chlorosis

黄化病
  • 文章类型: Journal Article
    铁(Fe)缺乏会引起植物萎黄病(IDC),并可能导致植物生产力降低。因此,铁高效植物的开发引起了人们的极大兴趣。为了更好地了解铁高效植物的生理学,从马铃薯(SolanumtubrosumL.var。\'Iwa\')在缺乏Fe或低Fe供应(0-5μMFe)下选择的愈伤组织培养物。基于视觉萎黄病等级(VCR),在缺铁条件下生长时,将23%的愈伤组织衍生的再生剂归类为Fe有效(EF),将77%归类为Fe无效(IFN)植物系。发现茎高与节间距离高度相关,在缺铁条件下生长的EF植物系的叶片和根长度。此外,与IFN植物系和对照亲本生物型相比,EF植物包括名为A1,B2和B9的品系,表现出侧根和根毛的形成增强,以及叶中铁蛋白(fer3)和根中铁调节转运蛋白(irt1)的表达增加。选定的EF马铃薯品系的fer3和irt1基因的这些形态适应和表达变化表明,它们与对低Fe供应胁迫的抗性有关。
    Iron (Fe) deficiency induces chlorosis (IDC) in plants and can result in reduced plant productivity. Therefore, development of Fe-efficient plants is of great interest. To gain a better understanding of the physiology of Fe-efficient plants, putative novel plant variants were regenerated from potato (Solanum tubersosum L. var. \'Iwa\') callus cultures selected under Fe deficient or low Fe supply (0-5 μM Fe). Based on visual chlorosis rating (VCR), 23% of callus-derived regenerants were classified as Fe-efficient (EF) and 77% as Fe-inefficient (IFN) plant lines when they were grown under Fe deficiency conditions. Stem height was found to be highly correlated with internodal distance, leaf and root lengths in the EF plant lines grown under Fe deficiency conditions. In addition, compared to the IFN plant lines and control parental biotype, the EF plants including the lines named A1, B2, and B9, exhibited enhanced formation of lateral roots and root hairs as well as increased expression of ferritin (fer3) in the leaf and iron-regulated transporter (irt1) in the root. These morphological adaptations and changes in expression the fer3 and irt1 genes of the selected EF potato lines suggest that they are associated with resistance to low Fe supply stress.
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  • 文章类型: Journal Article
    黄萎病是植物病害最常见的症状之一,包括病毒和类病毒引起的。最近,一项研究表明,桃子潜伏镶嵌类病毒(PLMVd)利用宿主RNA沉默机制,通过沉默叶绿体靶向热休克蛋白90(Hsp90C)来调节病毒疾病症状。为了了解黄萎病在这种类病毒疾病中的分子机制,我们建立了一个实验系统,适合研究转基因烟草中Hsp90CRNA沉默引起的萎黄病的机制。Hsp90C特异性区域的发夹RNA在地塞米松诱导型启动子的控制下表达,导致Hsp90C基因在2天内沉默,并伴有生长抑制表型。时程研究表明,早在2天就可以监测萎黄病的迹象,表明该实验模型适用于研究萎黄病发作前后发生的分子事件。在萎黄病发展的早期阶段,叶绿体和光合作用相关基因被下调。应当注意的是,尽管在该系统中不存在任何病原体来源的分子,一些发病机理相关的基因在萎黄病的早期被上调。
    Chlorosis is one of the most common symptoms of plant diseases, including those caused by viruses and viroids. Recently, a study has shown that Peach latent mosaic viroid (PLMVd) exploits host RNA silencing machinery to modulate the virus disease symptoms through the silencing of chloroplast-targeted heat shock protein 90 (Hsp90C). To understand the molecular mechanisms of chlorosis in this viroid disease, we established an experimental system suitable for studying the mechanism underlying the chlorosis induced by the RNA silencing of Hsp90C in transgenic tobacco. Hairpin RNA of the Hsp90C-specific region was expressed under the control of a dexamethasone-inducible promoter, resulted in the silencing of Hsp90C gene in 2 days and the chlorosis along with growth suppression phenotypes. Time course study suggests that a sign of chlorosis can be monitored as early as 2 days, suggesting that this experimental model is suitable for studying the molecular events taken place before and after the onset of chlorosis. During the early phase of chlorosis development, the chloroplast- and photosynthesis-related genes were downregulated. It should be noted that some pathogenesis related genes were upregulated during the early phase of chlorosis in spite of the absence of any pathogen-derived molecules in this system.
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  • 文章类型: Journal Article
    镁(Mg)是活细胞中第二丰富的阳离子。已知超过300种酶是Mg依赖性的,Mg浓度的变化显著影响膜电位。当Mg变得缺乏时,淀粉积累和萎黄病,由活性氧的产生桥接,常见于缺镁的年轻成熟叶片中。这些缺陷进一步导致光合作用的抑制并最终降低生物量。最近,转录组分析表明,在镁缺乏的早期阶段,叶绿素装置的转录下调,以及与激素信号和昼夜节律振荡有关的复杂网络的潜在参与。然而,常见症状的过程以及镁缺乏与信号传导之间的网络尚未完全了解。这里,为了定义缺失的部分,通过介绍有关镁缺乏的生理和转录反应的最新报道,考虑并解释了几个问题。此外,长期以来,尚不清楚Mg缺乏反应是否涉及Mg2转运系统的调节。在这次审查中,综述了Mg2+转运及相关转运蛋白的研究现状。尤其是,描述了植物MRS2基因家族的生理表征的快速进展以及有关细菌CorA蛋白作用的分子机制的基础研究。
    Magnesium (Mg) is the second most abundant cation in living cells. Over 300 enzymes are known to be Mg-dependent, and changes in the Mg concentration significantly affects the membrane potential. As Mg becomes deficient, starch accumulation and chlorosis, bridged by the generation of reactive oxygen species, are commonly found in Mg-deficient young mature leaves. These defects further cause the inhibition of photosynthesis and finally decrease the biomass. Recently, transcriptome analysis has indicated the transcriptinal downregulation of chlorophyll apparatus at the earlier stages of Mg deficiency, and also the potential involvement of complicated networks relating to hormonal signaling and circadian oscillation. However, the processes of the common symptoms as well as the networks between Mg deficiency and signaling are not yet fully understood. Here, for the purpose of defining the missing pieces, several problems are considered and explained by providing an introduction to recent reports on physiological and transcriptional responses to Mg deficiency. In addition, it has long been unclear whether the Mg deficiency response involves the modulation of Mg2+ transport system. In this review, the current status of research on Mg2+ transport and the relating transporters are also summarized. Especially, the rapid progress in physiological characterization of the plant MRS2 gene family as well as the fundamental investigation about the molecular mechanism of the action of bacterial CorA proteins are described.
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