PDPK1调控选择性自噬受体SQSTM1识别IBDV的机制研究

细胞自噬能够降解细胞中众多底物。而自噬受体在自噬识别底物中发挥核心作用，决定了自噬的选择性。已经有多篇自噬受体识别病毒并促进其自噬降解的报道。但是，自噬受体通过何种机制识别到细胞中的病毒还是一个迷。本团队于2020年报道选择性自噬受体SQSTM1通过识别传染性法氏囊病病毒（IBDV）促进其自噬降解，近期我们通过二次沉淀联合质谱分析鉴定出了调控SQSTM1识别IBDV的关键蛋白，磷酸化激酶PDPK1，但是调控识别的具体机制有待进一步解析。因此，本研究将继续深入探索PDPK1调控SQSTM1识别IBDV的分子机制，解析选择性自噬降解胞内病毒过程中“识别”这一核心环节,为选择性自噬做为一种天然免疫提供重要理论补充。

Autophagy can degrade many substrates in cells. Autophagy receptors play a central role in autophagy recognition substrates and determine the selectivity of autophagy. There have been many reports on autophagy receptors that recognize viruses and promote their autophagic degradation. However, the mechanism by which autophagy receptors recognize viruses in cells is still a mystery. Our team reported in 2020 that the selective autophagy receptor SQSTM1 promotes its autophagy degradation by recognizing infectious bursal disease virus (IBDV). Recently, we have identified the key phosphorylation kinase, PDPK1, that regulates SQSTM1 recognition of IBDV through secondary precipitation combined with mass spectrometry analysis, but the specific mechanism of regulating recognition needs further analysis. Therefore, this study will continue to explore in depth the molecular mechanism of PDPK1 regulating SQSTM1 to recognize IBDV, analyze the core link of "recognition" in the process of selective autophagy degradation of intracellular viruses, and provide an important supplement theory for selective autophagy as a kind of natural immunity.