RESTORATION OF NORMAL GLUTAMIC ACID TRANSPORT IN VITAMIN B6-DEFICIENT LACTOBACILLUS PLANTARUM BY ACETATE, AMMONIUM, AND VITAMIN B6,
CITY OF HOPE MEDICAL CENTER DUARTE CALIF DEPT OF BIOCHEMISTRY
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A vitamin B6-deficiency in Lactobacillus plantarum markedly reduces the amount of glutamate and other amino acids which can be taken up and accumulated from buffered solutions. The capacity for glutamate accumulation is restored to normal levels when acetate, ammonium, and pyridoxamine are included in the external buffer. The requirement for acetate was not satisfied by a large number of related organic acids. The stimulation of glutamic acid uptake occurred in the absence of significant changes in levels of cellular protein, RNA and DNA and was not inhibited by chloramphenicol. Cells pretreated with acetate, ammonium, and vitamin B6 were subsequently capable of accumulating nearly normal amounts of various amino acids in the absence of any supplemental additions to the buffer. This was true however, only if glutamic acid was included in the pretreatment solution. This requirement for glutamate during pretreatment to attain an expansion of amino acid accumulation capacity was specific and was observed regardless of which amino acid was subsequently used to measure the accumulation capacity. During pretreatment with acetate, ammonium, pyridoxamine, and glutamate there were substantial increases in cell-wall mass. Penicillin inhibited both the increases in cell wall mass and accumulation capacity. These findings support the hypothesis that the reduced capacity for amino acid accumulation by vitamin B6-deficient cells of L. plantarum arises from a failure to synthesize a normal cell wall.