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Significance The symptoms of neurological diseases such as autism and schizophrenia are often attributed to a loss of excitatory/inhibitory balance of neural network function. By showing that ATR and ATM impact inhibitory and excitatory vesicle trafficking differently, our work expands the known repertoire of cytoplasmic functions for the two kinases and provides a new perspective on the origins of the symptoms of ataxia-telangiectasia (A-T) and Seckel syndrome (ATM and ATR deficiency, respectively). While these findings have their most immediate implications for the neurologic and cognitive symptoms of A-T and Seckel syndrome, they have potential relevance to a much broader range of neurologic conditions.
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Cheng et al. (2017) studied this question.
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