Retooling spare parts: Gene duplication and cognition

Center for Autism Research and Treatment and the Program in Neurobehavioral Genetics, Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles, Los Angeles, California, USA.
Nature Neuroscience (Impact Factor: 16.1). 01/2013; 16(1):6-8. DOI: 10.1038/nn.3292
Source: PubMed


Two new studies provide experimental evidence of how ancient genomic duplications of synaptic genes provided the substrate for diversification that ultimately expanded vertebrate cognitive complexity.

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    • "Identifying such links can be valuable in personalized medicine and will extend our knowledge of recognized cholinergic controllers. The recently discovered role of gene duplication events in cognition [95] behooves the exploration of common variations in the expanded family of cholinergic regulators for genetic risks of autism and other mental diseases [96]. Also, de novo mutations in cholinergic regulators should be tested for impaired synaptic networks, as in schizophrenia [97], and the biogenesis of circular RNAs raises new questions in view of the involvement of changed circular RNA levels in controlling alternative splicing, which is essential for maintaining the cholinergic signaling process. "
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    ABSTRACT: The discovery of the first neurotransmitter — acetylcholine — was soon followed by the discovery of its hydrolysing enzyme, acetylcholinesterase. The role of acetylcholinesterase in terminating acetylcholine-mediated neurotransmission made it the focus of intense research for much of the past century. But the complexity of acetylcholinesterase gene regulation and recent evidence for some of the long-suspected 'non-classical' actions of this enzyme have more recently driven a profound revolution in acetylcholinesterase research. Although our understanding of the additional roles of acetylcholinesterase is incomplete, the time is ripe to summarize the evidence on a remarkable diversity of acetylcholinesterase functions.
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