Klaenhammer T R, Sanozky R B
J Gen Microbiol. 1985 Jun;131(6):1531-41. doi: 10.1099/00221287-131-6-1531.
Streptococcus lactis ME2 exhibits at least three mechanisms which confer resistance to virulent bacteriophage. These include plasmid-induced interference with phage adsorption, host-controlled restriction and modification activities, and a heat-sensitive mechanism which suppresses development of virulent phage. Conjugal mating experiments were done with S. lactis ME2 to determine if phage-defence mechanisms present in this strain could be mobilized, associated with plasmid DNA elements and phenotypically characterized in transconjugants. Agar-surface matings of S. lactis ME2 with S. lactis LM0230 demonstrated that lactose-fermenting ability (Lac+) was transferred in a conjugation-like process at frequencies of 10(-6) per donor cell and was associated with a 40 MDal plasmid designated pTR1040. Resistance to nisin (Nisr) was acquired or lost simultaneously with Lac+, indicating that pTR1040 carried determinants for both phenotypes. Lac+ Nisr transconjugants that carried a 30 MDal plasmid (pTR2030) exhibited a heat-sensitive phage-defence mechanism (Hsp+) which limited the burst size and plaque size of phage c2 without altering the efficiency of plaquing (e.o.p.) or the level of adsorption. The ability of phage c2 to initiate plaquing at an e.o.p. of 1.0 indicated that DNA injection and early viral gene expression are not affected in the Hsp+ transconjugants. We suggest, therefore, that the Hsp+ phenotype may result from plasmid-induced abortive infection of phage dependent on the presence of pTR2030. Hsp+ transconjugants carrying pTR2030 also promoted high-frequency conjugal transfer of Lac+ Nisr associated with pTR1040 (greater than 10(-1) per donor cell). It was concluded that Hsp+ and determinants for conjugal transfer ability (Tra+) are located on pTR2030.
乳酸链球菌ME2表现出至少三种赋予对烈性噬菌体抗性的机制。这些机制包括质粒诱导的对噬菌体吸附的干扰、宿主控制的限制和修饰活性,以及一种抑制烈性噬菌体发育的热敏感机制。用乳酸链球菌ME2进行接合交配实验,以确定该菌株中存在的噬菌体防御机制是否可以被转移、与质粒DNA元件相关联并在转接合子中进行表型鉴定。乳酸链球菌ME2与乳酸链球菌LM0230的琼脂表面交配表明,乳糖发酵能力(Lac+)在类似接合的过程中以每供体细胞10^(-6)的频率转移,并且与一个命名为pTR1040的40 MDal质粒相关联。对乳链菌肽的抗性(Nisr)与Lac+同时获得或丧失,表明pTR1040携带这两种表型的决定因素。携带30 MDal质粒(pTR2030)的Lac+ Nisr转接合子表现出一种热敏感噬菌体防御机制(Hsp+),该机制限制了噬菌体c2的爆发量和噬菌斑大小,而不改变噬菌斑形成效率(e.o.p.)或吸附水平。噬菌体c2以1.0的e.o.p.开始形成噬菌斑的能力表明,DNA注入和早期病毒基因表达在Hsp+转接合子中不受影响。因此,我们认为Hsp+表型可能是由质粒诱导的依赖于pTR2030存在的噬菌体流产感染导致的。携带pTR2030的Hsp+转接合子也促进了与pTR1040相关的Lac+ Nisr的高频接合转移(每供体细胞大于10^(-1))。得出的结论是,Hsp+和接合转移能力(Tra+)的决定因素位于pTR2030上。