RT Journal Article
SR Electronic
T1 RhlR, but not RhlI, allows P. aeruginosa bacteria to evade Drosophila Tep4-mediated opsonization
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 165530
DO 10.1101/165530
A1 Samantha Haller
A1 Adrien Franchet
A1 Abdul Hakkim
A1 Jing Chen
A1 Eliana Drenkard
A1 Shen Yu
A1 Stefanie Schirmeier
A1 Zi Li
A1 Frederick M. Ausubel
A1 Samuel Liégeois
A1 Dominique Ferrandon
YR 2017
UL http://biorxiv.org/content/early/2017/07/26/165530.abstract
AB When Drosophila flies feed on Pseudomonas aeruginosa strain PA14, some bacteria cross the intestinal barrier and start proliferating inside the hemocoel. This process is limited by hemocytes through phagocytosis. We have previously shown that the PA14 quorum-sensing regulator RhlR is required for these bacteria to elude the cellular immune response. RhlI synthesizes the auto-inducer signal that activates RhlR. Here, we compare the null mutant phenotypes of rhlR and rhlI in a variety of infection assays in Drosophila and in the nematode Caenorhabditis elegans. Surprisingly, in Drosophila, unlike ΔrhlR mutants, ΔrhlI mutants are only modestly attenuated for virulence and are poorly phagocytosed and opsonized in a Thioester-containing Protein4-dependent manner. Likewise, ΔrhlI but not ΔrhlR mutants colonize the digestive tract of C. elegans and kill it as efficiently as wild-type PA14. Thus, RhlR has an RhlI-independent function in eluding detection or counter-acting the action of the immune system. In contrast to the intestinal infection model, Tep4 mutant flies are more resistant to PA14 in a septic injury model, which also depends on rhlR. Thus, the Tep4 putative opsonin can either be protective or detrimental to host defense depending on the infection route.