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.
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.
Single-cell splicing of a conserved neuronal kinase is established by a combinatorial code of fate-determining transcription factors and neuronal RNA binding proteins, with different combinations in different neuron types.
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.
Transcriptome and eCLIP analyses in mouse and human reveal splicing factor proline/glutamine rich (SFPQ) as a conserved and critical guardian of long-intron integrity, splicing, and circular RNA (circRNA) production.
Transcriptome analysis reveals an alternative splicing program induced in the arterial endothelium under low-flow inflammatory conditions by platelet and macrophage recruitment and dependent upon the RNA-binding splice factor Rbfox2.
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.
