RT Journal Article
SR Electronic
T1 The Amyloid Precursor-like Protein APL-1 Regulates Axon Regeneration
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 305284
DO 10.1101/305284
A1 Lewie Zeng
A1 Rachid El Bejjani
A1 Marc Hammarlund
YR 2018
UL http://biorxiv.org/content/early/2018/04/20/305284.abstract
AB Members of the Amyloid Precursor Protein (APP) family have important functions during neuronal development. However, their physiological functions in the mature nervous system are not fully understood. Here we use the C. elegans GABAergic motor neurons to study the post-developmental function of the APP-like protein APL-1 in vivo. We find that apl-1 has minimum roles in the maintenance of gross neuron morphology and function. However, we show that apl-1 is an inhibitor of axon regeneration, acting on mature neurons to limit regrowth in response to injury. The small GTPase Rab6/RAB-6.2 also inhibits regeneration, and does so in part by maintaining protein levels of APL-1. To inhibit regeneration, APL-1 functions via the E2 domain of its ectodomain; the cytoplasmic tail, transmembrane anchoring, and the E1 domain are not required for this function. Our data defines a novel role for APL-1 in modulating the neuronal response to injury.