Drosophila embryos as model systems for monitoring bacterial infection in real time

Isabella Vlisidou1, Andrea J Dowling, Iwan R Evans

  • 1Department of Biology and Biochemistry, University of Bath, Bath, United Kingdom.

Plos Pathogens
|July 18, 2009
PubMed

Insights

Drosophila embryos model real-time bacterial infection. Embryonic hemocytes phagocytose E. coli but freeze upon Photorhabdus infection due to the Mcf1 toxin affecting actin.

Area of Science:

  • Developmental Biology
  • Immunology
  • Microbiology

Background:

  • Drosophila embryos serve as established models for development and wound repair.
  • Their utility is extended here to investigate bacterial infections in real-time.

Purpose of the Study:

  • To utilize Drosophila embryos as a model system for observing bacterial infections and hemocyte interactions dynamically.
  • To investigate the mechanisms underlying hemocyte responses to pathogenic and non-pathogenic bacteria.

Main Methods:

  • Time-lapse confocal microscopy was employed to observe bacterial behavior and hemocyte interactions within Drosophila embryos.
  • Pathogenic (Photorhabdus asymbiotica) and non-pathogenic (Escherichia coli) bacteria were injected into embryos.
  • The effects of the insecticidal toxin Makes Caterpillars Floppy 1 (Mcf1) and its genetic manipulation were analyzed.

Main Results:

  • Embryonic hemocytes demonstrated phagocytic competence, recognizing and engulfing non-pathogenic E. coli independently of Dscam.
  • Pathogenic Photorhabdus bacteria induced a rapid hemocyte 'freezing' phenotype, linked to actin cytoskeleton rearrangement.
  • This freezing was mimicked by Mcf1 toxin or recombinant E. coli expressing mcf1, dependent on shibire and modulated by Rac expression.

Conclusions:

  • Drosophila embryos provide a powerful system for real-time tracking of bacterial infections.
  • Hemocyte responses to bacterial virulence factors, like Mcf1, involve rapid cytoskeletal changes and endocytosis.
  • Mutant analysis in this system can dissect the genetic basis of bacterial virulence factor effects.

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