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. Author manuscript; available in PMC: 2012 Oct 20.
Published in final edited form as: Neuron. 2011 Oct 20;72(2):316–329. doi: 10.1016/j.neuron.2011.08.032

Fig 8.

Fig 8

Point mutants of conserved aspartates fail to rescue copulation defect. Transgenic expression with a ubiquitous driver (Da-Gal4) rescued the prt1 copulation phenotype with wild-type PRT (8th column, p < 0.001) but not with the D59A (9th column) or D483A mutations (10th column). In contrast, transgenic expression of the Q521A mutation did rescue the prt1 copulation phenotype (final column, p < 0.05). The driver or UAS-prt transgenes alone did not rescue the behavior (columns 3–7, p > 0.05 for all compared to prt1). * = p < 0.05, ** = p < 0.01, *** = p < 0.001, ANOVA with Bonferroni’s post test for multiple comparisons. Bars represent means ± SEMs. The n for each group is shown with each column. NS: not significant.