eprintid: 10050665 rev_number: 26 eprint_status: archive userid: 608 dir: disk0/10/05/06/65 datestamp: 2018-06-21 13:56:52 lastmod: 2021-09-18 21:50:35 status_changed: 2018-06-21 13:56:52 type: article metadata_visibility: show creators_name: Soutar, MPM creators_name: Kempthorne, L creators_name: Miyakawa, S creators_name: Annuario, E creators_name: Melandri, D creators_name: Harley, J creators_name: O'Sullivan, GA creators_name: Wray, S creators_name: Hancock, DC creators_name: Cookson, MR creators_name: Downward, J creators_name: Carlton, M creators_name: Plun-Favreau, H title: AKT signalling selectively regulates PINK1 mitophagy in SHSY5Y cells and human iPSC-derived neurons ispublished: pub divisions: UCL divisions: B02 divisions: C07 divisions: D07 divisions: F86 divisions: C08 divisions: D09 note: This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ abstract: The discovery of mutations within genes associated with autosomal recessive Parkinson's disease allowed for the identification of PINK1/Parkin regulated mitophagy as an important pathway for the removal of damaged mitochondria. While recent studies suggest that AKT-dependent signalling regulates Parkin recruitment to depolarised mitochondria, little is known as to whether this can also regulate PINK1 mitochondrial accumulation and downstream mitophagy. Here, we demonstrate that inhibition of AKT signalling decreases endogenous PINK1 accumulation in response to mitochondria depolarisation, subsequent Parkin recruitment, phosphorylation of ubiquitin, and ultimately mitophagy. Conversely, we show that upon stimulation of AKT signalling via insulin, the mitophagy pathway is increased in SHSY5Y cells. These data suggest that AKT signalling is an upstream regulator of PINK1 accumulation on damaged mitochondria. Importantly, we show that the AKT pathway also regulates endogenous PINK1-dependent mitophagy in human iPSC-derived neurons. date: 2018-06-11 date_type: published official_url: https://doi.org/10.1038/s41598-018-26949-6 oa_status: green full_text_type: pub language: eng primo: open primo_central: open_green article_type_text: Journal Article verified: verified_manual elements_id: 1561905 doi: 10.1038/s41598-018-26949-6 pii: 10.1038/s41598-018-26949-6 lyricists_name: Melandri, Daniela lyricists_name: Plun-Favreau, Helene lyricists_name: Soutar, Marc lyricists_name: Wray, Selina lyricists_id: DMELA56 lyricists_id: HPLUN15 lyricists_id: MSOUT43 lyricists_id: SWRAY93 actors_name: Plun-Favreau, Helene actors_id: HPLUN15 actors_role: owner full_text_status: public publication: Science Reports volume: 8 number: 1 article_number: 8855 event_location: England issn: 2045-2322 citation: Soutar, MPM; Kempthorne, L; Miyakawa, S; Annuario, E; Melandri, D; Harley, J; O'Sullivan, GA; ... Plun-Favreau, H; + view all <#> Soutar, MPM; Kempthorne, L; Miyakawa, S; Annuario, E; Melandri, D; Harley, J; O'Sullivan, GA; Wray, S; Hancock, DC; Cookson, MR; Downward, J; Carlton, M; Plun-Favreau, H; - view fewer <#> (2018) AKT signalling selectively regulates PINK1 mitophagy in SHSY5Y cells and human iPSC-derived neurons. Science Reports , 8 (1) , Article 8855. 10.1038/s41598-018-26949-6 <https://doi.org/10.1038/s41598-018-26949-6>. Green open access document_url: https://discovery.ucl.ac.uk/id/eprint/10050665/1/s41598-018-26949-6.pdf