Lysis inhibition (LIN) is a well known property of many of T-even family members of bacteriophages and phage T4 is the best known member of this group. LIN is a response of T4-infected cells to superinfection with other T-even phage at least 3 min after the primary infection occurred. This leads to the prolongation of a viral development inside host cell as well as increase of the number of progeny virons. This prolonged latent period then results in rapid, synchronous lysis of infected bacterial culture (LIN collapse). Proteins RI and RIII are known for their role in regulation of LIN. RI interacts with T4 holin (a protein responsible for degradation of the host's cell wall) and inhibits it’s function. The interaction between this two proteins is a key aspect of LIN. It is also speculated that RIII protein acts as a stabilizing agent in this holin-antiholin interaction. T4 phages that are mutants in either rI or rIII gene are unable to trigger LIN mechanism. Therefore there are known as “rapid-lysis mutants” or “r mutants”.
In this work we would like to present if overexpression of rIII gene influenced development of phage T4 and its mutants. We have investigated if it affected the time of lysis of bacterial cultures infected with bacteriophages. Since our previous work suggested that RIII protein may be located on cell poles during overexpression in uninfected bacteria, we have also tried to determine the location of RIII protein in bacterial cytoplasm during phage life cycle.