miR160 及其靶基因 ARF10、ARF16 和 ARF17 以光、BRZ 或 PAC 依赖的方式调节拟南芥下胚轴伸长：miR160 促进下胚轴伸长。

MiR160 and its target genes ARF10, ARF16 and ARF17 modulate hypocotyl elongation in a light, BRZ, or PAC-dependent manner in Arabidopsis: miR160 promotes hypocotyl elongation.

机构信息

The Key Laboratory of the Plant Development and Environmental Adaptation Biology, Ministry of Education, School of Life Sciences, Shandong University, Qingdao, 266237, Shandong, China.

出版信息

Plant Sci. 2021 Feb;303:110686. doi: 10.1016/j.plantsci.2020.110686. Epub 2020 Oct 20.

DOI:10.1016/j.plantsci.2020.110686

PMID:33487334

Abstract

Multiple hormonal and environmental signals participate in the regulation of plant hypocotyl elongation, which allow the plants to optimize their survival strategy from seed germination to seedling establishment. Auxin plays key roles in cell elongation via auxin signaling transduction and its interactions with other hormonal and environmental signals. However, the roles of auxin response factor (ARF) family in cross-talk between auxin and other hormonal or environmental signals during hypocotyl elongation are not fully understood. Here we show that miR160 and its target genes ARF10, ARF16 and ARF17 modulate hypocotyl elongation in a light, brassinazole (BRZ, a BR biosynthesis inhibitor), or paclobutrazol (PAC, a GA biosynthesis inhibitor)-dependent manner in Arabidopsis. miR160, ARF10, ARF16 and ARF17 have no effects on hypocotyl elongation in the dark. However, in the presence of either light, BRZ, or PAC, ARF10, ARF16 and ARF17 inhibit hypocotyl elongation, and miR160 promotes hypocotyl elongation via cleavage of their mRNA. miR160 and ARF10 are both expressed in the hypocotyl. ARF10 represses the expression of PACLOBUTRAZOL RESISTANCE1 (PRE1) and 35S::PRE1 could partly rescue the phenotype of mARF10 (a miR160-resistant form of ARF10), suggesting that PRE1 acts downstream of ARF10 in regulating hypocotyl elongation. In conclusion, our results indicate that miR160-ARF10/16/17 might serve as a molecular link in cross-talk of auxin, light, BR, and GA in hypocotyl elongation.

摘要

多种激素和环境信号参与调控植物下胚轴伸长，使植物能够从种子萌发到幼苗建立优化其生存策略。生长素通过生长素信号转导及其与其他激素和环境信号的相互作用在细胞伸长中发挥关键作用。然而，生长素响应因子（ARF）家族在生长素与其他激素或环境信号之间的交叉对话中在下胚轴伸长中的作用尚未完全阐明。在这里，我们表明 miR160 及其靶基因 ARF10、ARF16 和 ARF17 以光、油菜素内酯（BRZ，BR 生物合成抑制剂）或多效唑（PAC，GA 生物合成抑制剂）依赖的方式在拟南芥中调节下胚轴伸长。miR160、ARF10、ARF16 和 ARF17 在下胚轴伸长中在黑暗中没有影响。然而，在存在光、BRZ 或 PAC 的情况下，ARF10、ARF16 和 ARF17 抑制下胚轴伸长，miR160 通过切割其 mRNA 促进下胚轴伸长。miR160 和 ARF10 在下胚轴中都有表达。ARF10 抑制多效唑抗性 1（PRE1）的表达，而 35S::PRE1 可以部分挽救 mARF10（ARF10 的 miR160 抗性形式）的表型，表明 PRE1 在调节下胚轴伸长中作为 ARF10 的下游发挥作用。总之，我们的结果表明，miR160-ARF10/16/17 可能在下胚轴伸长中作为生长素、光、BR 和 GA 交叉对话的分子联系。