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bioRxiv
2025 ; ? (?): ? Nephropedia Template TP
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C elegans CED-1 acts in neurons to modulate ciliary protein abundance and
extracellular vesicle shedding
#MMPMID41341166
Ke T
; Tanis JE
bioRxiv
2025[Sep]; ? (?): ? PMID41341166
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The C. elegans receptor CED-1, along with orthologs mammalian MEGF10 and
Drosophila Draper, plays a well-established and conserved role in phagocytosis by
acting in engulfing cells. (1-7) Interestingly, CED-1 family members are also
expressed in neurons, but their functions in these non-engulfing cells remain
unclear. (6,8,9) Our study shows that CED-1 localizes to the dendrites and
primary cilia of male tail RnB neurons, which mediate sensory perceptions during
mating (10) and generate extracellular vesicles (EVs) that transfer bioactive
macromolecules for both intercellular and animal-to-animal communication. (11)
Loss of ced-1 leads to a reduction in the shedding of EVs that contain the
transient receptor potential (TRP) channel PKD-2 from the cilium distal tip, and
this is rescued by the expression of CED-1 in the neurons. CED-1 is required to
increase both the abundance of PKD-2 in the cilium and PKD-2 EV shedding in
response to the physiological stimulus of mating partners. Assessment of ced-1
mutant male mating indicates that neuronal CED-1 is also important for turning
behavior, which helps the male tail to maintain contact with a mate.
Collectively, these results reveal a new role for CED-1 in neurons as a regulator
of EV biogenesis in response to environmental cues, optimizing the shedding of
bioactive EVs for effective communication.