<i>unc-6</i>/netrin signaling via the <i>unc-5</i>/UNC5 receptor requires <i>lon-2</i>/glypican.

<p>(A) The axon of PVM normally migrates ventrally in the wild type, but it can be forced to migrate dorsally by misexpressing the repulsive receptor <i>unc-5</i>/UNC5. We quantified PVM since AVM could not be reliably identified (both AVM and neighboring ALMR axons project dorsally in P<i>mec-7</i>::<i>unc-5</i> transgenic animals.) (B) Upon misexpression of <i>unc-5</i>/UNC5 in PVM, using the transgene P<i>mec-7</i>::<i>unc-5</i>, the axon of PVM projects dorsally in an <i>unc-6</i>/netrin-, <i>unc-40</i>/DCC-, and <i>unc-34/</i>enabled-dependent manner. Loss of <i>lon-2</i>/glypican partially suppresses this forced dorsal migration, indicating that <i>unc-6</i>/netrin signaling depends on <i>lon-2</i>/glypican. Scale bar, 5 μm. Error bars are standard error of the proportion. Asterisks denote significant difference: *** <i>p</i> ≤ 0.001 (z-tests, <i>p</i>-values were corrected by multiplying by the number of comparisons). ns, not significant. Wild type (without <i>evIs25</i>) is the same as in <a href="http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.1002183#pbio.1002183.g001" target="_blank">Fig 1B</a>.