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海藻糖可诱导荧光假单胞菌ATCC 17400对德巴利腐霉产生拮抗作用。

Trehalose induces antagonism towards Pythium debaryanum in Pseudomonas fluorescens ATCC 17400.

作者信息

Gaballa A, Abeysinghe P D, Urich G, Matthijs S, De Greve H, Cornelis P, Koedam N

机构信息

Laboratorium Plantenfysiologie, Flanders Interuniversity Institute for Biotechnology, Vrije Universiteit Brussel, Belgium.

出版信息

Appl Environ Microbiol. 1997 Nov;63(11):4340-5. doi: 10.1128/aem.63.11.4340-4345.1997.

Abstract

Pseudomonas fluorescens ATCC 17400 shows in vitro activity against Pythium debaryanum under conditions of iron limitation. A lacZ reporter gene introduced by transposon mutagenesis into the P. fluorescens ATCC 17400 trehalase gene (treA) was induced by a factor released by the phytopathogen Pythium debaryanum. The induction of the lacZ gene was lost upon treatment of the Pythium supernatant with commercial trehalase. A trehalose concentration as low as 1 microM could induce the expression of treA. The mutation did not affect the wild-type potential for fungus antagonism but drastically decreased the osmotolerance of the mutant in liquid culture and suppressed the ability of P. fluorescens ATCC 17400 to utilize trehalose as a carbon source. A subsequent transposon insertion in treP, one of the trehalose phosphotransferase genes upstream of treA, silenced the lacZ gene. This double mutant restricted fungal growth only under conditions of high osmolarity, which probably results in internal trehalose accumulation. These data confirm the role of the disaccharide trehalose in osmotolerance, and they indicate its additional role as an initiator of or a signal for fungal antagonism.

摘要

荧光假单胞菌ATCC 17400在铁限制条件下对德巴利腐霉具有体外活性。通过转座子诱变导入荧光假单胞菌ATCC 17400海藻糖酶基因(treA)的lacZ报告基因,被植物病原菌德巴利腐霉释放的一种因子诱导。用商业海藻糖酶处理腐霉上清液后,lacZ基因的诱导作用消失。低至1微摩尔的海藻糖浓度就能诱导treA的表达。该突变不影响野生型对真菌的拮抗潜力,但显著降低了突变体在液体培养中的渗透压耐受性,并抑制了荧光假单胞菌ATCC 17400利用海藻糖作为碳源的能力。随后在treA上游的海藻糖磷酸转移酶基因之一treP中插入转座子,使lacZ基因沉默。这种双突变体仅在高渗透压条件下限制真菌生长,这可能导致内部海藻糖积累。这些数据证实了二糖海藻糖在渗透压耐受性中的作用,并表明其作为真菌拮抗作用的引发剂或信号的额外作用。

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