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miR160和miR166/165参与拟南芥体细胞胚胎发生诱导过程中生长素介导的反应。

miR160 and miR166/165 Contribute to the -Mediated Auxin Response Involved in the Somatic Embryogenesis Induction in Arabidopsis.

作者信息

Wójcik Anna M, Nodine Michael D, Gaj Małgorzata D

机构信息

Department of Genetics, University of Silesia, Faculty of Biology and Environmental Protection, Katowice, Poland.

Gregor Mendel Institute, Austrian Academy of Sciences, Vienna Biocenter (VBC), Vienna, Austria.

出版信息

Front Plant Sci. 2017 Dec 11;8:2024. doi: 10.3389/fpls.2017.02024. eCollection 2017.

DOI:10.3389/fpls.2017.02024
PMID:29321785
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5732185/
Abstract

MicroRNAs are non-coding small RNA molecules that are involved in the post-transcriptional regulation of the genes that control various developmental processes in plants, including zygotic embryogenesis (ZE). miRNAs are also believed to regulate somatic embryogenesis (SE), a counterpart of the ZE that is induced in plant somatic cells. However, the roles of specific miRNAs in the regulation of the genes involved in SE, in particular those encoding transcription factors (TFs) with an essential function during SE including ), remain mostly unknown. The aim of the study was to reveal the function of miR165/166 and miR160 in the -controlled pathway of SE that is induced in cultured Arabidopsis explants.In ZE, miR165/166 controls the / () genes, which are the positive regulators of , while miR160 targets the () that control the auxin signaling pathway, which plays key role in LEC2-mediated SE. We found that a deregulated expression/function of miR165/166 and miR160 resulted in a significant accumulation of auxin in the cultured explants and the spontaneous formation of somatic embryos. Our results show that miR165/166 might contribute to SE induction via targeting , a positive regulator of LEC2 that controls embryogenic induction via activation of auxin biosynthesis pathway (Wójcikowska et al., 2013). Similar to miR165/166, miR160 was indicated to control SE induction through auxin-related pathways and the negative impact of miR160 on was shown in an embryogenic culture. Altogether, the results suggest that the miR165/166- and miR160-node contribute to the LEC2-mediated auxin-related pathway of embryogenic transition that is induced in the somatic cells of Arabidopsis. A model summarizing the suggested regulatory interactions between the miR165/166-PHB and miR160-ARF10/ARF16/ARF17 nodes that control SE induction in Arabidopsis was proposed.

摘要

微小RNA是一类非编码小RNA分子,参与植物中控制各种发育过程的基因的转录后调控,包括合子胚发生(ZE)。微小RNA也被认为可调控体细胞胚发生(SE),这是合子胚发生在植物体细胞中诱导产生的对应过程。然而,特定微小RNA在调控体细胞胚发生相关基因中的作用,尤其是那些在体细胞胚发生过程中具有重要功能的转录因子(TFs)编码基因,大多仍不清楚。本研究的目的是揭示miR165/166和miR160在拟南芥培养外植体中诱导的体细胞胚发生调控途径中的功能。在合子胚发生中,miR165/166调控PHB/PHV(REVOLUTA/INTERFASCICULAR FIBERLESS)基因,这些基因是胚胎发生的正向调节因子,而miR160靶向ARF10/ARF16/ARF17(AUXIN RESPONSE FACTOR 10/16/17),它们控制生长素信号通路,该通路在LEC2介导的体细胞胚发生中起关键作用。我们发现,miR165/166和miR160表达/功能失调导致培养外植体中生长素大量积累以及体细胞胚的自发形成。我们的结果表明,miR165/166可能通过靶向BABY BOOM(BBM)促进体细胞胚发生诱导,BBM是LEC2的正向调节因子,通过激活生长素生物合成途径控制胚胎发生诱导(Wójcikowska等人,2013年)。与miR165/166类似,miR160被表明通过生长素相关途径控制体细胞胚发生诱导,并且在胚胎发生培养中显示出miR160对BBM的负面影响。总之,结果表明miR165/166和miR160节点有助于拟南芥体细胞中LEC2介导的生长素相关胚胎发生转变途径。提出了一个模型,总结了在拟南芥中控制体细胞胚发生诱导的miR165/166 - PHB和miR160 - ARF10/ARF16/ARF17节点之间建议的调控相互作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/097b/5732185/5082a7cb853d/fpls-08-02024-g0008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/097b/5732185/33228c125f9c/fpls-08-02024-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/097b/5732185/ea22cd68cf2a/fpls-08-02024-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/097b/5732185/4e771968b5ca/fpls-08-02024-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/097b/5732185/fa341210d5fa/fpls-08-02024-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/097b/5732185/3d249aa72441/fpls-08-02024-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/097b/5732185/b5c3b11d4883/fpls-08-02024-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/097b/5732185/f49598e7be8e/fpls-08-02024-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/097b/5732185/5082a7cb853d/fpls-08-02024-g0008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/097b/5732185/33228c125f9c/fpls-08-02024-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/097b/5732185/ea22cd68cf2a/fpls-08-02024-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/097b/5732185/4e771968b5ca/fpls-08-02024-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/097b/5732185/fa341210d5fa/fpls-08-02024-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/097b/5732185/3d249aa72441/fpls-08-02024-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/097b/5732185/b5c3b11d4883/fpls-08-02024-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/097b/5732185/f49598e7be8e/fpls-08-02024-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/097b/5732185/5082a7cb853d/fpls-08-02024-g0008.jpg

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