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噬菌体P22裂解周期早期抗生物合成的抑制作用。

Repression of ant synthesis early in the lytic cycle of phage P22.

作者信息

Harvey A M, Hava P, Oppenheim A B, Prell H H, Soska J

出版信息

Mol Gen Genet. 1981;181(1):74-81. doi: 10.1007/BF00339008.

Abstract

Using SDS-polyacrylamide gel electrophoresis to study the early expression of P22 genes we show that early expression of the ant-gene (imm I region) is turned off after 6-8 min, independent of the 'late' acting mnt-repressor. A semi-clear mutant called cir5 is defective for this early ant turn-off. The mutation cir5 maps in the imm I region of P22 between genes mnt and ant. P22 cir5 mutants are defective for a repressor which acts in trans to regulate early ant synthesis. There appears to be no absolute requirement of the cir5 allele for the establishment of lysogeny. The overproduction of ant in the P22 cir5 mutant leads to a marked increase in abortive infections, killing the infected cells. The cir5-phenotype can be suppressed by an ant- mutation.

摘要

利用SDS-聚丙烯酰胺凝胶电泳研究P22基因的早期表达,我们发现抗基因(imm I区域)的早期表达在6-8分钟后关闭,这与“晚期”起作用的mnt阻遏物无关。一个名为cir5的半透明突变体在这种抗基因早期关闭方面存在缺陷。cir5突变位于P22的imm I区域,在mnt和ant基因之间。P22 cir5突变体在一种反式作用的阻遏物方面存在缺陷,该阻遏物调节抗基因的早期合成。对于溶原性的建立,似乎对cir5等位基因没有绝对要求。P22 cir5突变体中抗基因的过量表达导致流产感染显著增加,杀死被感染的细胞。cir5表型可被抗基因突变抑制。

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