Speaker
Description
Contact-dependant interaction can be mediated by specific systems like the T6SS (Ikryannikova et al., 2020). This protein nanomachine, pierces target cells to inject toxic effector. If target cells don’t contain the corresponding Immunity protein they will not survive, contributing to colonization (Ducarmon et al., 2019). While competition is instrumental in the micro-community, cooperation is also vital. Biofilm is a prime example, in which individual bacteria build multi-cellular structures. Such communities are beneficial as they provide protection from predation/antibiotics. T6SS is associated with biofilm formation, however, the molecular mechanism remain elusive. Previously, we identified a mutation in a T6S effector, Spyo, that lead to an increase in biofilm fomation. In this project, we wanted to investigate the molecular mechanisms leading to Spyo increasing biofilm formation? We investigated the transcriptional profiles through over-expressed the effectors in the presence/absence of Immunity and performed RNA-seq. We observed increased expression in SOS response and biofilm-related genes, while also affecting c-di-GMP. Interestingly, we found that over-expression of the Immunity led to a decrease in biofilm formation. This leads us to ask, when would the amount of Spyo exceed the amount of Immunity in the cell? We have explored many possibilities, A)delivery Spyo, B) unstable Immunity, C) auto-regulation. Our results suggest that when the effector if free to act, its toxic nature allows it to drive biofilm formation.
