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. 2012 Feb 22;32(8):2628–2636. doi: 10.1523/JNEUROSCI.2901-11.2012

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Copyright © 2012 the authors 0270-6474/12/322628-09$15.00/0

This article is freely available online through the J Neurosci Open Choice option.

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Figure 4. — Binding of RAE-1 to RPM-1 is necessary for RPM-1 to be fully functional. Transgenic animals were generated on an rpm-1^−/− background to quantify rescue of rpm-1 (lf) defects. Rescue was analyzed for transgenic expression of wt RPM-1::GFP (Exrpm-1::GFP), or a point mutant of RPM-1::GFP (Exrpm-1::GFP VIR to AAA). A, ALM axon termination defects were quantified for the indicated genotypes. B, PLM axon termination defects were quantified for the indicated genotypes. Note, that data from 4–6 independently derived transgenic lines was pooled for this analysis, and n is the number of ALM or PLM neurons that were scored. A two-tailed Fisher exact test was used to determine significance. ***p < 0.0005.