Should it stay or should it go: gap junction protein GJA1/Cx43 conveys damaged lysosomes to the cell periphery to potentiate exocytosis.

Autophagy 2024 1 cites
2024:02025:02026:1
2024 2026
1

Domingues N, Ribeiro-Rodrigues T, Girão H

Abstract

  1. Autophagy. 2024 Dec;20(12):2816-2818. doi: 10.1080/15548627.2024.2408711. Epub 2024 Oct 21.

Should it stay or should it go: gap junction protein GJA1/Cx43 conveys damaged lysosomes to the cell periphery to potentiate exocytosis.

Domingues N(1)(2)(3)(4)(5), Ribeiro-Rodrigues T(1)(2)(3)(4), Girão H(1)(2)(3)(4).

Author information: (1)Coimbra Institute for Clinical and Biomedical Research (iCBR), Faculty of Medicine, University Coimbra, Coimbra, Portugal. (2)Faculty of Medicine, University Coimbra, Coimbra, Portugal. (3)Centre for Innovative Biomedicine and Biotechnology (CIBB), University Coimbra, Coimbra, Portugal. (4)Clinical and Academic Centre of Coimbra, Coimbra, Portugal. (5)Multidisciplinary Institute of Ageing, University of Coimbra, Coimbra, Portugal.

GJA1/Cx43 (gap junction protein alpha 1) has long been associated with gap junctions-mediated communication between adjacent cells. However, recent data have defied this concept, with studies implicating GJA1 in other biological processes, such as macroautophagy/autophagy regulation, mitochondrial activity and extracellular vesicles biology. In our recent study we unveiled an additional role played by GJA1 in lysosomal trafficking. We demonstrate that GJA1 promotes the exocytosis of damaged lysosomes, through a mechanism that relies on ACTR2/ARP2-ACTR3/ARP3-dependent actin remodeling. Our findings ascribe to GJA1 an important role during pathogen infection and lysosomal storage disorders, favoring the release of dysfunctional lysosomes.

DOI: 10.1080/15548627.2024.2408711 PMCID: PMC11587831 PMID: 39394955 [Indexed for MEDLINE]

Conflict of interest statement: No potential conflict of interest was reported by the author(s).

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