A novel protein domain in an ancestral splicing factor drove the evolution of neural microexons
Author:
Publisher
Springer Science and Business Media LLC
Subject
Ecology,Ecology, Evolution, Behavior and Systematics
Link
http://www.nature.com/articles/s41559-019-0813-6.pdf
Reference59 articles.
1. Irimia, M. et al. A highly conserved program of neuronal microexons is misregulated in autistic brains. Cell 159, 1511–1523 (2014).
2. Li, Y. I., Sanchez-Pulido, L., Haerty, W. & Ponting, C. P. RBFOX and PTBP1 proteins regulate the alternative splicing of micro-exons in human brain transcripts. Genome Res. 25, 1–13 (2015).
3. Quesnel-Vallières, M., Irimia, M., Cordes, S. P. & Blencowe, B. J. Essential roles for the splicing regulator nSR100/SRRM4 during nervous system development. Genes Dev. 29, 746–759 (2015).
4. Nakano, Y. et al. A mutation in the Srrm4 gene causes alternative splicing defects and deafness in the Bronx waltzer mouse. PLoS Genet. 8, e1002966 (2012).
5. Quesnel-Vallieres, M. et al. Misregulation of an activity-dependent splicing network as a common mechanism underlying autism spectrum disorders. Mol. Cell 64, 1023–1034 (2016).
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