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Dynamic change of mitochondrial morphology and distribution along neuronal branches are essential for neural circuitry formation and synaptic efficacy. However, the underlying mechanism remains elusive. We show here that  Pink1  knockout (KO) mice display defective dendritic spine maturation, reduced axonal synaptic vesicles, abnormal synaptic connection, and attenuated long-term synaptic potentiation (LTP). Drp1 activation via S616 phosphorylation rescues deficits of spine maturation in  Pink1  KO neurons. Notably, mice harboring a knockin (KI) phosphor-null  Drp1   S616A   recapitulate spine immaturity and synaptic abnormality identified in  Pink1  KO mice. Chemical LTP (cLTP) induces Drp1 S616  phosphorylation in a PINK1-dependent manner. Moreover, phosphor-mimetic Drp1 S616D  restores reduced dendritic spine localization of mitochondria in  Pink1  KO neurons. Together, this study provides the first in vivo evidence of functional regulation of Drp1 by phosphorylation and suggests that PINK1-Drp1 S616  phosphorylation coupling is essential for convergence between mitochondrial dynamics and neural circuitry formation and refinement.

PINK1-mediated Drp1S616 phosphorylation modulates synaptic development and plasticity via promoting mitochondrial fission