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Cofilin dysregulation alters actin turnover in frataxin-deficient neurons.

Abstract：

:Abnormalities in actin cytoskeleton have been linked to Friedreich's ataxia (FRDA), an inherited peripheral neuropathy characterised by an early loss of neurons in dorsal root ganglia (DRG) among other clinical symptoms. Despite all efforts to date, we still do not fully understand the molecular events that contribute to the lack of sensory neurons in FRDA. We studied the adult neuronal growth cone (GC) at the cellular and molecular level to decipher the connection between frataxin and actin cytoskeleton in DRG neurons of the well-characterised YG8R Friedreich's ataxia mouse model. Immunofluorescence studies in primary cultures of DRG from YG8R mice showed neurons with fewer and smaller GCs than controls, associated with an inhibition of neurite growth. In frataxin-deficient neurons, we also observed an increase in the filamentous (F)-actin/monomeric (G)-actin ratio (F/G-actin ratio) in axons and GCs linked to dysregulation of two crucial modulators of filamentous actin turnover, cofilin-1 and the actin-related protein (ARP) 2/3 complex. We show how the activation of cofilin is due to the increase in chronophin (CIN), a cofilin-activating phosphatase. Thus cofilin emerges, for the first time, as a link between frataxin deficiency and actin cytoskeleton alterations.

journal_name

Sci Rep

journal_title

Scientific reports

authors

Muñoz-Lasso DC,Mollá B,Calap-Quintana P,García-Giménez JL,Pallardo FV,Palau F,Gonzalez-Cabo P

doi

10.1038/s41598-020-62050-7

subject

Has Abstract

pub_date

2020-03-23 00:00:00

pages

5207

issue

1

issn

2045-2322

pii

10.1038/s41598-020-62050-7

journal_volume

10

pub_type

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