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Free Radic Biol Med. 2018 Feb 20;116:101-113. doi: 10.1016/j.freeradbiomed.2018.01.008. Epub 2018 Jan 10.

Crosstalk between Rac1-mediated actin regulation and ROS production.

Author information

1
FONDAP Geroscience Center for Brain Health and Metabolism, Santiago, Chile. Electronic address: a.acevedo.aracena@gmail.com.
2
FONDAP Geroscience Center for Brain Health and Metabolism, Santiago, Chile; Department of Biology, Faculty of Sciences, Universidad de Chile, 7800024, Chile; The Buck Institute for Research on Aging, Novato, USA. Electronic address: chrgonza@uchile.cl.

Abstract

The small RhoGTPase Rac1 is implicated in a variety of events related to actin cytoskeleton rearrangement. Remarkably, another event that is completely different from those related to actin regulation has the same relevance; the Rac1-mediated production of reactive oxygen species (ROS) through NADPH oxidases (NOX). Each outcome involves different Rac1 downstream effectors; on one hand, events related to the actin cytoskeleton require Rac1 to bind to WAVEs proteins and PAKs that ultimately promote actin branching and turnover, on the other, NOX-derived ROS production demands active Rac1 to be bound to a cytosolic activator of NOX. How Rac1-mediated signaling ends up promoting actin-related events, NOX-derived ROS, or both is poorly understood. Rac1 regulators, including scaffold proteins, are known to exert tight control over its functions. Hence, evidence of Rac1 regulatory events leading to both actin remodeling and NOX-mediated ROS generation are discussed. Moreover, cellular functions linked to physiological and pathological conditions that exhibit crosstalk between Rac1 outcomes are analyzed, while plausible roles in neuronal functions (and dysfunctions) are highlighted. Together, discussed evidence shed light on cellular mechanisms which requires Rac1 to direct either actin- and/or ROS-related events, helping to understand crucial roles of Rac1 dual functionality.

KEYWORDS:

Actin cytoskeleton regulation; NADPH oxidases; Neurodegeneration; Polarity; ROS and actin crosstalk; Rac1; Reactive oxygen species (ROS); Redox signaling; Scaffolding proteins

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