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UDP-葡萄糖:糖蛋白葡糖基转移酶(UGGT)是内质网质量控制中的关键酶,在拟南芥的植物生长以及生物和非生物胁迫中发挥着重要作用。

The UDP-glucose: glycoprotein glucosyltransferase (UGGT), a key enzyme in ER quality control, plays a significant role in plant growth as well as biotic and abiotic stress in Arabidopsis thaliana.

作者信息

Blanco-Herrera Francisca, Moreno Adrián A, Tapia Rodrigo, Reyes Francisca, Araya Macarena, D'Alessio Cecilia, Parodi Armando, Orellana Ariel

机构信息

Centro de Biotecnología Vegetal, Facultad de Ciencias Biológicas, Universidad Andrés Bello, Avenida República 217, Santiago, 837-0146, RM, Chile.

FONDAP Center for Genome Regulation, Santiago, RM, Chile.

出版信息

BMC Plant Biol. 2015 May 28;15:127. doi: 10.1186/s12870-015-0525-2.

DOI:10.1186/s12870-015-0525-2
PMID:26017403
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4465474/
Abstract

BACKGROUND

UDP-glucose: glycoprotein glucosyltransferase (UGGT) is a key player in the quality control mechanism (ER-QC) that newly synthesized glycoproteins undergo in the ER. It has been shown that the UGGT Arabidopsis orthologue is involved in ER-QC; however, its role in plant physiology remains unclear.

RESULTS

Here, we show that two mutant alleles in the At1g71220 locus have none or reduced UGGT activity. In wild type plants, the AtUGGT transcript levels increased upon activation of the unfolded protein response (UPR). Interestingly, mutants in AtUGGT exhibited an endogenous up-regulation of genes that are UPR targets. In addition, mutants in AtUGGT showed a 30% reduction in the incorporation of UDP-Glucose into the ER suggesting that this enzyme drives the uptake of this substrate for the CNX/CRT cycle. Plants deficient in UGGT exhibited a delayed growth rate of the primary root and rosette as well as an alteration in the number of leaves. These mutants are more sensitive to pathogen attack as well as heat, salt, and UPR-inducing stressors. Additionally, the plants showed impairment in the establishment of systemic acquired resistance (SAR).

CONCLUSIONS

These results show that a lack of UGGT activity alters plant vegetative development and impairs the response to several abiotic and biotic stresses. Moreover, our results uncover an unexpected role of UGGT in the incorporation of UDP-Glucose into the ER lumen in Arabidopsis thaliana.

摘要

背景

UDP-葡萄糖:糖蛋白葡糖基转移酶(UGGT)是内质网中新生糖蛋白所经历的质量控制机制(内质网质量控制,ER-QC)的关键参与者。研究表明,UGGT在拟南芥中的同源物参与内质网质量控制;然而,其在植物生理学中的作用仍不清楚。

结果

在此,我们表明At1g71220基因座中的两个突变等位基因没有UGGT活性或UGGT活性降低。在野生型植物中,未折叠蛋白反应(UPR)激活后AtUGGT转录水平升高。有趣的是,AtUGGT突变体表现出作为UPR靶标的基因的内源性上调。此外,AtUGGT突变体显示UDP-葡萄糖向内质网的掺入减少30%,这表明该酶驱动这种底物进入CNX/CRT循环。缺乏UGGT的植物主根和莲座叶的生长速率延迟,叶片数量也发生改变。这些突变体对病原体攻击以及热、盐和诱导UPR的应激源更敏感。此外,这些植物在系统获得性抗性(SAR)的建立方面存在缺陷。

结论

这些结果表明,UGGT活性的缺乏会改变植物营养发育,并损害对几种非生物和生物胁迫的反应。此外,我们的结果揭示了UGGT在拟南芥中将UDP-葡萄糖掺入内质网腔中的意外作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b96c/4465474/19fd444ae671/12870_2015_525_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b96c/4465474/3e3344daec24/12870_2015_525_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b96c/4465474/d5637e8d6f2a/12870_2015_525_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b96c/4465474/c465b744cb8b/12870_2015_525_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b96c/4465474/2378e17c9ec9/12870_2015_525_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b96c/4465474/0e40c6ae2afb/12870_2015_525_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b96c/4465474/e3c6c1872e24/12870_2015_525_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b96c/4465474/9829308fa338/12870_2015_525_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b96c/4465474/4f25777a14e1/12870_2015_525_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b96c/4465474/19fd444ae671/12870_2015_525_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b96c/4465474/3e3344daec24/12870_2015_525_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b96c/4465474/d5637e8d6f2a/12870_2015_525_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b96c/4465474/c465b744cb8b/12870_2015_525_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b96c/4465474/2378e17c9ec9/12870_2015_525_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b96c/4465474/0e40c6ae2afb/12870_2015_525_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b96c/4465474/e3c6c1872e24/12870_2015_525_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b96c/4465474/9829308fa338/12870_2015_525_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b96c/4465474/4f25777a14e1/12870_2015_525_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b96c/4465474/19fd444ae671/12870_2015_525_Fig9_HTML.jpg

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