Serratia marcescens T2SS SECRETES POTENTIAL EFFECTOR PROTEINS AND IS REGULATED BY IRON

SARTORI, MARIA SOL; GARCÍA VÉSCOVI, ELEONORA; MARISCOTTI, JAVIER F.

Congreso; SAIB - SAMIGE Joint meeting 2021 on line; 2021

SAIB - SAMIGE

Serratia marcescens is an opportunistic human pathogen that represents a growing problem for public health, particularly in hospitalized or immunocompromised patients. Despite its clinical prevalence, factors and mechanisms that contribute to Serratia pathogenesis remain unclear. S. marcescens ability to adapt to and survive in either hostile or changing environments also relates to the bacterial capacity to express a wide range of secreted enzymes, including chitinases, phospholipase, haemolysin, nuclease and proteases. The T2SS is a multiprotein secretion complex, present in a wide variety of organisms and frequently implicated in virulence. In our clinical RM66262 strain, we found the presence of a type II secretion system (T2SS), which is chromosomally encoded in the majority of clinical isolates, but absent from most non-clinical isolates, including the reference, S. marcescens strain Db11. However, the substrates of the RM66262 T2SS, environmental signals and regulatory factors that modulate its expression are unknown. In this work, we have assessed the regulation of T2SS using gfp-containing reporter plasmid and we have searched for potential effector proteins secreted by the system. Results showed that T2SS expression is induced during the stationary growth phase. One conspicuous defense of vertebrates against bacterial infections is nutrient deprivation, which prevents bacterial growth in a process termed nutritional immunity. The most significant form of nutritional immunity is the sequestration of iron. We found that under iron-depleted conditions, the transcription levels of PT2SS-gfp is two-times increased compared to iron-suppled medium. Our preliminary results suggest that the S. marcescens T2SS secretes effector proteins in response to signals from the extracellular environment, a mechanism that could contribute to Serratia virulence strategies.