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- W2607888630 abstract "Genetic changes in the HECT ubiquitin ligase HUWE1 are associated with intellectual disability, but it remains unknown whether HUWE1 functions in post-mitotic neurons to affect circuit function. Using genetics, pharmacology, and electrophysiology, we show that EEL-1, the HUWE1 ortholog in C. elegans, preferentially regulates GABAergic presynaptic transmission. Decreasing or increasing EEL-1 function alters GABAergic transmission and the excitatory/inhibitory (E/I) balance in the worm motor circuit, which leads to impaired locomotion and increased sensitivity to electroshock. Furthermore, multiple mutations associated with intellectual disability impair EEL-1 function. Although synaptic transmission defects did not result from abnormal synapse formation, sensitizing genetic backgrounds revealed that EEL-1 functions in the same pathway as the RING family ubiquitin ligase RPM-1 to regulate synapse formation and axon termination. These findings from a simple model circuit provide insight into the molecular mechanisms required to obtain E/I balance and could have implications for the link between HUWE1 and intellectual disability." @default.
- W2607888630 created "2017-05-05" @default.
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- W2607888630 date "2017-04-01" @default.
- W2607888630 modified "2023-09-28" @default.
- W2607888630 title "The HECT Family Ubiquitin Ligase EEL-1 Regulates Neuronal Function and Development" @default.
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- W2607888630 doi "https://doi.org/10.1016/j.celrep.2017.04.003" @default.
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