YggS (COG0325) is a pyridoxal 5′-phosphate (PLP)-binding protein proposed to be involved in homeostasis of B₆ vitamers. In Salmonella enterica, lack of yggS resulted in phenotypes that were distinct and others that were similar to those of a yggS mutant of Escherichia coli. Like other organisms, yggS mutants of S. enterica accumulate endogenous pyridoxine 5′-phosphate (PNP). Data herein show that strains lacking YggS accumulated ∼10-fold more PLP in growth medium than a parental strain. The deoxyxylulose 5-phosphate-dependent biosynthetic pathway for PLP and the PNP/pyridoxamine 5′-phosphate (PMP) oxidase credited with interconverting B₆ vitamers were replaced with a single PLP synthase from Saccharomyces cerevisiae. The impact of a yggS deletion on the intracellular and extracellular levels of B₆ vitamers in this restructured strain supported a role for PdxH in PLP homeostasis and led to a general model for YggS function in PLP-PMP cycling. Our findings uncovered broader consequences of a yggS mutation than previously reported and suggest that the accumulation of PNP is not a direct effect of lacking YggS but rather a downstream consequence.

中文翻译：

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YggS在肠道沙门氏菌中维生素B6稳态中的作用是由酵母SNZ3的异源表达所决定的。

YggS（COG0325）是一种吡ido醛5'-磷酸（PLP）结合蛋白，被提议参与B ₆维生素的体内平衡。在沙门氏菌中，缺乏yggS导致明显的表型和其他与大肠杆菌yggS突变体相似的表型。像其他生物体，yggS的突变体肠道沙门氏菌累加内源性吡哆醇5'-磷酸（PNP）。本文中的数据显示，缺乏YggS的菌株在生长培养基中的PLP积累是亲代菌株的10倍。PLP的脱氧木糖5磷酸依赖性生物合成途径和PNP /吡py胺5'-磷酸（PMP）氧化酶被认为是相互转化的B ₆用来自酿酒酵母的一个PLP合酶代替了维生素。一的影响yggS缺失上B的胞内和胞外的水平_6个同效维生素在本重组菌株支持PdxH作用在PLP稳态和导致对在PLP-PMP循环YggS功能的一般模型。我们的发现揭示了yggS突变比以前报道的更广泛的后果，并表明PNP的积累不是缺乏YggS的直接影响，而是下游的后果。