Fig. 7. Innervation defects are strongly enhanced in tlr1,side double mutants. Arrows indicate missing or mislocalized NMJs on muscles 12, 13, 6 and 7. Asterisks mark NMJs outside of the intended focal plane. (A-C) Confocal images of tlr1^D427 (A) and side^C137/side^I1563 (B) single and tlr1^D427,side^C137/tlr1^K788,side^C137 (C) double mutant third instar larvae stained with CD8-GFP-Sh. Double mutant larvae (C) show a strong enhancement of the innervation phenotype and lack almost all NMJs on ventral muscles, only muscle 12 is innervated at an unusual dorsal-posterior position in this example. (A'-C') Confocal images of dissected tlr1^D427/tlr1^K788 (A') and side^C137/side^I1563 (B') single and tlr1^D427,side^C137/tlr1^K788,side^C137 (C') double mutant third instar larvae stained with CD8-GFP-Sh (green) and anti-Fas II antibodies (red). In this double mutant hemisegment (C'), all NMJs are missing on ventral muscles, including NMJs formed by type II boutons. (A"-C") Schematic representation of the quantitative evaluation of the larval innervation defects as presented in Table 1. The frequency of innervation errors for a respective muscle in wild type was subtracted from the frequency observed in mutants. Misinnervation frequencies were then transformed into a color code, as depicted in (A"). Muscles 4 and 25 were not evaluated. In tlr1 mutants (A"), the misinnervation phenotype is weaker than in side mutants (B"), and creation of a double mutant aggravates the innervation defects in ventral, lateral and dorsal body wall regions (C").