Neuronal Autophagy Regulates Presynaptic Neurotransmission by Controlling the Axonal Endoplasmic Reticulum

This is the authors' abstract. We don't add key points for this paper.

(Neuron 109, 299–313.e1–e9; January 20, 2021) The authors noticed two inadvertent errors in their publication. In Figure 6G, the DAPI channels of the wild-type and knockout brain slices were erroneously swapped. In Figure S5A, an incorrect representative immunoblot for calnexin was shown that originated from a different experiment. The corrected Figures 6G and S5A are shown below. These corrections do not affect the analysis of data or statements in the text and do not affect the conclusion of this paper. The authors sincerely apologize for both errors.Figure S5ALoss of ATG5 does not affect mitochondrial acidification, axonal lipid levels or ER integrityView Large Image Figure ViewerDownload Hi-res image Download (PPT) Neuronal Autophagy Regulates Presynaptic Neurotransmission by Controlling the Axonal Endoplasmic ReticulumKuijpers et al.NeuronNovember 5, 2020In BriefAutophagy is crucial for nervous system function. However, its physiological substrates are largely unknown. Kuijpers et al. demonstrate, using knockout mice conditionally lacking the essential autophagy protein ATG5 and quantitative proteomics paired with electrophysiology and functional imaging experiments, that neuronal autophagy regulates presynaptic neurotransmission by controlling the axonal endoplasmic reticulum.