A selective role for a component of the autophagy pathway in coupling the Golgi apparatus to dendrite polarity in pyramidal neurons.

Pyramidal neurons have a characteristic morphology that is critical to their ability to integrate into functional neural circuits. In addition to axon dendrite polarity, pyramidal neurons also exhibit dendritic polarity such that apical and basolateral dendrites differ in size, structure and inputs. Dendrite polarity in pyramidal neurons coincides with polarity of the Golgi apparatus, a key feature relevant to directed secretory trafficking, both in vitro and in vivo. We identify a novel autophagy based mechanism that uncouples the polarity of the Golgi apparatus from dendrite polarity. Autophagy is a universal cellular pathway that promotes cellular homeostasis via degradation of cellular components. Our data indicate that knockdown of ATG7, a key component of the autophagy mechanism, disrupts the polarity of the Golgi apparatus without impacting dendritic polarity in primary pyramidal neurons, providing the first evidence that dendrite polarity can be uncoupled from Golgi polarity. Interestingly, these effects are restricted to ATG7 knockdown and are not replicated by the knockdown of ATG16L1, another component of the autophagy mechanism. We propose that cellular mechanisms exist to couple Golgi polarity to dendrite polarity. Components of the autophagy mechanism are leveraged to actively couple Golgi polarity to dendrite polarity, thus impacting secretory trafficking into individual dendrites in pyramidal neurons.