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miRNAs 在拟南芥中介导 SnRK1 依赖的能量信号转导。

miRNAs mediate SnRK1-dependent energy signaling in Arabidopsis.

机构信息

Plant Stress Signaling, Instituto Gulbenkian de Ciência Oeiras, Portugal.

出版信息

Front Plant Sci. 2013 Jun 20;4:197. doi: 10.3389/fpls.2013.00197. eCollection 2013.

DOI:10.3389/fpls.2013.00197
PMID:23802004
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3687772/
Abstract

The SnRK1 protein kinase, the plant ortholog of mammalian AMPK and yeast Snf1, is activated by the energy depletion caused by adverse environmental conditions. Upon activation, SnRK1 triggers extensive transcriptional changes to restore homeostasis and promote stress tolerance and survival partly through the inhibition of anabolism and the activation of catabolism. Despite the identification of a few bZIP transcription factors as downstream effectors, the mechanisms underlying gene regulation, and in particular gene repression by SnRK1, remain mostly unknown. microRNAs (miRNAs) are 20-24 nt RNAs that regulate gene expression post-transcriptionally by driving the cleavage and/or translation attenuation of complementary mRNA targets. In addition to their role in plant development, mounting evidence implicates miRNAs in the response to environmental stress. Given the involvement of miRNAs in stress responses and the fact that some of the SnRK1-regulated genes are miRNA targets, we postulated that miRNAs drive part of the transcriptional reprogramming triggered by SnRK1. By comparing the transcriptional response to energy deprivation between WT and dcl1-9, a mutant deficient in miRNA biogenesis, we identified 831 starvation genes misregulated in the dcl1-9 mutant, out of which 155 are validated or predicted miRNA targets. Functional clustering analysis revealed that the main cellular processes potentially co-regulated by SnRK1 and miRNAs are translation and organelle function and uncover TCP transcription factors as one of the most highly enriched functional clusters. TCP repression during energy deprivation was impaired in miR319 knockdown (MIM319) plants, demonstrating the involvement of miR319 in the stress-dependent regulation of TCPs. Altogether, our data indicates that miRNAs are components of the SnRK1 signaling cascade contributing to the regulation of specific mRNA targets and possibly tuning down particular cellular processes during the stress response.

摘要

SnRK1 蛋白激酶是植物中与哺乳动物 AMPK 和酵母 Snf1 同源的蛋白,它可以被逆境环境导致的能量耗竭所激活。在激活后,SnRK1 会引发广泛的转录变化,以恢复体内平衡,并通过抑制合成代谢和激活分解代谢来促进应激耐受和生存。尽管已经鉴定出一些 bZIP 转录因子作为下游效应子,但基因调控的机制,特别是 SnRK1 对基因的抑制作用,仍然大部分未知。microRNAs(miRNAs)是 20-24nt 的 RNA,通过驱动互补 mRNA 靶标切割和/或翻译衰减,在后转录水平上调节基因表达。除了在植物发育中的作用外,越来越多的证据表明 miRNAs 参与了环境胁迫的响应。鉴于 miRNAs 在应激反应中的作用,以及一些 SnRK1 调节的基因是 miRNA 靶标,我们假设 miRNAs 驱动了由 SnRK1 触发的部分转录重编程。通过比较 WT 和 dcl1-9(miRNA 生物发生缺陷突变体)在能量剥夺下的转录响应,我们在 dcl1-9 突变体中鉴定出 831 个饥饿基因失调,其中 155 个是已验证或预测的 miRNA 靶标。功能聚类分析显示,可能由 SnRK1 和 miRNAs 共同调节的主要细胞过程是翻译和细胞器功能,并揭示 TCP 转录因子是最富集的功能簇之一。在能量剥夺期间,miR319 敲低(MIM319)植物中的 TCP 抑制作用受损,证明了 miR319 在依赖应激的 TCP 调节中的作用。总之,我们的数据表明,miRNAs 是 SnRK1 信号级联的组成部分,有助于调节特定的 mRNA 靶标,并可能在应激反应中下调特定的细胞过程。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f227/3687772/cd0d1a2f1a96/fpls-04-00197-a0006.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f227/3687772/cd0d1a2f1a96/fpls-04-00197-a0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f227/3687772/5047b3dec138/fpls-04-00197-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f227/3687772/0f34f92f7530/fpls-04-00197-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f227/3687772/c9499499aa95/fpls-04-00197-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f227/3687772/824a18674a7b/fpls-04-00197-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f227/3687772/1a7a14a2bb55/fpls-04-00197-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f227/3687772/de39cf4e9b2f/fpls-04-00197-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f227/3687772/9641c62bad63/fpls-04-00197-a0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f227/3687772/0346f57299d0/fpls-04-00197-a0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f227/3687772/ebbd3693d1a5/fpls-04-00197-a0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f227/3687772/d5fbe66e35d9/fpls-04-00197-a0004.jpg
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