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The Multifaceted Interactions of Dictyostelium Atg1 with Mitochondrial Function, Endocytosis, Growth, and Development.

Authors :
Sen, Melodi Gizem
Sanislav, Oana
Fisher, Paul Robert
Annesley, Sarah Jane
Source :
Cells (2073-4409); Jul2024, Vol. 13 Issue 14, p1191, 32p
Publication Year :
2024

Abstract

Autophagy is a degradative recycling process central to the maintenance of homeostasis in all eukaryotes. By ensuring the degradation of damaged mitochondria, it plays a key role in maintaining mitochondrial health and function. Of the highly conserved autophagy proteins, autophagy-related protein 1 (Atg1) is essential to the process. The involvement of these proteins in intracellular signalling pathways, including those involving mitochondrial function, are still being elucidated. Here the role of Atg1 was investigated in the simple model organism Dictyostelium discoideum using an atg1 null mutant and mutants overexpressing or antisense-inhibiting atg1. When evaluated against the well-characterised outcomes of mitochondrial dysfunction in this model, altered atg1 expression resulted in an unconventional set of phenotypic outcomes in growth, endocytosis, multicellular development, and mitochondrial homeostasis. The findings here show that Atg1 is involved in a tightly regulated signal transduction pathway coordinating energy-consuming processes such as cell growth and multicellular development, along with nutrient status and energy production. Furthermore, Atg1's effects on energy homeostasis indicate a peripheral ancillary role in the mitochondrial signalling network, with effects on energy balance rather than direct effects on electron transport chain function. Further research is required to tease out these complex networks. Nevertheless, this study adds further evidence to the theory that autophagy and mitochondrial signalling are not opposing but rather linked, yet strictly controlled, homeostatic mechanisms. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
20734409
Volume :
13
Issue :
14
Database :
Complementary Index
Journal :
Cells (2073-4409)
Publication Type :
Academic Journal
Accession number :
178692004
Full Text :
https://doi.org/10.3390/cells13141191