Retrograde Ret signaling controls sensory pioneer axon outgrowth

Author:

Tuttle Adam1ORCID,Drerup Catherine M1ORCID,Marra Molly12,McGraw Hillary1,Nechiporuk Alex V1ORCID

Affiliation:

1. Department of Cell, Developmental, and Cancer Biology, Oregon Health & Science University, Portland, United States

2. Neuroscience Graduate Program, Oregon Health & Science University, Portland, United States

Abstract

The trafficking mechanisms and transcriptional targets downstream of long-range neurotrophic factor ligand/receptor signaling that promote axon growth are incompletely understood. Zebrafish carrying a null mutation in a neurotrophic factor receptor, Ret, displayed defects in peripheral sensory axon growth cone morphology and dynamics. Ret receptor was highly enriched in sensory pioneer neurons and Ret51 isoform was required for pioneer axon outgrowth. Loss-of-function of a cargo adaptor, Jip3, partially phenocopied Ret axonal defects, led to accumulation of activated Ret in pioneer growth cones, and reduced retrograde Ret51 transport. Jip3 and Ret51 were also retrogradely co-transported, ultimately suggesting Jip3 is a retrograde adapter of active Ret51. Finally, loss of Ret reduced transcription and growth cone localization of Myosin-X, an initiator of filopodial formation. These results show a specific role for Ret51 in pioneer axon growth, and suggest a critical role for long-range retrograde Ret signaling in regulating growth cone dynamics through downstream transcriptional changes.

Funder

Eunice Kennedy Shriver National Institute of Child Health and Human Development

National Institute of Neurological Disorders and Stroke

Publisher

eLife Sciences Publications, Ltd

Subject

General Immunology and Microbiology,General Biochemistry, Genetics and Molecular Biology,General Medicine,General Neuroscience

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