期刊
MOLECULAR CELL
卷 72, 期 3, 页码 496-+出版社
CELL PRESS
DOI: 10.1016/j.molcel.2018.09.033
关键词
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资金
- European Research Council [617837]
- Wellcome Trust [103760/Z/14/Z, FC001002]
- Marie Curie Intraeuropean Fellowship [627783]
- Francis Crick Institute
- Cancer Research UK [FC001002]
- UK Medical Research Council [FC001002, MR/N013867/1]
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [T32GM007266] Funding Source: NIH RePORTER
- MRC [1764955] Funding Source: UKRI
Recursive splicing (RS) starts by defining an RS-exon,'' which is then spliced to the preceding exon, thus creating a recursive 5' splice site (RS-5ss). Previous studies focused on cryptic RS-exons, and now we find that the exon junction complex (EJC) represses RS of hundreds of annotated, mainly constitutive RS-exons. The core EJC factors, and the peripheral factors PNN and RNPS1, maintain RS-exon inclusion by repressing spliceosomal assembly on RS-5ss. The EJC also blocks 5ss located near exon-exon junctions, thus repressing inclusion of cryptic microexons. The prevalence of annotated RS-exons is high in deuterostomes, while the cryptic RS-exons are more prevalent in Drosophila, where EJC appears less capable of repressing RS. Notably, incomplete repression of RS also contributes to physiological alternative splicing of several human RS-exons. Finally, haploinsufficiency of the EJC factor Magoh in mice is associated with skipping of RS-exons in the brain, with relevance to the microcephaly phenotype and human diseases.
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