鼠伤寒沙门氏菌的突变体，可引导感染性噬菌体P22走向溶原化。
Mutant of Salmonella typhimurium that channels infecting bacteriophage P22 toward lysogenization.
作者信息
Tokuno S I, Goldschmidt E P, Gough M
出版信息
J Bacteriol. 1974 Aug;119(2):508-13. doi: 10.1128/jb.119.2.508-513.1974.
Abstract
A slowly growing, polymyxin-sensitive mutant of Salmonella typhimurium was isolated. Wild-type phage P22 form plaques on the mutant at 5 x 10(-4), the frequency observed on wild-type hosts. All P22 clear mutants form plaques with near normal frequency. The inability of the mutant to form plaques is correlated with an increase in lysogenization frequency. The cause of the increased lysogenization frequency is not known, but it is not the result of overproduction of cyclic adenosine 5'-monophosphate.
摘要
分离出一株生长缓慢、对多粘菌素敏感的鼠伤寒沙门氏菌突变体。野生型噬菌体P22在该突变体上形成噬菌斑的频率为5×10⁻⁴，这与在野生型宿主上观察到的频率相同。所有P22清亮突变体形成噬菌斑的频率接近正常。该突变体无法形成噬菌斑与溶原化频率增加相关。溶原化频率增加的原因尚不清楚，但不是5'-环磷酸腺苷过量产生的结果。
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