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A highly conserved program of neuronal microexons is misregulated in autistic brains #MMPMID25525873
Irimia M; Weatheritt RJ; Ellis J; Parikshak NN; Gonatopoulos-Pournatzis T; Babor M; Quesnel-Vallières M; Tapial J; Raj B; O?Hanlon D; Barrios-Rodiles M; Sternberg MJ; Cordes SP; Roth FP; Wrana JL; Geschwind DH; Blencowe BJ
Cell 2014[Dec]; 159 (7): 1511-23 PMID25525873show ga
Alternative splicing (AS) generates vast transcriptomic and proteomic complexity. However, which of the myriad of detected AS events provide important biological functions is not well understood. Here, we define the largest program of functionally coordinated, neural-regulated AS described to date in mammals. Relative to all other types of AS within this program, 3-15 nucleotide ?microexons? display the most striking evolutionary conservation and switch-like regulation. These microexons modulate the function of interaction domains of proteins involved in neurogenesis. Most neural microexons are regulated by the neuronal-specific splicing factor nSR100/SRRM4, through its binding to adjacent intronic enhancer motifs. Neural microexons are frequently misregulated in the brains of individuals with autism spectrum disorder, and this misregulation is associated with reduced levels of nSR100. The results thus reveal a highly conserved program of dynamic microexon regulation associated with the remodeling of protein interaction networks during neurogenesis, the misregulation of which is linked to autism.