Einzeltreffer — DigiBib

The organelle contact site of the endoplasmic reticulum and mitochondria, known as the mitochondria-associated membrane (MAM), is a multifunctional microdomain in cellular homeostasis. We previously reported that MAM disruption is a common pathological feature in amyotrophic lateral sclerosis (ALS); however, the precise role of MAM in ALS was uncovered. Here, we show that the MAM is essential for TANK-binding kinase 1 (TBK1) activation under proteostatic stress conditions. A MAM-specific E3 ubiquitin ligase, autocrine motility factor receptor, ubiquitinated nascent proteins to activate TBK1 at the MAM, which results in ribosomal protein degradation. MAM or TBK1 deficiency under proteostatic stress conditions resulted in increased cellular vulnerability in vitro and motor impairment in vivo. Thus, MAM disruption exacerbates proteostatic stress via TBK1 inactivation in ALS. Our study has revealed a proteostatic mechanism mediated by the MAM-TBK1 axis, highlighting the physiological importance of the organelle contact sites.

Titel:	Mitochondria-associated membrane collapse impairs TBK1-mediated proteostatic stress response in ALS.
Autor/in / Beteiligte Person:	Watanabe, S ; Murata, Y ; Oka, Y ; Oiwa, K ; Horiuchi, M ; Iguchi, Y ; Komine, O ; Sobue, A ; Katsuno, M ; Ogi, T ; Yamanaka, K
Link:	Zum Volltext
Zeitschrift:	Proceedings of the National Academy of Sciences of the United States of America, Jg. 120 (2023-11-21), Heft 47, S. e2315347120
Veröffentlichung:	Washington, DC : National Academy of Sciences, 2023
Medientyp:	academicJournal
ISSN:	1091-6490 (electronic)
DOI:	10.1073/pnas.2315347120
Schlagwort:	Humans Mitochondria metabolism Mitochondrial Membranes metabolism Endoplasmic Reticulum metabolism Protein Serine-Threonine Kinases genetics Protein Serine-Threonine Kinases metabolism Amyotrophic Lateral Sclerosis metabolism
Sonstiges:	Nachgewiesen in: MEDLINE Sprachen: English Publication Type: Journal Article Language: English [Proc Natl Acad Sci U S A] 2023 Nov 21; Vol. 120 (47), pp. e2315347120. <i>Date of Electronic Publication: </i>2023 Nov 15. MeSH Terms: Amyotrophic Lateral Sclerosis* / metabolism ; Humans ; Mitochondria / metabolism ; Mitochondrial Membranes / metabolism ; Endoplasmic Reticulum / metabolism ; Protein Serine-Threonine Kinases / genetics ; Protein Serine-Threonine Kinases / metabolism References: Trends Endocrinol Metab. 2017 Jan;28(1):32-45. (PMID: 27670636) ; Trends Mol Med. 2016 Jun;22(6):511-527. (PMID: 27211305) ; Trends Neurosci. 2016 Mar;39(3):146-157. (PMID: 26899735) ; Autophagy. 2019 Sep;15(9):1539-1557. (PMID: 30871407) ; Sci Adv. 2018 Nov 21;4(11):eaav0443. (PMID: 30627666) ; FASEB J. 2017 Mar;31(3):864-867. (PMID: 28246299) ; Genes Dev. 2008 Jun 1;22(11):1451-64. (PMID: 18519638) ; Biochim Biophys Acta. 2014 Apr 4;1841(4):595-609. 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(PMID: 36736924) Grant Information: 17H04986 23K06826 Ministry of Education, Culture, Sports, Science and Technology (MEXT); 18H02740 18H04860 19KK0214 22H00467 Ministry of Education, Culture, Sports, Science and Technology (MEXT); JP21ek0109426 JP23wm0425014 Japan Agency for Medical Research and Development (AMED); Uehara Memorial Foundation (UMF); Public Foundation of Chubu Science and Technology Center (CSTC) Contributed Indexing: Keywords: TANK-binding kinase 1; amyotrophic lateral sclerosis; mitochondria-associated membrane; sigma-1 receptor; stress granules Substance Nomenclature: EC 2.7.11.1 (TBK1 protein, human) ; EC 2.7.11.1 (Protein Serine-Threonine Kinases) Entry Date(s): Date Created: 20231115 Date Completed: 20231117 Latest Revision: 20231125 Update Code: 20231215 PubMed Central ID: PMC10666035

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Mitochondria-associated membrane collapse impairs TBK1-mediated proteostatic stress response in ALS.