The carboxy-terminal fragment of TMEM59 promotes autophagy via interaction with ATG5-ATG16L1-LC3B proteins
Objective To investigate the induction of autophagy by transmembrane protein 59(TMEM59)and the site of autophagy induced by TMEM59,and to explore the related pathways of autophagy induced by TMEM59.Methods The ability of TMEM59 to induce autophagy and the site of autophagy induction were clarified using techniques such as cell transfection,Co-immunoprecipitation,immunofluorescence,etc.The related pathways of autophagy induced by TMEM59 were clarified through treatment with inhibitors of autophagy flux.Results Studies confirmed that overexpression of TMEM59 and the carboxy-terminal fragment(CTF)of TMEM59 in cells increased the level of autophagy marker protein microtubule-associated protein 1 light chain 3(LC3B)-Ⅱ and promoted the occurrence of autophagy flux,with statistically significant differences(P＜0.05).However,the difference in the overexpression of amino-terminal fragment(NTF)of TMEM59 was not statistically significant(P＞0.05).Overexpression of TMEM59 did not affect the increase in the level of LC3B-Ⅱ induced by the autophagy activator rapamycin,with no statistically significant difference(P＞0.05).But it promoted the increase in the level of LC3B-Ⅱ due to the inhibition of autolysosome fusion,with a statistically significant difference(P＜0.05).TMEM59 and TMEM59-CTF were confirmed to interact with the autophagy-associated gene protein(ATG)5,ATG16L1 and LC3B.Conclusion TMEM59-CTF can induce autophagy at a stage after the initiation of autophagy and before the formation of autolysosome,and interact with ATG5-ATG16L1-LC3B proteins to promote autophagy.
Transmembrane protein 59AutophagyAutophagy marker protein microtubule-associated protein 1 light chain 3Signaling pathway
万方数据
维普
