Alternative splicing has been recently implicated in cocaine addiction (Cates et al. 2018). Transcription factor E2F3a regulates cocaine-induced alternative splicing in the mouse nucleus accumbens, and E2F3b mediates cocaine responses in the prefrontal cortex (Cates et al. 2019). Drosophila E2F1 was expressed in our MB nuclei data set (Figure 1Cii), although it was not alternatively spliced in response to alcohol or alcohol-cue training (see transcript count data in Gene Expression Omnibus). We speculate that cocaine utilizes the E2F transcription factor family more than alcohol does to drive drug-cue memory formation and retention. Future investigations will likely identify both conserved drug-specific and convergent molecular mechanisms that influence transcriptional activity in reward circuitry.
