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MICAL-like Regulates Fasciclin II Membrane Cycling and Synaptic Development

  • Nahm, Minyeop (Department of Brain and Cognitive Sciences, College of Natural Sciences) ;
  • Park, Sunyoung (Interdisciplinary Graduate Program in Brain Science, College of Natural Sciences, Seoul National University) ;
  • Lee, Jihye (Department of Oral Pathology and BK21 PLUS Project, School of Dentistry and Institute of Translational Dental Sciences, Pusan National University) ;
  • Lee, Seungbok (Department of Brain and Cognitive Sciences, College of Natural Sciences)
  • Received : 2016.08.24
  • Accepted : 2016.09.12
  • Published : 2016.10.31

Abstract

Fasciclin II (FasII), the Drosophila ortholog of neural cell adhesion molecule (NCAM), plays a critical role in synaptic stabilization and plasticity. Although this molecule undergoes constitutive cycling at the synaptic membrane, how its membrane trafficking is regulated to ensure proper synaptic development remains poorly understood. In a genetic screen, we recovered a mutation in Drosophila mical-like that displays an increase in bouton numbers and a decrease in FasII levels at the neuromuscular junction (NMJ). Similar phenotypes were induced by presynaptic, but not postsynaptic, knockdown of mical-like expression. FasII trafficking assays revealed that the recycling of internalized FasII molecules to the cell surface was significantly impaired in mical-like-knockdown cells. Importantly, this defect correlated with an enhancement of endosomal sorting of FasII to the lysosomal degradation pathway. Similarly, synaptic vesicle exocytosis was also impaired in mical-like mutants. Together, our results identify Mical-like as a novel regulator of synaptic growth and FasII endocytic recycling.

Keywords

References

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