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Spt1 function is required for appropriate larval nociceptive responses to rising heat. Targeted Spt1C129W expression under control of the ppk-GAL4 driver in the class IV da neurons, and global hypomorphic conditions of Spt1 causes defective nociception similar to that observed during da neuron silencing (ppk-GAL4 driving expression of UAS-TNTE) and in the painless (pain1) mutant. ****P ≤ 0.0001, ANOVA, ns = non-significant compared with control.
