SRP118479 PRJNA408240 GSE104100 Traumatic brain injury in Drosophila causes retention of long introns. Traumatic brain injury (TBI) can cause persistent pathological alteration of neurons. This may lead to cognitive dysfunctions, depression, and even increased susceptibility to life threatening diseases, such as epilepsy. To investigate the underlying genetic and molecular basis of TBI, Wasserman and colleagues developed an inexpensive and reproducible model for simulating TBI in Drosophila melanogaster (Fruit Fly). Using a modified version of this model, we subjected w1118 fruit flies to mild closed head trauma. To determine the transcriptomic changes which contribute to survival post TBI, we collected fly heads from the survivors at 2 time points; 4 hours and 24 hours post-trauma. We observed that the induction of transcriptomic changes occur 24 hours post-trauma in fly heads. Classification of these AS changes showed selective retention of long introns (>81bps), with a mean size of ~3000bps. Gene ontology analysis of the genes containing retained introns showed significant enrichment for critical regulators of glycolysis, citric acid cycle as well as vesicle mediated neurotransmitter release. Some of these genes also showed a significant reduction in transcript abundance. The retained introns were enriched for CA-rich motifs known to bind to Smooth (SM), an hnRNPL class of splicing factor. Overall design: mRNA profile of w1118 wild-type heads (±TBI) were generated by deep sequencing using 100bps paired-end reads. GSE104100 pubmed 29187863