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USP1(泛素特异性肽酶 1)靶向 ULK1 并调节其细胞区室化和自噬。

USP1 (ubiquitin specific peptidase 1) targets ULK1 and regulates its cellular compartmentalization and autophagy.

机构信息

a L.N.C.I.B. Laboratorio Nazionale Consorzio Interuniversitario Biotecnologie , AREA Science Park , Trieste , Italy.

b Department of Medicine , University of Udine , Udine , Italy.

出版信息

Autophagy. 2019 Apr;15(4):613-630. doi: 10.1080/15548627.2018.1535291. Epub 2018 Oct 29.

Abstract

ULK1 (unc-51 like autophagy activating kinase 1) is a core component at multiple steps of canonical macroautophagy/autophagy. The activity of ULK1 is tightly regulated by several post-translational modifications, including ubiquitination, yet the deubiquitinase (DUB) responsible for its reversible deubiquitination has not been described. Here, we identified USP1 (ubiquitin specific peptidase 1) as a key player in the modulation of ULK1 K63-linked deubiquitination. Moreover, both USP1 depletion and its chemical inhibition by pimozide are coupled to a reduction of ULK1 in Triton X-100 soluble cellular lysates, and its compartmentalization to a fraction that can be solubilized in 5 M urea. In USP1-depleted cells this fraction is also enriched in SQSTM1 (sequestosome 1), the aggresome marker HDAC6 (histone deacetylase 6), and the prototype of USP1 targets FANCD2 (FA complementation group D2). Consistently, in USP1-depleted and pimozide-treated cells, ULK1 forms protein aggregates enriched in SQSTM1, as detected by both immummunofluorescence and co-immunoprecipitation studies. Notably, depletion of USP1 inhibits canonical autophagic flux and promotes an alternative route leading to lysosomal-mediated degradation of SQSTM1. Our findings reveal a novel function of the USP1-ULK1 axis as a modulator of the switch between canonical and unconventional autophagy. Further, we provide the first evidence supporting the existence of a subset of breast tumors co-expressing ULK1 and MAP1LC3B (microtubule associated protein 1 light chain 3 beta) proteins. Because the USP1 inhibitor pimozide affects breast cancer cell growth, targeting USP1 in those tumors relying on autophagy for growth might prove to be a convenient therapeutic strategy. Abbreviations: ATG13: autophagy related 13; BECN1: beclin 1; BZ: bortezomib; CAPN1: calpain 1; DUB: deubiquitinase; FANCI: FA complementation group I; FANCD2: FA complementation group D2; FZR1: fizzy and cell division cycle 20 related 1; HDAC6: histone deacetylase 6; MAP1LC3B: microtubule associated protein 1 light chain 3 beta; PMZ: pimozide; SH3GLB1: SH3 domain containing GRB2 like, endophilin B1; SQSTM1: sequestosome 1; TRAF6: TNF receptor associated factor 6; ULK1: unc-51 like autophagy activating kinase 1; USP1: ubiquitin specific peptidase 1; WDR48: WD repeat domain 48.

摘要

ULK1(与自噬激活激酶 1 相似的 UNC-51 )是经典巨自噬/自噬的多个步骤中的核心成分。ULK1 的活性受到几种翻译后修饰的严格调节,包括泛素化,但负责其可逆去泛素化的去泛素酶(DUB)尚未被描述。在这里,我们确定 USP1(泛素特异性肽酶 1)是调节 ULK1 K63 连接去泛素化的关键因子。此外,USP1 的耗竭及其化学抑制剂匹莫齐都与 Triton X-100 可溶性细胞裂解物中 ULK1 的减少以及其向可溶于 5M 尿素的部分的区室化相关。在 USP1 耗竭的细胞中,该部分也富含 SQSTM1(自噬体 1)、聚集物标志物 HDAC6(组蛋白去乙酰化酶 6)和 USP1 靶标 FANCD2(FA 补体组 D2)的原型。一致地,在 USP1 耗竭和匹莫齐处理的细胞中,ULK1 形成富含 SQSTM1 的蛋白聚集体,这通过免疫荧光和共免疫沉淀研究都可以检测到。值得注意的是,USP1 的耗竭抑制了经典的自噬通量,并促进了导致 SQSTM1 溶酶体介导降解的替代途径。我们的发现揭示了 USP1-ULK1 轴作为调节经典和非经典自噬之间转换的调节剂的新功能。此外,我们提供了第一个证据,支持存在一组共同表达 ULK1 和 MAP1LC3B(微管相关蛋白 1 轻链 3β)蛋白的乳腺癌肿瘤。因为 USP1 抑制剂匹莫齐会影响乳腺癌细胞的生长,因此针对那些依赖自噬生长的肿瘤中的 USP1 可能是一种方便的治疗策略。缩写:ATG13:自噬相关 13;BECN1:自噬相关基因 13;BZ:硼替佐米;CAPN1:钙蛋白酶 1;DUB:去泛素化酶;FANCI:FA 补体组 I;FANCD2:FA 补体组 D2;FZR1:有活力和细胞分裂周期 20 相关 1;HDAC6:组蛋白去乙酰化酶 6;MAP1LC3B:微管相关蛋白 1 轻链 3β;PMZ:匹莫齐;SH3GLB1:SH3 结构域包含 GRB2 样内收蛋白 B1;SQSTM1:自噬体 1;TRAF6:肿瘤坏死因子受体相关因子 6;ULK1:与自噬激活激酶 1 相似的 UNC-51;USP1:泛素特异性肽酶 1;WDR48:WD 重复域 48。

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