Serratia marcescens Type VI Secretion System is transcriptionally upregulated by RcsB in response to the attack of bacterial competitors

LAZZARO, MARTINA; GARCÍA VÉSCOVI, ELEONORA; FELDMAN, MARIO F.

Ciudad Autónoma de Buenos Aires

Congreso; Reunión Conjunta de Sociedades de BioCiencias. LIII Reunión de la Sociedad Argentina de Investigación Bioquímica y Biología Molecular (SAIB).; 2017

Serratia marcescens (Sma) is an opportunistic human pathogen that represents a growing problem for public health. It has been reported that the type VI secretion system (T6SS) of Sma has a role in bacterial competition. We have previously showed that the T6SS of Sma is transcriptionally regulated by RcsB. The aim of this work is to analyze the RcsB-dependent regulation. Performing killing assays between Sma Db10 and Sma RM66262, we have determined that both strains were able to kill their wild-type counterparts but unable to kill the T6SS mutants (tssM). Using a fusion to GFP as a reporter of the transcriptional activity of T6SS promoter, we have demonstrated that this activity increased when Sma RM66262 was challenged by Sma Db10. In contrast, Sma Db10 tssM was not able to induce the T6SS transcriptional activity. Lack of RcsB expression resulted in the inability of the T6SS promoter to be induced when challenged by Sma Db10. We also performed inter-species competition assays using Acinetobacter baumannii or A. nosocomialis as attackers. The wild-type strains were able to kill Sma and to induce the transcriptional activity in a T6SS-dependent manner. To determine the signal that activates the T6SS in Serratia, we designed different approaches to detect if there is a danger signal detected by the prey. Finally, we analyzed whether the action of bacterial envelope damaging agents were able to promote T6SS expression. None of these challenges induced T6SS activity, indicating that non-specific envelope damage or the presence of endogenous molecules released as the result of bacterial lysis or T6SS-provoked death does not suffice to induce T6SS expression. Taken together, our results demonstrate that in Serratia, RcsB-controlled up-regulation of the T6SS over basal expression levels would constitute a survival strategy triggered by specific lethal threats posed by interbacterial competition.