The tep1 gene of Sinorhizobium meliloti coding for a putative transmembrane efflux protein and N-acetyl glucosamine affect nod gene expression and nodulation of alfalfa plants.

The tep1 gene of Sinorhizobium meliloti coding for a putative transmembrane efflux protein and N-acetyl glucosamine affect nod gene expression and nodulation of alfalfa plants.
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DOI:
10.1186/1471-2180-9-17
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发表时间:
2009-01-27
期刊:
影响因子:
4.2
通讯作者:
Soto MJ
Soto MJ
中科院分区:
生物学3区
文献类型:
--
作者:
van Dillewijn P;Sanjuán J;Olivares J;Soto MJ

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土壤细菌统称为根瘤菌,其特征在于它们能够与豆科植物建立有益的共生关系,在感染宿主植物时与病原菌具有几个共同特征。最近,它被证明,苜蓿中华根瘤菌的fadD突变体的改变,在控制群集,一种类型的协调运动先前与致病性,也削弱了苜蓿根的促生长效率。在植物病原体野油菜黄单胞菌中,fadD同源物(rpfB)形成参与致病因子调节的基因簇的一部分。本工作研究了一株嗜热链球菌SMc 02161在集群和共生中的作用。苜蓿fadD连锁基因。在S.苜蓿表现出与转运蛋白的主要促进剂超家族(MFS)成员的相似性。色葡萄苜蓿属无效突变体对氯霉素的敏感性增加。这一指示使我们将位点重新命名为跨膜流出蛋白tep 1。tep 1的缺乏并不影响群集运动的出现。有趣的是,在相互作用的第一天,尽管nod基因的表达低于野生型菌株,但tep 1突变体在苜蓿植物上的根瘤形成效率得到了提高。令人好奇的是,在野生型菌株中添加NoctanC突变或N-乙酰葡糖胺导致nod基因表达与tep 1突变体相似的减少。此外,结瘤因子的氨基糖前体抑制结瘤。tep 1质粒编码一种跨膜蛋白,该蛋白可赋予沙门氏菌氯霉素抗性。通过将抗生素排出细菌外来治疗苜蓿草。在tep 1突变体中观察到的苜蓿生长的改善但nod基因表达的减少表明,Tep 1转运影响生长的化合物。与慢生型大豆根瘤菌(Bradyrhizobium japonicum)相比,慢生型大豆根瘤菌(S.苜蓿不存在反馈调控的促生长基因。此外,结瘤因子前体N-乙酰葡糖胺在以毫摩尔浓度存在时降低结瘤基因表达和结瘤效率。Tep 1在Nod因子前体流出中的作用可以解释与Tep 1失活相关的表型。
Soil bacteria collectively known as Rhizobium, characterized by their ability to establish beneficial symbiosis with legumes, share several common characteristics with pathogenic bacteria when infecting the host plant. Recently, it was demonstrated that a fadD mutant of Sinorhizobium meliloti is altered in the control of swarming, a type of co-ordinated movement previously associated with pathogenicity, and is also impaired in nodulation efficiency on alfalfa roots. In the phytopathogen Xanthomonas campestris, a fadD homolog (rpfB) forms part of a cluster of genes involved in the regulation of pathogenicity factors. In this work, we have investigated the role in swarming and symbiosis of SMc02161, a S. meliloti fadD-linked gene. The SMc02161 locus in S. meliloti shows similarities with members of the Major Facilitator Superfamily (MFS) of transporters. A S. meliloti null-mutant shows increased sensitivity to chloramphenicol. This indication led us to rename the locus tep1 for transmembrane efflux protein. The lack of tep1 does not affect the appearance of swarming motility. Interestingly, nodule formation efficiency on alfalfa plants is improved in the tep1 mutant during the first days of the interaction though nod gene expression is lower than in the wild type strain. Curiously, a nodC mutation or the addition of N-acetyl glucosamine to the wild type strain lead to similar reductions in nod gene expression as in the tep1 mutant. Moreover, aminosugar precursors of Nod factors inhibit nodulation. tep1 putatively encodes a transmembrane protein which can confer chloramphenicol resistance in S. meliloti by expelling the antibiotic outside the bacteria. The improved nodulation of alfalfa but reduced nod gene expression observed in the tep1 mutant suggests that Tep1 transports compounds which influence nodulation. In contrast to Bradyrhizobium japonicum, we show that in S. meliloti there is no feedback regulation of nodulation genes. Moreover, the Nod factor precursor, N-acetyl glucosamine reduces nod gene expression and nodulation efficiency when present at millimolar concentrations. A role for Tep1 in the efflux of Nod factor precursors could explain the phenotypes associated with tep1 inactivation.
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