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双链RNA结合蛋白下胚轴叶1的缺陷会增加拟南芥对内质网应激诱导剂衣霉素的敏感性。

Deficiency in the double-stranded RNA binding protein HYPONASTIC LEAVES1 increases sensitivity to the endoplasmic reticulum stress inducer tunicamycin in Arabidopsis.

作者信息

Hirata Rikako, Mishiba Kei-Ichiro, Koizumi Nozomu, Iwata Yuji

机构信息

Graduate School of Life and Environmental Sciences, Osaka Prefecture University, 1-1 Gakuen-cho, Naka-ku, Sakai, 599-8531, Osaka, Japan.

出版信息

BMC Res Notes. 2019 Sep 14;12(1):580. doi: 10.1186/s13104-019-4623-3.

DOI:10.1186/s13104-019-4623-3
PMID:31521187
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6744651/
Abstract

OBJECTIVE

microRNA (miRNA) is a small non-coding RNA that regulates gene expression by sequence-dependent binding to protein-coding mRNA in eukaryotic cells. In plants, miRNA plays important roles in a plethora of physiological processes, including abiotic and biotic stress responses. The present study was conducted to investigate whether miRNA-mediated regulation is important for the endoplasmic reticulum (ER) stress response in Arabidopsis.

RESULTS

We found that hyl1 mutant plants are more sensitive to tunicamycin, an inhibitor of N-linked glycosylation that causes ER stress than wild-type plants. Other miRNA-related mutants, se and ago1, exhibited similar sensitivity to the wild-type, indicating that the hypersensitive phenotype is attributable to the loss-of-function of HYL1, rather than deficiency in general miRNA biogenesis and function. However, the transcriptional response of select ER stress-responsive genes in hyl1 mutant plants was indistinguishable from that of wild-type plants, suggesting that the loss-of-function of HYL1 does not affect the ER stress signaling pathways.

摘要

目的

微小RNA(miRNA)是一种小的非编码RNA,通过在真核细胞中与蛋白质编码mRNA进行序列依赖性结合来调节基因表达。在植物中,miRNA在众多生理过程中发挥重要作用,包括非生物和生物胁迫反应。本研究旨在调查miRNA介导的调控对拟南芥内质网(ER)应激反应是否重要。

结果

我们发现hyl1突变体植株比野生型植株对衣霉素更敏感,衣霉素是一种N-糖基化抑制剂,可引起内质网应激。其他与miRNA相关的突变体se和ago1对衣霉素的敏感性与野生型相似,这表明超敏表型归因于HYL1功能的丧失,而非一般miRNA生物合成和功能的缺陷。然而,hyl1突变体植株中选定的内质网应激反应基因的转录反应与野生型植株并无差异,这表明HYL1功能的丧失不会影响内质网应激信号通路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c618/6744651/e1faefa738ac/13104_2019_4623_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c618/6744651/a02f863549c0/13104_2019_4623_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c618/6744651/e1faefa738ac/13104_2019_4623_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c618/6744651/a02f863549c0/13104_2019_4623_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c618/6744651/e1faefa738ac/13104_2019_4623_Fig2_HTML.jpg

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