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. Author manuscript; available in PMC: 2013 Apr 20.
Published in final edited form as: Immunity. 2012 Mar 29;36(4):612–622. doi: 10.1016/j.immuni.2012.01.019

Figure 3. Phosphoinositide binding by dMyD88 is necessary for immune defenses in flies.

Figure 3

(a) Schematic representation of the dMyD88 constructs used to generate transgenic flies. The molecular weights (MW) of the resulting proteins are indicated. (b) Fluorescence micrographs of S2 cells expressing the indicated dMyD88 constructs. The localization of full length dMyD88 (FL) is phenocopied by the PIP2-specific chimera (dMyD88-PLC). Scale bars represent 5µm. (c,d) Lysates from dMyD88 homozygous mutant (c03881), wild type dMyD88 heterozygote (WT), and dMyD88 homozygous mutant flies complemented with the transgenes described in (a) were analyzed either by immunoblotting with a dMyD88 antibody (obtained from S. Wassermann (Sun et al., 2002) or by performing RT-PCR using dMyD88 Taqman probes. No significant difference in RNA or protein amounts was observed between the various transgenic flies. (e, f, g) Male flies of the indicated genotype were infected with E. facaelis (e), S. epidermidis (f), or E. coli (g). Each infection was done with at least 25 flies for each genotype, and the surviving flies were counted daily. Log-rank analysis demonstrated a statistically significant difference between survival of dMyD88-FL flies and dMyD88 mutants (p=<0.0001) for both E. facaelis and S. epidermidis infections, but not following E. coli infection (p=0.1986). Survival of dMyD88-FL flies and dMyD88-Cyto flies was statistically significant following treatment with E. facaelis (p=0.0091) and S. epidermidis (p= 0.0020), but not following E. coli infection (p=0.2673). The difference between survival of dMyD88-FL flies and dMyD88-PLC was not significant for any of the above infections. See also Figure S3.