Key result
Disruption of the actin cytoskeleton by Cytochalasin D increased the lateral mobility of reggie-1/flotillin-2 (t1/2 = 11.1 s), while stabilization by Jasplakinolide decreased it (t1/2 = 20.2 s) compared to controls (16.2 s).
Absolute Event Rate: 11.1% vs 16.2%
p-value: p=<0.05
The study demonstrates that the lateral mobility of reggie-1/flotillin-2 microdomains is regulated by their interaction with the actin cytoskeleton.
Actin-flotillin regulation in animal cells leaves open any role in human cardiomyocyte membrane function or cardiovascular disease.
The reggies/flotillins are oligomeric scaffolding proteins for membrane microdomains. We show here that reggie-1/flotillin-2 microdomains are organized along cortical F-actin in several cell types. Interaction with F-actin is mediated by the SPFH domain as shown by in vivo co-localization and in vitro binding experiments. Reggie-1/flotillin-2 microdomains form independent of actin, but disruption or stabilization of the actin cytoskeleton modulate the lateral mobility of reggie-1/flotillin-2 as shown by FRAP. Furthermore, reggie/flotillin microdomains can efficiently be immobilized by actin polymerisation, while exchange of reggie-1/flotillin-2 molecules between microdomains is enhanced by actin disruption as shown by tracking of individual microdomains using TIRF microscopy.
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Langhorst et al. (2007) studied this question. Actin cytoskeleton disruption or stabilization (Cytochalasin D, Jasplakinolide) vs. Untreated control cells was evaluated on Lateral mobility of reggie-1/flotillin-2 (half time of fluorescence recovery, t1/2) (p=<0.05). Disruption of the actin cytoskeleton by Cytochalasin D increased the lateral mobility of reggie-1/flotillin-2 (t1/2 = 11.1 s), while stabilization by Jasplakinolide decreased it (t1/2 = 20.2 s) compared to controls (16.2 s).
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