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. 2013 Jan 23;33(4):1672–1677. doi: 10.1523/JNEUROSCI.3042-12.2013

Figure 1.

Figure 1.

oamb-null mutants are impaired in appetitive learning, which is rescued by temporarily restored expression of either OAMB-K3 or OAMB-AS isoform. Flies were trained with EA and IAA as CS and sucrose reward or electric shock punishment as US. A, oamb286 flies exhibited impaired performance immediately or 1 and 3 h after training in appetitive olfactory conditioning (***p < 0.001, n = 6–12, Dunnett's test) but their memory decay was comparable to that of the control Canon-S flies (ANCOVA, p > 0.05). B, Three oamb-null alleles (oamb584, oamb286, and oamb96) showed learning performance comparable to that in the ry control in aversive conditioning (NS, not significant; n = 6, Tukey–Kramer test). C, The oamb286- (§) and oamb96 (§§)-null alleles and the oamb286 carrying HS-GAL4 along with UAS-OAMB-KS or UAS-OAMB-AS or both, when reared at 20°C (Uninduced), exhibited significantly reduced performance compared with Canton-S (top). Upon heat treatment (Induced), the oamb mutants carrying the same transgenes showed learning performance comparable to that of Canton-S but significantly different from that of oamb-null alleles (bottom). Two independent UAS-OAMB lines for each isoform were used for rescue experiments and the chromosomes (| for X, ‖ and |‖) containing the transgene are noted in the genotype table. NS, not significant; **p < 0.01; ***p < 0.001, n = 6, Tukey–Kramer.