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对苜蓿根瘤菌syrA(一种胞外多糖丰度调节因子)的多重遗传控制。

Multiple genetic controls on Rhizobium meliloti syrA, a regulator of exopolysaccharide abundance.

作者信息

Barnett M J, Swanson J A, Long S R

机构信息

Department of Biological Sciences, Stanford University, California 94305, USA.

出版信息

Genetics. 1998 Jan;148(1):19-32. doi: 10.1093/genetics/148.1.19.

DOI:10.1093/genetics/148.1.19
PMID:9475718
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1459771/
Abstract

Exopolysaccharides (EPS) are produced by a wide assortment of bacteria including plant pathogens and rhizobial symbionts. Rhizobium meliloti mutants defective in EPS production fail to invade alfalfa nodules. Production of EPS in R. meliloti is likely controlled at several levels. We have characterized a new gene of this regulatory circuit. syrA was identified by its ability to confer mucoid colony morphology and by its ability to suppress the colonial phenotype of an exoD mutant. Here we show that syrA encodes a 9-kD hydrophobic protein that has sequence similarity to two other EPS regulatory proteins: ExoX of Rhizobium NGR234 and R. meliloti, and Psi of R. leguminosarum bv. phaseoli. The syrA transcription start site lies 522 nucleotides upstream of a non-canonical TTG start codon. The syrA promoter region is similar to the promoter region of the nodulation regulatory protein, nodD3. We found that in free-living bacteria, syrA expression is activated by the regulatory locus, syrM, but not by nodD3. In planta, syrM is not required for expression of syrA. Instead, expression of the nitrogen fixation (nifHDKE) genes upstream of syrA plays a role. Specific and distinct sets of genetic controls may operate at different times during nodule invasion.

摘要

胞外多糖(EPS)由多种细菌产生,包括植物病原体和根瘤菌共生体。苜蓿中华根瘤菌中EPS产生缺陷的突变体无法侵入苜蓿根瘤。苜蓿中华根瘤菌中EPS的产生可能在多个水平受到调控。我们鉴定了这个调控回路中的一个新基因。syrA是通过其赋予黏液菌落形态的能力以及抑制exoD突变体菌落表型的能力而被鉴定出来的。在这里我们表明,syrA编码一种9-kD的疏水蛋白,该蛋白与另外两种EPS调控蛋白具有序列相似性:根瘤菌NGR234和苜蓿中华根瘤菌的ExoX,以及菜豆根瘤菌菜豆生物型的Psi。syrA转录起始位点位于一个非典型TTG起始密码子上游522个核苷酸处。syrA启动子区域与结瘤调控蛋白nodD3的启动子区域相似。我们发现,在自由生活的细菌中,syrA的表达由调控位点syrM激活,而不是由nodD3激活。在植物体内,syrA的表达不需要syrM。相反,syrA上游的固氮(nifHDKE)基因的表达起作用。在根瘤侵染过程中的不同时间可能会有特定且不同的遗传控制机制发挥作用。

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