Atlastin-1 regulates morphology and function of endoplasmic reticulum in dendrites

Xianzhuang Liu, Xiangyang Guo, Liling Niu, Xixia Li, Fei Sun, Junjie Hu, Xiangming Wang () and Kang Shen ()
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Xianzhuang Liu: Institute of Biophysics, Chinese Academy of Sciences
Xiangyang Guo: Nankai University
Liling Niu: Nankai University
Xixia Li: Institute of Biophysics, Chinese Academy of Sciences
Fei Sun: Institute of Biophysics, Chinese Academy of Sciences
Junjie Hu: Institute of Biophysics, Chinese Academy of Sciences
Xiangming Wang: Institute of Biophysics, Chinese Academy of Sciences
Kang Shen: Institute of Biophysics, Chinese Academy of Sciences

Nature Communications, 2019, vol. 10, issue 1, 1-15

Abstract: Abstract Endoplasmic reticulum (ER) is characterized by interconnected tubules and sheets. Neuronal ER adopts specific morphology in axons, dendrites and soma. Here we study mechanisms underlying ER morphogenesis in a C. elegans sensory neuron PVD. In PVD soma and dendrite branch points, ER tubules connect to form networks. ER tubules fill primary dendrites but only extend to some but not all dendritic branches. We find that the Atlastin-1 ortholog, atln-1 is required for neuronal ER morphology. In atln-1 mutants with impaired GTPase activity, ER networks in soma and dendrite branch points are reduced and replaced by tubules, and ER tubules retracted from high-order dendritic branches, causing destabilized microtubule in these branches. The abnormal ER morphology likely causes defects in mitochondria fission at dendritic branch points. Mutant alleles of Atlastin-1 found in Hereditary Spastic Paraplegia (HSP) patients show similar ER phenotypes, suggesting that neuronal ER impairment contributes to HSP disease pathogenesis.

Date: 2019
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DOI: 10.1038/s41467-019-08478-6

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