The research focuses on the stringent response of bacteria. Stringent response is a universal mechanism in bacteria to survive stress. It is governed by the alarmone (p)ppGpp that is produced by RSH (RelA-SpoT homologue) enzymes. When the level of (p)ppGpp in cells increases, the growth of bacteria decreases, which helps them survive stressful conditions.
Bacteria encounter several stresses, one of the most common of them is attacks by phages, viruses. Upon lytic cycle they kill the cell after forcing it to produce new viruses. On the other hand, temperate phages can integrate into bacterial genome as prophages, where they can be beneficial for the cell by protecting it from superinfection with other phages. Yet, prophage can switch to the lytic cycle and kill its host. It has been suggested that stringent response may have a role in defence against phages and their lytic-lysogenic choice.
I have recently returned from abroad, where my postdoctoral research was directed towards unravelling the molecular mechanisms behind stringent response. Here, I aim to shed light onto the connections between stringent response and phage attacks and the role of (p)ppGpp in temperate phages’ lifecycle choice.
Scheme used in the header: Pseudomonas putida stringent response (by Hedvig Tamman)