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. Author manuscript; available in PMC: 2022 May 26.
Published in final edited form as: Nature. 2015 Jun 17;523(7558):83–87. doi: 10.1038/nature14545

Extended Data Figure 7: The IgC2 domain is necessary for OIG-1 function.

Extended Data Figure 7:

At the L1 stage when only the DD MNs are present, ectopic SNB-1::GFP puncta (from juIs1-unc-25p::SNB-1::GFP) localize to the dorsal nerve cord (DNC) of oig-1 mutant L1s (red bar) but not in wild-type animal (black bar) (see Fig. 3A). Based on an alignment with the hidden Markov model (HMM) Ig domain (top), a highly conserved residue (W75) and a nonconserved residue (E64) in the OIG-1 Ig domain were mutated in the context of an unc-30p::oig-1 transgene that is able to rescue the L1 ectopic synapse defects (see Fig. 3A). The unc-30p::oig-1E64A transgenes (otEx6212, otEx6213) were still able to rescue the synaptic defects of oig-1 L1 animals (green bars), whereas the unc-30p::oig-1W75A transgenes (otEx6214,otEx6215) had no rescue ability (blue bars). L1 animals were obtained by hypochlorite-treating gravid adult animals and letting embryos hatch and arrest in M9 for 16-18 hours. n>20 for each strain scored, **p < 0.01, *p < 0.05.