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fou8/fry1 突变对硫代谢的影响:内部硫酸盐减少是硫酸盐饥饿反应的触发因素吗?

Effects of fou8/fry1 mutation on sulfur metabolism: is decreased internal sulfate the trigger of sulfate starvation response?

机构信息

John Innes Centre, Norwich Research Park, Norwich, United Kingdom.

出版信息

PLoS One. 2012;7(6):e39425. doi: 10.1371/journal.pone.0039425. Epub 2012 Jun 18.

DOI:10.1371/journal.pone.0039425
PMID:22724014
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3377649/
Abstract

The fou8 loss of function allele of adenosine bisphosphate phosphatase FIERY1 results in numerous phenotypes including the increased enzymatic oxygenation of fatty acids and increased jasmonate synthesis. Here we show that the mutation causes also profound alterations of sulfur metabolism. The fou8 mutants possess lower levels of sulfated secondary compounds, glucosinolates, and accumulate the desulfo-precursors similar to previously described mutants in adenosine 5'phosphosulfate kinase. Transcript levels of genes involved in sulfate assimilation differ in fou8 compared to wild type Col-0 plants and are similar to plants subjected to sulfate deficiency. Indeed, independent microarray analyses of various alleles of mutants in FIERY1 showed similar patterns of gene expression as in sulfate deficient plants. This was not caused by alterations in signalling, as the fou8 mutants contained significantly lower levels of sulfate and glutathione and, consequently, of total elemental sulfur. Analysis of mutants with altered levels of sulfate and glutathione confirmed the correlation of sulfate deficiency-like gene expression pattern with low internal sulfate but not low glutathione. The changes in sulfur metabolism in fou8 correlated with massive increases in 3'-phosphoadenosine 5'-phosphate levels. The analysis of fou8 thus revealed that sulfate starvation response is triggered by a decrease in internal sulfate as opposed to external sulfate availability and that the presence of desulfo-glucosinolates does not induce the glucosinolate synthesis network. However, as well as resolving these important questions on the regulation of sulfate assimilation in plants, fou8 has also opened an array of new questions on the links between jasmonate synthesis and sulfur metabolism.

摘要

腺苷二磷酸磷酸酶 FIERY1 的功能丧失突变等位基因导致多种表型,包括脂肪酸的酶促氧化增加和茉莉酸合成增加。在这里,我们表明该突变还导致硫代谢的深刻改变。 fou8 突变体具有较低水平的硫酸化次生化合物、硫苷和积累类似先前报道的腺苷 5'磷酸硫酸激酶突变体的脱硫前体。与野生型 Col-0 植物相比, fou8 中的硫酸盐同化相关基因的转录水平不同,并且与硫酸盐缺乏的植物相似。事实上,对 FIERY1 突变体的各种等位基因的独立微阵列分析显示出与硫酸盐缺乏植物相似的基因表达模式。这不是由信号转导的改变引起的,因为 fou8 突变体含有显著较低水平的硫酸盐和谷胱甘肽,因此总元素硫含量较低。改变硫酸盐和谷胱甘肽水平的突变体分析证实了硫酸盐缺乏样基因表达模式与低内部硫酸盐而不是低谷胱甘肽相关。 fou8 中的硫代谢变化与 3'-磷酸腺苷 5'-磷酸水平的大量增加相关。因此, fou8 的分析表明,硫酸盐饥饿反应是由内部硫酸盐的减少而不是外部硫酸盐的可用性引发的,并且脱硫硫苷的存在不会诱导硫苷合成网络。然而,除了解决植物硫酸盐同化调控的这些重要问题外, fou8 还提出了关于茉莉酸合成和硫代谢之间联系的一系列新问题。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f063/3377649/4c893527c61d/pone.0039425.g010.jpg
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