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. 2007 Jun 20;27(25):6852–6857. doi: 10.1523/JNEUROSCI.0933-07.2007

Figure 2.

Figure 2.

Rescue of learning and LTM defects by expressing hNF1 as well as heat shock NF1 (hsNF1) transgene in Nf1-null mutants. A, Crosses performed to generate F1 progeny expressing UAS-hNF1 constructs under the control of the pan-neuronal elav-Gal4 driver. B, Rescue of learning and LTM by expressing hNF1 transgene in Nf1-null mutants. Transgenic flies expressing hNF1 pan-neuronally (elav/+/Y;UAS-hNF1/+;Nf1P1/P2) exhibit significant increases (*p < 0.001) in both learning (left) and LTM (right) from parental lines (elav;Nf1P1 and UAS_hNF1;Nf1P2). The wild-type control is 2202u, an isogenic line from which transgenic parental lines were generated (Hannan et al., 2006). C, Normal ARM performance in all transgenic lines. None of the transgenes show any nonspecific effect on ARM (n = 4 PIs per group). D, Acute expression of NF1 rescues LTM. Heat shock-induced expression of NF1 (hsNF1/+;Nf1P2) before spaced training significantly rescues (*p < 0.001) the LTM defect found in Nf1 mutants when compared with both 2202u (control) and K33 wild-type flies. This indicates the importance of NF1 in LTM formation. HS+, raised at 18°C and shifted to 30°C for 30 min 2 h before training; HS−, no heat shock treatment. PI scores are expressed as mean ± SEM, n = 8 unless otherwise indicated.