Suppr超能文献

ERF转录因子EPI1是黑暗诱导和茉莉酸刺激的衰老过程中的负调控因子。

The ERF transcription factor EPI1 is a negative regulator of dark-induced and jasmonate-stimulated senescence in .

作者信息

Chung KwiMi, Nakano Toshitsugu, Fujiwara Sumire, Mitsuda Nobutaka, Otsuki Namie, Tsujimoto-Inui Yayoi, Naito Yuki, Ohme-Takagi Masaru, Suzuki Kaoru

机构信息

Bioproduction Research Institute, National Institute of Advanced Industrial Science and Technology (AIST), Tsukuba, Ibaraki 305-8566, Japan.

Graduate School of Science and Engineering, Saitama University, Saitama 338-8570, Japan.

出版信息

Plant Biotechnol (Tokyo). 2016;33(4):235-243. doi: 10.5511/plantbiotechnology.16.0127a. Epub 2016 Apr 9.

Abstract

Identification of the factors involved in the regulation of senescence and the analysis of their function are important for both a biological understanding of the senescence mechanism and the improvement of agricultural productivity. In this study, we identified an gene termed " (EPI1) as a possible regulator of senescence in . We found that EPI1 possesses transcriptional repression activity and that the transgenic plants overexpressing and expressing its chimeric repressor, , commonly suppressed the darkness-induced senescence in their excised aerial parts. These transgenic plants additionally maintained a high level of chlorophyll, even after the methyl jasmonate (MeJA) treatment, which stimulated senescence in the dark. In addition, we found that senescence-induced and -reduced genes are down- and upregulated, respectively, in the MeJA-treated transgenic plants under darkness. Our results suggest that EPI1 functions as a negative regulator of the dark-induced and JA-stimulated senescence.

摘要

确定参与衰老调控的因素并分析其功能,对于从生物学角度理解衰老机制以及提高农业生产力都很重要。在本研究中,我们鉴定出一个名为“(EPI1)”的基因,它可能是[植物名称]衰老的调控因子。我们发现EPI1具有转录抑制活性,过表达EPI1及其嵌合阻遏物的转基因植物,通常会抑制其离体地上部分的黑暗诱导衰老。这些转基因植物即使在茉莉酸甲酯(MeJA)处理后,仍能维持高水平的叶绿素,而MeJA处理会在黑暗中刺激衰老。此外,我们发现,在黑暗条件下经MeJA处理的转基因植物中,衰老诱导基因和衰老减少基因分别下调和上调。我们的结果表明,EPI1作为黑暗诱导和茉莉酸刺激衰老的负调控因子发挥作用。

相似文献

本文引用的文献

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验