Samantha Haller
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Samantha Haller has a total of 10 co-authors. Here are the top co-authors by number of shared publications:
- Abdul Hakkim
Department of Genetics, Harvard Medical School, Boston
1 shared publication - Adrien Franchet
Universite de Strasbourg CNRS UPR9022
1 shared publication - Dominique Ferrandon
Institut de Biologie Moléculaire et Cellulaire
1 shared publication Eliana Drenkard
Department of Genetics, Harvard Medical School, Boston
1 shared publicationFrederick M. Ausubel
Department of Genetics, Harvard Medical School, Boston, MA 02115 USA
1 shared publication- Jing Chen
Sino-French Hoffman Institute, Guangzhou Medical University
1 shared publication
Latest Publications
- Open Access
RhlR, but not RhlI, allows P. aeruginosa bacteria to evade Drosophila Tep4-mediated opsonization
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, Δ rhlI but not Δ rhlR 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.
Open AccessRhlR, but not RhlI, allows P. aeruginosa bacteria to evade Drosophila Tep4-mediated opsonization
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, Δ rhlI but not Δ rhlR 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.