serC is involved in vitamin B6 biosynthesis in Escherichia coli but not in Bacillus subtilis.

The possible involvement of serC in vitamin B6 (B6) biosynthesis in Bacillus subtilis was investigated and compared with that in Escherichia coli. The genes of E. coli and B. subtilis were disrupted with pBEN66 and pMutin1-derived integration vectors, respectively. Nutrient requirement analyses showed that the serC-disrupted E. coli mutant required pyridoxine (PN) and L-serine, and lacked the ability to synthesize B6. Glycolaldehyde (GA), a confirmed precursor of B6, could replace PN and support the growth of the disruptant. However, the serC-disrupted E. coli mutant grown in a minimal medium supplemented with L-serine and GA synthesized B6 at a level less than 20% of that synthesized by the wild type. In contrast to E. coli, the serC-disrupted B. subtilis mutant required L-serine or glycine for growth, but did not require PN. The serC disruptant retained its ability for B6 biosynthesis and produced almost the same amount of PN as the wild type. GA had no effect on the growth and level of B6 biosynthesis of both the wild type and the serC disruptant. These results lead to the conclusion that serC is directly involved in B6 biosynthesis in E. coli, but not in B. subtilis.