The pea nodule environment restores the ability of a Rhizobium leguminosarum lipopolysaccharide acpXL mutant to add 27-hydroxyoctacosanoic acid to its lipid A.

The pea nodule environment restores the ability of a Rhizobium leguminosarum lipopolysaccharide acpXL mutant to add 27-hydroxyoctacosanoic acid to its lipid A.
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豌豆根瘤环境恢复了豆根瘤菌脂多糖acpXL突变体向其脂质A添加27-羟基二十八烷酸的能力。

DOI:
10.1128/jb.188.6.2126-2133.2006
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发表时间:
2006
影响因子:
3.2
通讯作者:
Carlson,RussellW
Carlson,RussellW
中科院分区:
生物学3区
文献类型:
--
作者:
Vedam,Vinata;Kannenberg,Elmar;Datta,Anup;Brown,Dusty;Haynes-Gann,JanineG;Sherrier,DJanine;Carlson,RussellW

文献摘要

相似文献

根瘤菌科的成员在其脂质A中含有27-羟基二十八烷酸(27 OHC 28:0)。缺乏功能性特化酰基载体的ARhizobium leguminosarum 3841 acpXL突变体(在此命名为Rlv 22)在其脂质A中缺乏27 OHC 28:0,具有改变的生长和生理特性(例如,它不能在高盐浓度[0.5%NaCl]存在下生长),并形成不规则形状的拟杆菌,并且该突变体和宿主植物来源的共生体膜的同步分裂被破坏。尽管有这些缺陷,突变体能够坚持根瘤细胞内,并最终形成,虽然效率低下,固氮类杆菌。这一结果表明,该突变体在寄主根瘤中可能存在某种机制来适应脂质A中27 OHC 28:0的丢失。为了进一步确定该脂肪酰基残基的功能,有必要检查从突变类细菌分离的脂质A。在这份报告中,我们表明,除了27 OHC 28:0的脂A的Rlv 22脂多糖是部分恢复在Rlv 22 acpXL突变体类杆菌。我们假设R.豆科植物VICiaE 3841包含替代机制(例如,另一种替代机制)用于合成27 OHC 28:0,当细菌处于结核环境中时,27 OHC 28:0被激活,并且正是这种替代机制在功能上抑制了Rlv 22 acpXL类杆菌中含27 OHC 28:0的脂质A的合成。
Members of theRhizobiaceaecontain 27-hydroxyoctacosanoic acid (27OHC28:0) in their lipid A. ARhizobium leguminosarum 3841 acpXLmutant (named here Rlv22) lacking a functional specialized acyl carrier lacked 27OHC28:0in its lipid A, had altered growth and physiological properties (e.g., it was unable to grow in the presence of an elevated salt concentration [0.5% NaCl]), and formed irregularly shaped bacteroids, and the synchronous division of this mutant and the host plant-derived symbiosome membrane was disrupted. In spite of these defects, the mutant was able to persist within the root nodule cells and eventually form, albeit inefficiently, nitrogen-fixing bacteroids. This result suggested that while it is in a host root nodule, the mutant may have some mechanism by which it adapts to the loss of 27OHC28:0from its lipid A. In order to further define the function of this fatty acyl residue, it was necessary to examine the lipid A isolated from mutant bacteroids. In this report we show that addition of 27OHC28:0to the lipid A of Rlv22 lipopolysaccharides is partially restored in Rlv22acpXLmutant bacteroids. We hypothesize thatR. leguminosarumbv. viciae 3841 contains an alternate mechanism (e.g., anotheracpgene) for the synthesis of 27OHC28:0, which is activated when the bacteria are in the nodule environment, and that it is this alternative mechanism which functionally replacesacpXLand is responsible for the synthesis of 27OHC28:0-containing lipid A in the Rlv22acpXLbacteroids.