Figure 2

Figure 2

Loss of function of Annexin11a results in defects of zebrafish neuromuscular junctions. (A) Fixed wild-type (WT) and homozygous (HOM) larvae were stained to label pre and postsynaptic junctions with ZNP1 (blue), αBTX (red) and merge respectively with representative images shown. HOM larvae [(iv–vi), n = 9 embryos] show a loss of branching reflected by a loss of Znp1/Btx co-localization compared to WT [A(i–iii) (n = 8 embryos) and in B]. This was significant on quantification (C) (Pearson’s r coefficients of co-localization, P ≤ 0.0001). Injection with human WT Annexin A11 mRNA had no detrimental effect on the WT larvae [A(vii–ix) (n = 8 embryos)]. Homozygous embryos injected with human WT Annexin A11 (n = 9 embryos) rescued the loss of ZNP1 and αBTX co-localization [A(x–xii)] that was significant (C, unpaired t-test; ****P ≤ 0.0001). Max projections, ×40 oil objective. Scale bar = 100μm. hpf = hours post-fertilization.