SNX6 is an important molecular mechanism for long-range transport of synhapus post-stent proteins in synapses.

Membrane protrusions on the surface of neuron degeneratives in the central nervous system, known as destetic ratchets, are the primary receiving points for excitable neurotransmitter.
synactal rear stent protein located in the synapse ratchet is essential to maintain its structure and function.
because of the highly polarized structure of neurons, how stent proteins are transported to synapses that are synthesized by the cells is an important and interesting question in cell biology.
previous studies in HeLa skin cells by Liu Jiajia of the National Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, have shown that SNX6 is a cargo-mediated molecule for the dynein-u2012dynactin power protein complex.
it connects the power protein complex to the vesicle cargo binding to the retromer by acting directly with dynactin sub-base p150Glued and retromer sub-base SNX1, mediated reverse transport from the cytosome to the trans-gorki membrane (Hong et et al. Cell Research 2009, Niu et al. Nat Cell Biol 2013).
recently, Liu Jiajia's research team and The Shi Yun Group, a professor at Nanjing University, worked together to reveal the important biological function of SNX6 in transporting the synth post stent protein Homer1 b/c in excitable neurons.
they used behavioral tests to find that SNX6's gene knock-out in the central nervous system led to spatial learning memory impairment in mice.
Because spatial learning memory depends on the hippoc marker region of the cerebral cortical layer, they then analyzed the morphology and function of CA1 and CA3 neurons in the sponge region of Snx6-/- mice and found that the density of deducination at the far end of the top dextamination of CA1 neurons decreased, while the excitability synapses of CA1 neurons decreased and the mass membrane expression level of Glutamate-like subjectivity AMPAR decreased.
electrophysiological analysis found that the synapse transmission of AMPAR mediated was impaired.
they then found that SNX6 binds to the synaptic backstent protein Homer1b/c through the PX domain, while homer1b/c is reduced in the synaptic trunk and dexterity in the remote end of the Snx6-/- mouse CA1 neuron.
further studies have found that SNX6 mediates a combination of Homer1b/c vesicles and dynein'u2012dynactin, and that the absence of SNX6 leads to a decrease in home1c vesicles in the dendrine.
Because Homer1b/c is highly expressed in CA1 neurons and regulates the structure of dendracts and the internal swallowing transport of AMPAR, these results suggest that SNX6 regulates the formation/stabilization of tree synapses and their synapses by mediated long-range vesicle transport driven by dynein/u2012dynactin in the trunk.
the first time that an important molecular mechanism for long-range transport of synhapus post-synoptic stent proteins in synapses has been revealed.
study was published online January 30 in eLife in the form of a study entitled Ablation of SNX6 leads to defects in synaptic function of CA1al pyramid neurons and spatial memory.
Liu Jiajia Research Group Ph.D. student Niu Yang, assistant researcher Dai China and Nanjing University master's student Liu Literary are co-authors of the paper, Shi Yun and Liu Jiajia are co-authors of the paper.
the study was supported by the National Natural Science Foundation of China, the Ministry of Science and Technology and the Chinese Academy of Sciences.
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