Purine limitation prevents the exogenous pyridoxal 5′-phosphate accumulation of <i>Salmonella enterica yggS</i> mutants

Pyridoxal 5'-phosphate is the active form of vitamin B<sub>6</sub> and is an essential cofactor in all domains of life. PLP can be synthesized <i>de novo</i> or salvaged from the environment from one of the six B<sub>6</sub> vitamers. B<sub>6</sub> vitamer levels appear to be tightly regulated, and alterations in their levels can have deleterious effects, most notably being the development of B6-dependent epilepsy in humans. YggS homologs are broadly conserved across multiple organisms and considered to be involved in maintaining B<sub>6</sub> homeostasis, though no specific mechanism has been defined. The current study showed that the exogenous accumulation of PLP caused by a lack of YggS can be prevented by purine limitation. The demonstration that purine limitation impacts exogenous PLP accumulation separates one consequence of a <i>yggS</i> mutation for further study and contributes to continuing efforts to define the biochemical and physiological roles of the COG0325 family of proteins.

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Publication Details

Journal
Microbiology Spectrum
Published
2024-10-22
DOI
https://doi.org/10.1128/spectrum.02075-24
Primary Topic
Enzyme Structure and Function
Type
article
Field-Weighted Citation Impact
0.00

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article

Purine limitation prevents the exogenous pyridoxal 5′-phosphate accumulation of Salmonella enterica yggS mutants

Diana M. Downs
Microbiology Spectrum
Enzyme Structure and Function
article

Purine limitation prevents the exogenous pyridoxal 5′-phosphate accumulation of Salmonella enterica yggS mutants

Diana M. Downs
article en

Abstract

Pyridoxal 5'-phosphate is the active form of vitamin B<sub>6</sub> and is an essential cofactor in all domains of life. PLP can be synthesized <i>de novo</i> or salvaged from the environment from one of the six B<sub>6</sub> vitamers. B<sub>6</sub> vitamer levels appear to be tightly regulated, and alterations in their levels can have deleterious effects, most notably being the development of B6-dependent epilepsy in humans. YggS homologs are broadly conserved across multiple organisms and considered to be involved in maintaining B<sub>6</sub> homeostasis, though no specific mechanism has been defined. The current study showed that the exogenous accumulation of PLP caused by a lack of YggS can be prevented by purine limitation. The demonstration that purine limitation impacts exogenous PLP accumulation separates one consequence of a <i>yggS</i> mutation for further study and contributes to continuing efforts to define the biochemical and physiological roles of the COG0325 family of proteins.

Microbiology SpectrumVol. 12(12)
University of Georgia (US)
National Institutes of Health
Openalex Percentile: Top 89%
Enzyme Structure and Function
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