established a carpel regeneration system in which two types of carpels were induced by exogenous cytokinin. For type I, all the floral organs in the regenerated inflorescence were transformed into carpels. For type II, carpels were generated directly from callus. The transcript level of AGAMOUS (AG), the carpel identity gene, was up-regulated during carpel induction. The expression signals of AG were detected in the initiating carpel primordia and regenerating carpels, and co-localized with those of two Type-B ARABIDOPSIS RESPONSE REGULATORs (ARRs), ARR1 and ARR10. Repression of either AG or type-B ARRs reduced carpel regeneration. Binding analyses showed that ARR1 and ARR10 directly bound to transcriptional regulatory regions of AG and positively regulated its expression. In addition, the expression of type-B ARRs overlapped with that of AG in the floral primordia in planta. Defects in type-B ARRs reduced the number of carpels. The results indicate that type-B ARRs control carpel regeneration through activating AG expression. Our results provide new information for understanding the mechanism of carpel formation. Oxford University Press 2018-04 2017-11-24 /pmc/articles/PMC6018948/ /pubmed/29186581 http://dx.doi.org/10.1093/pcp/pcx187 Text en © The Author 2017. Published by Oxford University Press on behalf of Japanese Society of Plant Physiologists. http://creativecommons.org/licenses/by-nc/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com |
spellingShingle | Special Issue – Regular Papers Rong, Xiao Fei Sang, Ya Lin Wang, Liang Meng, Wen Jing Zou, Chun Hao Dong, Yu Xiu Bie, Xiao Min Cheng, Zhi Juan Zhang, Xian Sheng Type-B ARRs Control Carpel Regeneration Through Mediating AGAMOUS Expression in Arabidopsis |
title | Type-B ARRs Control Carpel Regeneration Through Mediating AGAMOUS Expression in Arabidopsis |
title_full | Type-B ARRs Control Carpel Regeneration Through Mediating AGAMOUS Expression in Arabidopsis |
title_fullStr | Type-B ARRs Control Carpel Regeneration Through Mediating AGAMOUS Expression in Arabidopsis |
title_full_unstemmed | Type-B ARRs Control Carpel Regeneration Through Mediating AGAMOUS Expression in Arabidopsis |
title_short | Type-B ARRs Control Carpel Regeneration Through Mediating AGAMOUS Expression in Arabidopsis |
title_sort | type-b arrs control carpel regeneration through mediating agamous expression in arabidopsis |
topic | Special Issue – Regular Papers |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6018948/ https://www.ncbi.nlm.nih.gov/pubmed/29186581 http://dx.doi.org/10.1093/pcp/pcx187 |
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