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Article

Functional Redundancy of Cyclase-Associated Proteins CAP1 and CAP2 in Differentiating Neurons

1
Molecular Neurobiology Group, Institute of Physiological Chemistry, University of Marburg, 35032 Marburg, Germany
2
Center for Mind, Brain and Behavior (CMBB), University of Marburg, Justus-Liebig-University Giessen, Hans-Meerwein-Strasse 6, 35032 Marburg, Germany
3
DFG Research Training Group, Membrane Plasticity in Tissue Development and Remodeling, GRK 2213, University of Marburg, 35032 Marburg, Germany
*
Author to whom correspondence should be addressed.
Academic Editor: Karl-Wilhelm Koch
Cells 2021, 10(6), 1525; https://doi.org/10.3390/cells10061525
Received: 14 May 2021 / Revised: 11 June 2021 / Accepted: 14 June 2021 / Published: 17 June 2021
(This article belongs to the Special Issue Molecular Mechanisms of Neuronal Actin Cytoskeleton Dynamics)
Cyclase-associated proteins (CAPs) are evolutionary-conserved actin-binding proteins with crucial functions in regulating actin dynamics, the spatiotemporally controlled assembly and disassembly of actin filaments (F-actin). Mammals possess two family members (CAP1 and CAP2) with different expression patterns. Unlike most other tissues, both CAPs are expressed in the brain and present in hippocampal neurons. We recently reported crucial roles for CAP1 in growth cone function, neuron differentiation, and neuron connectivity in the mouse brain. Instead, CAP2 controls dendritic spine morphology and synaptic plasticity, and its dysregulation contributes to Alzheimer’s disease pathology. These findings are in line with a model in which CAP1 controls important aspects during neuron differentiation, while CAP2 is relevant in differentiated neurons. We here report CAP2 expression during neuron differentiation and its enrichment in growth cones. We therefore hypothesized that CAP2 is relevant not only in excitatory synapses, but also in differentiating neurons. However, CAP2 inactivation neither impaired growth cone morphology and motility nor neuron differentiation. Moreover, CAP2 mutant mice did not display any obvious changes in brain anatomy. Hence, differently from CAP1, CAP2 was dispensable for neuron differentiation and brain development. Interestingly, overexpression of CAP2 rescued not only growth cone size in CAP1-deficient neurons, but also their morphology and differentiation. Our data provide evidence for functional redundancy of CAP1 and CAP2 in differentiating neurons, and they suggest compensatory mechanisms in single mutant neurons. View Full-Text
Keywords: cyclase-associated protein; CAP2; CAP1; SRV2; growth cone; actin dynamics; F-actin cyclase-associated protein; CAP2; CAP1; SRV2; growth cone; actin dynamics; F-actin
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MDPI and ACS Style

Schneider, F.; Metz, I.; Khudayberdiev, S.; Rust, M.B. Functional Redundancy of Cyclase-Associated Proteins CAP1 and CAP2 in Differentiating Neurons. Cells 2021, 10, 1525. https://doi.org/10.3390/cells10061525

AMA Style

Schneider F, Metz I, Khudayberdiev S, Rust MB. Functional Redundancy of Cyclase-Associated Proteins CAP1 and CAP2 in Differentiating Neurons. Cells. 2021; 10(6):1525. https://doi.org/10.3390/cells10061525

Chicago/Turabian Style

Schneider, Felix, Isabell Metz, Sharof Khudayberdiev, and Marco B. Rust. 2021. "Functional Redundancy of Cyclase-Associated Proteins CAP1 and CAP2 in Differentiating Neurons" Cells 10, no. 6: 1525. https://doi.org/10.3390/cells10061525

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