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JAZ7 negatively regulates dark-induced leaf senescence in Arabidopsis
JASMONATE ZIM-domain (JAZ) proteins play important roles in plant defence and growth by regulating jasmonate signalling. Through data mining, we discovered that the JAZ7 gene was up-regulated in darkness. In the dark, the jaz7 mutant displayed more severe leaf yellowing, quicker chlorophyll degradat...
Autores principales: | , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Oxford University Press
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4737072/ https://www.ncbi.nlm.nih.gov/pubmed/26547795 http://dx.doi.org/10.1093/jxb/erv487 |
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author | Yu, Juan Zhang, Yixiang Di, Chao Zhang, Qunlian Zhang, Kang Wang, Chunchao You, Qi Yan, Hong Dai, Susie Y. Yuan, Joshua S Xu, Wenying Su, Zhen |
author_facet | Yu, Juan Zhang, Yixiang Di, Chao Zhang, Qunlian Zhang, Kang Wang, Chunchao You, Qi Yan, Hong Dai, Susie Y. Yuan, Joshua S Xu, Wenying Su, Zhen |
author_sort | Yu, Juan |
collection | PubMed |
description | JASMONATE ZIM-domain (JAZ) proteins play important roles in plant defence and growth by regulating jasmonate signalling. Through data mining, we discovered that the JAZ7 gene was up-regulated in darkness. In the dark, the jaz7 mutant displayed more severe leaf yellowing, quicker chlorophyll degradation, and higher hydrogen peroxide accumulation compared with wild-type (WT) plants. The mutant phenotype of dark-induced leaf senescence could be rescued in the JAZ7-complemented and -overexpression lines. Moreover, the double mutants of jaz7 myc2 and jaz7 coi1 exhibited delayed leaf senescence. We further employed GeneChip analysis to study the molecular mechanism. Some key genes down-regulated in the triple mutant myc2 myc3 myc4 were up-regulated in the jaz7 mutant under darkness. The Gene Ontology terms ‘leaf senescence’ and ‘cell death’ were significantly enriched in the differentially expressed genes. Combining the genetic and transcriptomic analyses together, we proposed a model whereby darkness can induce JAZ7, which might further block MYC2 to suppress dark-induced leaf senescence. In darkness, the mutation of JAZ7 might partially liberate MYC2/MYC3/MYC4 from suppression, leading the MYC proteins to bind to the G-box/G-box-like motifs in the promoters, resulting in the up-regulation of the downstream genes related to indole-glucosinolate biosynthesis, sulphate metabolism, callose deposition, and JA-mediated signalling pathways. In summary, our genetic and transcriptomic studies established the JAZ7 protein as an important regulator in dark-induced leaf senescence. |
format | Online Article Text |
id | pubmed-4737072 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Oxford University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-47370722016-02-03 JAZ7 negatively regulates dark-induced leaf senescence in Arabidopsis Yu, Juan Zhang, Yixiang Di, Chao Zhang, Qunlian Zhang, Kang Wang, Chunchao You, Qi Yan, Hong Dai, Susie Y. Yuan, Joshua S Xu, Wenying Su, Zhen J Exp Bot Research Paper JASMONATE ZIM-domain (JAZ) proteins play important roles in plant defence and growth by regulating jasmonate signalling. Through data mining, we discovered that the JAZ7 gene was up-regulated in darkness. In the dark, the jaz7 mutant displayed more severe leaf yellowing, quicker chlorophyll degradation, and higher hydrogen peroxide accumulation compared with wild-type (WT) plants. The mutant phenotype of dark-induced leaf senescence could be rescued in the JAZ7-complemented and -overexpression lines. Moreover, the double mutants of jaz7 myc2 and jaz7 coi1 exhibited delayed leaf senescence. We further employed GeneChip analysis to study the molecular mechanism. Some key genes down-regulated in the triple mutant myc2 myc3 myc4 were up-regulated in the jaz7 mutant under darkness. The Gene Ontology terms ‘leaf senescence’ and ‘cell death’ were significantly enriched in the differentially expressed genes. Combining the genetic and transcriptomic analyses together, we proposed a model whereby darkness can induce JAZ7, which might further block MYC2 to suppress dark-induced leaf senescence. In darkness, the mutation of JAZ7 might partially liberate MYC2/MYC3/MYC4 from suppression, leading the MYC proteins to bind to the G-box/G-box-like motifs in the promoters, resulting in the up-regulation of the downstream genes related to indole-glucosinolate biosynthesis, sulphate metabolism, callose deposition, and JA-mediated signalling pathways. In summary, our genetic and transcriptomic studies established the JAZ7 protein as an important regulator in dark-induced leaf senescence. Oxford University Press 2016-02 2015-11-07 /pmc/articles/PMC4737072/ /pubmed/26547795 http://dx.doi.org/10.1093/jxb/erv487 Text en © The Author 2015. Published by Oxford University Press on behalf of the Society for Experimental Biology. http://creativecommons.org/licenses/by/3.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Paper Yu, Juan Zhang, Yixiang Di, Chao Zhang, Qunlian Zhang, Kang Wang, Chunchao You, Qi Yan, Hong Dai, Susie Y. Yuan, Joshua S Xu, Wenying Su, Zhen JAZ7 negatively regulates dark-induced leaf senescence in Arabidopsis |
title | JAZ7 negatively regulates dark-induced leaf senescence in Arabidopsis
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title_full | JAZ7 negatively regulates dark-induced leaf senescence in Arabidopsis
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title_fullStr | JAZ7 negatively regulates dark-induced leaf senescence in Arabidopsis
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title_full_unstemmed | JAZ7 negatively regulates dark-induced leaf senescence in Arabidopsis
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title_short | JAZ7 negatively regulates dark-induced leaf senescence in Arabidopsis
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title_sort | jaz7 negatively regulates dark-induced leaf senescence in arabidopsis |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4737072/ https://www.ncbi.nlm.nih.gov/pubmed/26547795 http://dx.doi.org/10.1093/jxb/erv487 |
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