期刊
JOURNAL OF CELL BIOLOGY
卷 218, 期 1, 页码 125-133出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.201804207
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- National Institutes of Health Office of Research Infrastructure Programs [P40 OD010440]
- Canadian Institutes of Health Research [123513]
- Natural Sciences and Engineering Research Council of Canada [312460-2012]
- National Institutes of Health [R01 NS093588]
Neuronal morphology and circuitry established during early development must often be maintained over the entirety of animal lifespans. Compared with neuronal development, the mechanisms that maintain mature neuronal structures and architecture are little understood. The conserved disco-interacting protein 2 (DIP2) consists of a DMAP1-binding domain and two adenylate-forming domains (AFDs). We show that the Caenorhabditis elegans DIP-2 maintains morphology of mature neurons. dip-2 loss-of-function mutants display a progressive increase in ectopic neurite sprouting and branching during late larval and adult life. In adults, dip-2 also inhibits initial stages of axon regeneration cell autonomously and acts in parallel to DLK-1 MAP kinase and EFA-6 pathways. The function of DIP-2 in maintenance of neuron morphology and in axon regrowth requires its AFD domains and is independent of its DMAP1-binding domain. Our findings reveal a new conserved regulator of neuronal morphology maintenance and axon regrowth after injury.
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