The tissue-specific deployment of highly extended neural 3’ UTR isoforms, generated by alternative polyadenylation (APA), is a broad and conserved feature of metazoan genomes. However, the factors and mechanisms that control neural APA isoforms are not well-understood. Here, we show that three ELAV/Hu RNA binding proteins (Elav, Rbp9 and Fne) have similar capacities to induce a lengthened 3’ UTR landscape in an ectopic setting. These factors promote accumulation of chromatin-associated, 3’ UTR-extended, nascent transcripts, through inhibition of proximal polyadenylation site (PAS) usage. Notably, Elav represses an unannotated splice isoform of fne , switching the normally cytoplasmic Fne towards the nucleus in elav mutants. We use genomic profiling to reveal strong and broad loss of neural APA in elav/fne double mutant CNS, the first genetic background to largely abrogate this distinct APA signature. Overall, we demonstrate how regulatory interplay and functionally overlapping activities of neural ELAV/Hu RBPs drives the neural APA landscape. Neurons express much longer 3’ UTRs than other celltypes. Here, Wei and Lee et al. determine that roles of Drosophila ELAV/Hu RNA binding proteins are necessary and sufficient to determine the extended 3’ UTR landscape. Moreover, their compensatory functions involve splicing and subcellular regulation between ELAV/Hu members.