Previous studies have confirmed that the beclin 1 complex plays a key role in the initial stage of autophagy and deregulated autophagy might involve in amyotrophic lateral sclerosis.However,the mechanism underlying altered autophagy associated with the beclin 1 complex remains unclear.In this study,we transfected the Cu/Zn superoxide dismutase 1 G93A mutant protein into the motor neuron-like cell line NSC34 cultured in vitro.Western blotting and co-immunoprecipitation showed that the Cu/Zn superoxide dismutase 1 G93A mutant enhanced the turnover of autophagic marker microtubule-associated protein light chain 3II(LC3II)and stimulated the conversion of EGFP-LC3I to EGFP-LC3II,but had little influence on the binding capacity of the autophagy modulators ATG14L,rubicon,UVRAG,and hVps34 to beclin 1 during autophagosome formation.These results suggest that the amyotrophic lateral sclerosis-linked Cu/Zn superoxide dismutase 1 G93A mutant can upregulate autophagic activity in NSC34 cells,but that this does not markedly affect beclin 1 complex components.
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