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. Author manuscript; available in PMC: 2011 Mar 1.
Published in final edited form as: J Neurogenet. 2010 Mar;24(1):33–41. doi: 10.3109/01677060903419751

Figure 4.

Figure 4

A wild-type amn+ gene whose expression is driven by amn28A and amnX8 GAL4 activities rescues the thermal nociception defect in amn mutants. Nociception assays were performed for animals trans-heterozygous for amn28A and amnX8, with or without the UAS-amn+ transgene. Latencies of the responses to a noxious heat stimulus are shown as box plots, for larvae (A) and adult flies (B). The amn28A/amnX8; UAS-amn+/+ flies displayed response latencies that were reduced in comparison to those of amn28A/amnX8 flies. ***P < 0.001 (Mann-Whitney Rank Sum Test).