期刊
GENOME RESEARCH
卷 25, 期 1, 页码 1-13出版社
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/gr.181990.114
关键词
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资金
- University of Oxford Nuffield Department of Medicine
- Medical Research Council UK
- Wellcome Trust [090532/Z/09/Z]
- BBSRC [BBS/E/T/000PR5885, BBS/E/T/000PR6193] Funding Source: UKRI
- MRC [MC_UU_12021/1, MC_U137761446] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BBS/E/T/000PR5885, BBS/E/T/000PR6193] Funding Source: researchfish
- Medical Research Council [MC_UU_12021/1, MC_U137761446] Funding Source: researchfish
Ninety-four percent of mammalian protein-coding exons exceed 51 nucleotides (nt) in length. The paucity of micro-exons (<= 51 nt) suggests that their recognition and correct processing by the splicing machinery present greater challenges than for longer exons. Yet, because thousands of human genes harbor processed micro-exons, specialized mechanisms may be in place to promote their splicing. Here, we survey deep genomic data sets to define 13,085 micro-exons and to study their splicing mechanisms and molecular functions. More than 60% of annotated human micro-exons exhibit a high level of sequence conservation, an indicator of functionality. While most human micro-exons require splicing-enhancing genomic features to be processed, the splicing of hundreds of micro-exons is enhanced by the adjacent binding of splice factors in the introns of pre-messenger RNAs. Notably, splicing of a significant number of micro-exons was found to be facilitated by the binding of RBFOX proteins, which promote their inclusion in the brain, muscle, and heart. Our analyses suggest that accurate regulation of micro-exon inclusion by RBFOX proteins and PTBP1 plays an important role in the maintenance of tissue-specific protein-protein interactions.
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