Mozola M A, Friedman D I
Virology. 1985 Jan 30;140(2):313-27. doi: 10.1016/0042-6822(85)90368-x.
Bacteriophage phi 80 and lambda-phi 80 hybrid phage of the type lambda (QSR)80, in which the rightmost 10% of the lambda genome is replaced by corresponding phi 80 material, are unable to grow lytically in himA and hip/himD mutants of Escherichia coli K12 at 32 degrees. The genetic element responsible for the growth defect, rha, has been mapped to the (QSR)80 region and was located more precisely by restriction enzyme and DNA heteroduplex analysis of mutations that result in loss of the Rha phenotype. Such an Rha mutant carrying a 1.5-kb deletion beginning 0.58 kb from the right end of the chromosome and extending leftward locates the rha locus at least in part within this region of (QSR)80. In addition, a substitution derivative of lambda (QSR)80 was isolated which does not exhibit the Rha phenotype. In this phage, lambda-80hy95, the right half of the (QSR)80 region is replaced by DNA homologous to the 95-100% segment of lambda. In mixed infections in the himA42 host at 32 degrees, lambda + does not complement lambda (QSR)80 for growth and the burst size of the coinfecting lambda + is reduced in comparison to that in a single infection. Deletion mutants of lambda (QSR)80 that grow normally in himA42 at 32 degrees in single infections are inhibited for growth in mixed infections with lambda (QSR)80. These results suggest the existence of a trans-acting function which inhibits phage growth in the absence of HimA or Hip/HimD function. It is likely that the rha gene either encodes that function or indirectly controls its action.
噬菌体φ80和λ-φ80杂合噬菌体λ(QSR)80(其中λ基因组最右侧10%被相应的φ80物质取代)在32℃时无法在大肠杆菌K12的himA和hip/himD突变体中进行裂解生长。导致生长缺陷的遗传元件rha已被定位到(QSR)80区域,并通过对导致Rha表型丧失的突变进行限制酶和DNA异源双链分析更精确地定位。这样一个Rha突变体携带一个1.5kb的缺失,从染色体右端0.58kb处开始并向左延伸,这至少部分地将rha基因座定位在(QSR)80的这个区域内。此外,分离出了一种λ(QSR)80的替代衍生物,其不表现出Rha表型。在这种噬菌体λ-80hy95中,(QSR)80区域的右半部分被与λ的95 - 100%区段同源的DNA取代。在32℃的himA42宿主中进行混合感染时,λ+不能互补λ(QSR)80的生长,并且与单一感染相比,共感染的λ+的爆发量减少。在单一感染中能在32℃的himA42中正常生长的λ(QSR)80缺失突变体,在与λ(QSR)80的混合感染中生长受到抑制。这些结果表明存在一种反式作用功能,在没有HimA或Hip/HimD功能时抑制噬菌体生长。rha基因很可能要么编码该功能,要么间接控制其作用。