Journal
HISTOCHEMISTRY AND CELL BIOLOGY
Volume 138, Issue 5, Pages 737-748Publisher
SPRINGER
DOI: 10.1007/s00418-012-0989-1
Keywords
Local translation; mRNA transport; Motoneuron; Laminin; Actin; Spinal muscular atrophy
Categories
Funding
- Deutsche Forschungsgemeinschaft SFB581 [B1, B24]
- Hermann und Lilly Schilling Stiftung im Stifterverband der Deutschen Wissenschaft
Ask authors/readers for more resources
Reduced levels of the SMN (survival of motoneuron) protein cause spinal muscular atrophy, the main form of motoneuron disease in children and young adults. In cultured motoneurons, reduced SMN levels lead to disturbed axon growth that correlates with reduced actin mRNA and protein in growth cones, indicating that anterograde transport and local translation of beta-actin mRNA are altered in this disease. However, it is not fully understood how local translation of the beta-actin mRNA is regulated in SMN-deficient motoneurons. Here, we established a lentiviral GFP-based reporter construct to monitor local translation of beta-actin mRNA. Time-lapse imaging of fluorescence recovery after photobleaching (FRAP) in living motoneurons revealed that beta-actin is locally translated in the growth cones of embryonic motoneurons. Interestingly, local translation of the beta-actin reporter construct was differentially regulated by various Laminin isoforms, indicating that Laminins provide extracellular cues for the regulation of local translation in growth cones. Notably, local translation of beta-actin mRNA was deregulated in motoneurons from a mouse model for the most severe form of SMA (Smn (-/-) ;SMN2). Taken together our findings suggest that local translation of beta-actin in growth cones of motoneurons is regulated by Laminin signalling and that this signalling is disturbed in SMA.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available