Deposition of the exon junction complex is thought to be the missing link between pre-mRNA splicing and translation in multicellular organisms, but no evidence of such deposition has been found in Drosophila.
The need for efficient pre-RNA splicing during early embryonic development of Drosophila indicates that the constraints imposed by the cell cycle are a force capable of driving changes in Eukaryotic gene architecture.
Surprising connections between gene architecture and splicing kinetics are illuminated using short, progressive metabolic labeling/RNA sequencing and novel computational modeling approaches in Drosophila cells.
Diverse and widespread novel alternative pre-mRNA splicing isoforms as well as cycling alternative splicing events that undergo time-of-day dependent changes are identified in isolated Drosophila neuron groups.
Hinokiflavone is identified as a splicing modulator that blocks progression from spliceosome complex A to complex B and inhibits SUMO protease SENP1, causing hyper-SUMOylation affecting 6 U2 snRNP proteins.
Structural and functional analyses show how the spliceosomal Prp3 protein concomitantly binds double- and single- stranded regions in U4/U6 di-snRNAs and serves to stabilize the U4/U6•U5 tri-snRNP for splicing.
During evolutionary progression of Alu-exons, repressive U-tracts buffer sudden gains in 3' splice site strength and prevent inclusion of cryptic exons.
