A tentative unifying view of bacteria.
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Biomedical subjects
Publications and source records attributed to S Sonea.
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Nine hemin-deficient mutants of Salmonella typhimurium LT2 were isolated as neomycin-resistant colonies. Five of these mutants could be stimulated by Delta-aminolevulinic acid (Delta-ALA), thus representing hemA mutants. Since S. typhimurium LT2 is not able to incorporate hemin, the identification of the mutants not stimulated by Delta-ALA was made on the basis of the simultaneous loss of catalase activity and cytochromes. The hemA gene was mapped by conjugation in the trp region, probably in the order purB-pyrD-hemA-trp; the episome FT(71)trp does not carry the hemA gene. Transductional intercrosses by phage P22 indicate that hemA 11, 12, 13, and 37 are at very closely linked sites, whereas hemA14 is at a more distant site in the same or an adjacent gene. No joint transduction was detected between hemA and trp or pyrF. The loci affected in the other hemin-deficient mutants were linked in conjugation to the pro(+) marker (frequency of linkage, 88 to 97%), but cotransduction of the two markers could not be obtained. The episome F lac hem purE, which originates from Escherichia coli K-12, could complement these hemin-deficient mutants of S. typhimurium LT2. As a result, the sequence of the markers on the chromosome of S. typhimurium LT2 is probably pro heme purE, analogous to the sequence found in E. coli K-12. Thus, the chromosome of S. typhimurium also possesses two hem regions, with a location similar to that described in E. coli K-12.
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The lethal activity of a thymineless mutant of Staphylococcus aureus Wood 46 strain has been compared with that of three naturally occurring strains: parent Wood 46, Smith, and coagulase-negative SA-13. The thymineless mutant and the parent Wood 46 strain showed a sharp decline in culturable units from the peritoneal cavity in the first 4 hr after their injection. After 6 hr, that is, 2 hr before the mice began to die, the number of culturable units of the thymineless mutant was still declining, whereas that of the parent strain increased; for both strains, the number of units was still lower than that of the inoculum. Although the thymineless mutant, unlike the parent strain, was apparently unable to multiply in mouse peritoneal cavity, it killed mice at a similar rate. The highly virulent Smith strain known to multiply rapidly and the avirulent coagulase-negative SA-13 strain were used as additional controls. Under our experimental conditions, death of mice after the injection of the thymineless mutant in the peritoneal cavity did not seem to be due to bacterial multiplication but to toxicity, death being delayed by antitoxin. The pyrimidine-requiring auxotroph we used could be better material than killed bacteria to study some aspects of the lethal activity of S. aureus.