Reciprocal regulation of actin filaments and cellular metabolism

For cells to adhere, migrate and proliferate, remodeling of the actin cytoskeleton is required. This process consumes a large amount of ATP while having an intimate connection with cellular metabolism. Signaling pathways that regulate energy homeostasis can also affect actin dynamics, whereas a vari...

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Bibliographic Details
Published in:	European journal of cell biology Vol. 101; no. 4; p. 151281
Main Authors:	Liu, Geyao, Li, Jiayi, Wu, Congying
Format:	Journal Article
Language:	English
Published:	Germany Elsevier GmbH 01-09-2022 Elsevier
Subjects:	Actin Actin Cytoskeleton - metabolism Actins - metabolism Cancer Cytoskeleton - metabolism Glycolysis Metabolism Microfilament Proteins - metabolism Stress fiber Glycolysis Stress fiber Metabolism Actin Cancer
Online Access:	Get full text
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Summary:	For cells to adhere, migrate and proliferate, remodeling of the actin cytoskeleton is required. This process consumes a large amount of ATP while having an intimate connection with cellular metabolism. Signaling pathways that regulate energy homeostasis can also affect actin dynamics, whereas a variety of actin binding proteins directly or indirectly interact with the anabolic and catabolic regulators in cells. Here, we discuss the inter-regulation between actin filaments and cellular metabolism, reviewing recent discoveries on key metabolic enzymes that respond to actin remodeling as well as historical findings on metabolic stress-induced cytoskeletal reorganization. We also address emerging techniques that would benefit the study of cytoskeletal dynamics and cellular metabolism in high spatial-temporal resolution. •Cell motility and mechanics are intimately coupled to energy metabolism.•Cellular energetic states affect actin network through the AMPK and mTOR pathways.•Hippo-YAP pathway responds to mechanical cues and regulate F-actin and metabolism.•F-actin remodeling directly and indirectly impacts glucose and lipid metabolism.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	0171-9335 1618-1298
DOI:	10.1016/j.ejcb.2022.151281