Mirroring their unparalleled morphological and cellular richness, vertebrate brains are built by uniquely complex transcriptomes and proteomes. Multiple post-transcriptional mechanisms contribute to expand this molecular complexity; in particular, alternative splicing (AS) – the differential processing of introns and exons to generate multiple mRNA isoforms from a single gene – is believed to be the largest contributor to proteomic diversification in animals. With the advent of next generation sequencing, we can now comprehensively identify the isoforms that are unique to neural cells and start elucidating their functions. For example, neural-specific alternative exons in proteins involved in neurogenesis and synaptic functions have been shown to often impact protein-protein interactions, contributing to rewire interaction networks in a cell typespecific manner. Moreover, we have recently uncovered in mammalian brains a large number of microexons (exons as short as 3–27 nucleotides) that display the most striking evolutionary conservation and switch-like regulation during neuronal regulation. These microexons modulate the function of interaction domains of proteins involved in neurogenesis, and we are only starting to glimpse their multiple biological roles. Remarkably, they are frequently misregulated in the brains of individuals with autism spectrum disorder, providing a new perspective to investigating the molecular bases of this complex disease.
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