Prell H H, Harvey A M
Mol Gen Genet. 1981;184(1):147-50. doi: 10.1007/BF00271211.
Phage P22 defective in gene 24 and harbouring the Oc mutation k5 in OR exhibits a strongly increased c2-repressor synthesis after infection of non-lysogenic S. typhimurium. The repressor synthesis depends strictly on an intact c1 gene. The kinetics of its synthesis, as monitored by polyacrylamide gel electrophoresis, is the same as with P22 c+, namely a turn off 8-10 min after infection. - After infection of P22-lysogenic bacteria with either P22 24- k5 or P22 24- k5 c1, much lower amounts of repressor are synthesized but again with the same kinetics. These results suggest a cro-like function acting at PRE and PRM of P22. The possible reason for the c2 overproduction is discussed.
基因24有缺陷且在OR区带有Oc突变k5的噬菌体P22在感染非溶原性鼠伤寒沙门氏菌后，c2阻遏物的合成显著增加。阻遏物的合成严格依赖完整的c1基因。通过聚丙烯酰胺凝胶电泳监测，其合成动力学与P22 c+相同，即在感染后8 - 10分钟关闭。 - 用P22 24 - k5或P22 24 - k5 c1感染P22溶原性细菌后，阻遏物的合成量要低得多，但动力学相同。这些结果表明存在一种类似cro的功能作用于P22的PRE和PRM。文中讨论了c2过量产生的可能原因。
