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SLC35D3 increases autophagic activity in midbrain dopaminergic neurons by enhancing BECN1-ATG14-PIK3C3 complex formation

By Z.B. Wei, Y.F. Yuan, F. Jaouen, M.S. MA, C.J. Hao, Zhongkai Zhang, Q. Chen, Z. Yuan, C. Beurrier and W. Li


International audienceSearching for new regulators of autophagy involved in selective dopaminergic (DA) neuron loss is a hallmark in the pathogenesis of Parkinson disease (PD). We here report that an endoplasmic reticulum (ER)-associated transmembrane protein SLC35D3 is selectively expressed in subsets of midbrain DA neurons in about 10% TH (tyrosine hydroxylase)-positive neurons in the substantia nigra pars compacta (SNc) and in about 22% TH-positive neurons in the ventral tegmental area (VTA). Loss of SLC35D3 in ros (roswell mutant) mice showed a reduction of 11.9% DA neurons in the SNc and 15.5% DA neuron loss in the VTA with impaired autophagy. We determined that SLC35D3 enhanced the formation of the BECN1-ATG14-PIK3C3 complex to induce autophagy. These results suggest that SLC35D3 is a new regulator of tissue-specific autophagy and plays an important role in the increased autophagic activity required for the survival of subsets of DA neurons

Topics: BECN1-ATG14-PIK3C3 complex, Parkinson disease, SLC35D3, autophagy, dopaminergic neuron, neurodegeneration, [SDV.BC]Life Sciences [q-bio]/Cellular Biology
Publisher: 'Informa UK Limited'
Year: 2016
DOI identifier: 10.1080/15548627.2016.1179402.
OAI identifier: oai:HAL:hal-01445052v1
Provided by: HAL AMU
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