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P J WHITE

Publications and source records attributed to P J WHITE.

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PURIFICATION AND PROPERTIES OF DIAMINOPIMELATE DECARBOXYLASE FROM ESCHERICHIA COLI.

1. Diaminopimelate decarboxylase from a soluble extract of Escherichia coli A.T.C.C. 9637 was purified 200-fold by precipitation of nucleic acids, fractionation with acetone and then with ammonium sulphate, adsorption on calcium phosphate gel and chromatography on DEAE-cellulose or DEAE-Sephadex. 2. The purified enzyme showed only one component in the ultracentrifuge, with a sedimentation coefficient of 5.4s. One major peak and three much smaller peaks were observed on electrophoresis of the enzyme at pH8.9. 3. The mol.wt. of the enzyme was approx. 200000. The catalytic constant was 2000mol. of meso-diaminopimelic acid decomposed/min./mol. of enzyme, at 37 degrees . The relative rates of decarboxylation at 25 degrees , 37 degrees and 45 degrees were 0.17:1.0:1.6. At 37 degrees the Michaelis constant was 1.7mm and the optimum pH was 6.7-6.8. 4. There was an excess of acidic amino acids over basic amino acids in the enzyme, which was bound only on basic cellulose derivatives at pH6.8. 5. The enzyme had an absolute requirement for pyridoxal phosphate as a cofactor; no other derivative of pyridoxine had activity. A thiol compound (of which 2,3-dimercaptopropan-1-ol was the most effective) was also needed as an activator. 6. In the presence of 2,3-dimercaptopropan-1-ol (1mm), heavy-metal ions (Cu(2+), Hg(2+)) did not inhibit the enzyme, but there was inhibition by several amino acids with analogous structures to diaminopimelate, generally at high concentrations relative to the substrate. Penicillamine was inhibitory at relatively low concentrations; its action was prevented by pyridoxal phosphate.

Amino Acids↗

Effects of uracil and thymidine on the development of resistance to 5-fluorouracil in Pediococcus cerevisiae.

White, P. J. (Roswell Park Memorial Institute, Buffalo, N.Y.) and C. A. Nichol. Effects of uracil and thymidine on the development of resistance to 5-fluorouracil in Pediococcus cerevisiae. J. Bacteriol. 85:97-105. 1963.-Growth of Pediococcus cerevisiae ATCC 8081 in a basal semidefined medium was inhibited by 5-fluorouracil (FU) and 5-fluoro-2'-deoxyuridine (FUDR). Addition of uracil slightly decreased sensitivity to FU, but did not affect inhibition by FUDR. Addition of thymidine alone increased sensitivity to FUDR 500-fold, but did not appreciably affect sensitivity to FU. This organism was able to grow in the presence of high concentrations of either drug when both uracil and thymidine were added to the medium. Substrains resistant to FU were developed in the basal medium, or in basal medium with added uracil, or with thymidine. The substrains developed in the presence of uracil or thymidine were not resistant when these compounds were omitted from the medium. Cross resistance to FUDR was shown only when thymidine was present. The ability to use thymidine as a growth factor in the absence of leucovorin was lost in the substrains developed in the presence of uracil, though not in the other substrains. Washed suspensions of organisms of all strains hydrolyzed FUDR to FU, the parent strain being most active in this respect. The cellular uptake of fluorouracil-2-C(14) was less in all of the resistant substrains than in the parent strain, whether or not uracil or thymidine was present during the incubation. This uptake of FU-C(14) was decreased most markedly in the substrains which became resistant to FU in the absence of uracil.

Deoxyuridine↗