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质体逆行调控 miRNA 表达响应光胁迫。

Plastid retrograde regulation of miRNA expression in response to light stress.

机构信息

Department of Plant Genetics, Breeding and Biotechnology, Institute of Biology, Warsaw University of Life Sciences-SGGW, 02-776, Warsaw, Poland.

Institute of Biochemistry and Biophysics Polish Academy of Sciences, 02-106, Warsaw, Poland.

出版信息

BMC Plant Biol. 2022 Mar 26;22(1):150. doi: 10.1186/s12870-022-03525-9.

DOI:10.1186/s12870-022-03525-9
PMID:35346032
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8962581/
Abstract

BACKGROUND

MicroRNAs (miRNAs) are a class of endogenous noncoding RNAs that play a pivotal role in the regulation of plant development and responses to the surrounding environment. Despite the efforts made to elucidate their function in the adaptation of plants to many abiotic and biotic stresses, their role in high light (HL) stress is still vague. HL stress often arises upon plant exposure to full sunlight. Subsequent changes in nuclear gene expression are triggered by chloroplast-derived retrograde signals.

RESULTS

In this study, we show that HL is involved in miRNA-dependent regulation in Arabidopsis thaliana rosettes. Microtranscriptomic screening revealed a limited number of miRNAs reacting to HL. To explain the miRNA regulation mechanisms at the different biogenesis stages, chemical and genetic approaches were applied. First, we tested the possible role of plastoquinone (PQ) redox changes using photosynthetic electron transport chain inhibitors. The results suggest that increased primary transcript abundance (pri-miRNAs) of HL-regulated miRNAs is dependent on signals upstream of PQ. This indicates that such signals may originate from photosystem II, which is the main singlet oxygen (O) source. Nevertheless, no changes in pri-miRNA expression upon a dark-light shift in the conditional fluorescent (flu) mutant producing O were observed when compared to wild-type plants. Thus, we explored the O signaling pathway, which is initiated independently in HL and is related to β-carotene oxidation and production of volatile derivatives, such as β-cyclocitral (β-CC). Pri-miRNA induction by β-CC, which is a component of this O pathway, as well as an altered response in the methylene blue sensitivity 1 (mbs1) mutant support the role of O signaling in miRNA regulation.

CONCLUSIONS

We show that light stress triggers changes in miRNA expression. This stress response may be regulated by reactive oxygen species (ROS)-related signaling. In conclusion, our results link ROS action to miRNA biogenesis, suggesting its contribution to inconsistent pri- and mature miRNA dynamics.

摘要

背景

MicroRNAs (miRNAs) 是一类内源性非编码 RNA,在调控植物发育和对周围环境的响应方面发挥着关键作用。尽管已经努力阐明它们在植物适应多种非生物和生物胁迫中的功能,但它们在高光(HL)胁迫中的作用仍然不清楚。HL 胁迫通常发生在植物暴露于全日照下。随后,叶绿体衍生的逆行信号触发核基因表达的变化。

结果

在本研究中,我们表明 HL 参与了拟南芥莲座叶中 miRNA 依赖的调节。微转录组筛选显示,只有少数 miRNAs 对 HL 有反应。为了解释不同生物发生阶段 miRNA 调节机制,我们应用了化学和遗传方法。首先,我们使用光合作用电子传递链抑制剂测试了质体醌(PQ)氧化还原变化的可能作用。结果表明,HL 调控 miRNA 的初级转录本丰度(pri-miRNAs)的增加依赖于 PQ 上游的信号。这表明这些信号可能来自于光系统 II,它是单线态氧(O)的主要来源。然而,与野生型植物相比,在条件荧光(flu)突变体中进行暗-光转换时,pri-miRNA 的表达没有变化。因此,我们探索了 O 信号通路,该通路在 HL 中独立启动,与β-胡萝卜素氧化和挥发性衍生物(如β-环柠檬醛(β-CC))的产生有关。β-CC 诱导 pri-miRNA 的表达,这是 O 途径的一个组成部分,以及在亚甲基蓝敏感性 1(mbs1)突变体中的改变反应,支持 O 信号在 miRNA 调节中的作用。

结论

我们表明,光照胁迫会引发 miRNA 表达的变化。这种应激反应可能受到活性氧(ROS)相关信号的调节。总之,我们的结果将 ROS 作用与 miRNA 生物发生联系起来,表明其对不一致的 pri-和成熟 miRNA 动力学的贡献。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db66/8962581/f795af48eccc/12870_2022_3525_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db66/8962581/39b49b33b8bb/12870_2022_3525_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db66/8962581/68860374fd7f/12870_2022_3525_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db66/8962581/977f546b2afd/12870_2022_3525_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db66/8962581/f795af48eccc/12870_2022_3525_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db66/8962581/39b49b33b8bb/12870_2022_3525_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db66/8962581/68860374fd7f/12870_2022_3525_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db66/8962581/977f546b2afd/12870_2022_3525_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db66/8962581/f795af48eccc/12870_2022_3525_Fig4_HTML.jpg

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