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. 2014 Nov 15;141(22):4395–4405. doi: 10.1242/dev.110437

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© 2014. Published by The Company of Biologists Ltd

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed.

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Fig. 6. — Excessive filopodial protrusion correlates with axon branching defects in adult animals. Quantification of VD/DD axon pathfinding defects and ectopic axon branches as described in Fig. 3. Activated ced-10(G12V) and mig-2(G16V), which suppress excessive growth cone filopodial protrusion of unc-73(rh40), also suppress ectopic axon branching but not other guidance defects. ced-10(G12V) and mig-2(G16V) did not suppress excessive growth cone filopodial protrusion of unc-33 and unc-44, nor did they suppress ectopic axon branching of these mutants. M+ indicates that the animals had wild-type maternal ced-10(+) contribution. Error bars represent 2× standard error of proportion. Fisher's exact tests were used to determine statistical significance.