Université de Paris, ITODYS, Paris, France.
Institute for Interdisciplinary Research, Jianghan University, Wuhan, China.
PLoS One. 2020 Aug 13;15(8):e0237110. doi: 10.1371/journal.pone.0237110. eCollection 2020.
Serine/threonine phosphatases are responsible for modulating the activities of the protein kinases implicated in the development of several pathologies. Here we identified by a PEP-scan approach a peptide of LRRK2, a Parkinson's disease associated protein, interacting with the phosphatase PP1. In order to study its biological activity, the peptide was fused via its N-terminal to an optimized cell penetrating peptide. We synthesized from the original peptide five interfering peptides and identified two (Mut3DPT-LRRK2-Short and Mut3DPT-LRRK2-Long) able to disrupt the LRRK2/PP1 interaction by competition in anti-LRRK2 immunoprecipitates. Using FITC-labelled peptides, we confirmed their internalization into cell lines as well as into primary cells obtained from healthy or ill human donors. We confirmed by ELISA test the association of Mut3DPT-LRRK2-Long peptide to purified PP1 protein. The peptides Mut3DPT-LRRK2-5 to 8 with either N or C-terminal deletions were not able to disrupt the association LRRK2/PP1 nor to associate with purified PP1 protein. The interfering sequences blocking the PP1/LRRK2 interaction were also fused to a shuttle peptide able to cross the blood brain barrier and showed that the newly generated peptides BBB-LRRK2-Short and BBB-LRRK2-Long were highly resistant to protease degradation. Furthermore, they blocked PP1/LRRK2 interaction and they penetrated into cells. Hence, these newly generated peptides can be employed as new tools in the investigation of the role of the LRRK2/PP1 interaction in normal and pathological conditions.
丝氨酸/苏氨酸磷酸酶负责调节几种病理发生中涉及的蛋白激酶的活性。在这里,我们通过 PEP 扫描方法鉴定了与帕金森病相关蛋白 LRRK2 相互作用的肽与磷酸酶 PP1。为了研究其生物学活性,该肽通过其 N 端融合到优化的穿透肽。我们从原始肽合成了五个干扰肽,并鉴定了两个(Mut3DPT-LRRK2-Short 和 Mut3DPT-LRRK2-Long)能够通过在抗 LRRK2 免疫沉淀物中竞争来破坏 LRRK2/PP1 相互作用。使用 FITC 标记的肽,我们证实它们能够进入细胞系以及从健康或患病的人类供体获得的原代细胞内化。我们通过 ELISA 测试证实了 Mut3DPT-LRRK2-Long 肽与纯化的 PP1 蛋白的结合。具有 N 或 C 末端缺失的肽 Mut3DPT-LRRK2-5 至 8 均不能破坏 LRRK2/PP1 的结合,也不能与纯化的 PP1 蛋白结合。阻断 PP1/LRRK2 相互作用的干扰序列也融合到一个能够穿过血脑屏障的穿梭肽上,并表明新生成的肽 BBB-LRRK2-Short 和 BBB-LRRK2-Long 对蛋白酶降解具有高度抗性。此外,它们阻断了 PP1/LRRK2 相互作用并穿透了细胞。因此,这些新生成的肽可作为研究 LRRK2/PP1 相互作用在正常和病理条件下的作用的新工具。