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Neurite outgrowth of mature retinal ganglion cells and PC12 cells requires activity of CK1delta and CK1epsilon.

Authors: Bischof, J  Muller, A  Fander, M  Knippschild, U  Fischer, D 
Citation: Bischof J, etal., PLoS One. 2011;6(6):e20857. doi: 10.1371/journal.pone.0020857. Epub 2011 Jun 16.
Pubmed: (View Article at PubMed) PMID:21698236
DOI: Full-text: DOI:10.1371/journal.pone.0020857

Mature retinal ganglion cells (RGCs) do not normally regenerate severed axons after optic nerve injury and show only little neurite outgrowth in culture. However, RGCs can be transformed into an active regenerative state after lens injury (LI) enabling these neurons to regrow axons in vitro and in vivo. In the current study we investigated the role of CK1delta and CK1epsilon activity in neurite outgrowth of LI stimulated RGCs and nerve growth factor (NGF) stimulated PC12 cells, respectively. In both cell types CK1delta and epsilon were localized in granular particles aligned at microtubules in neurites and growth cones. Although LI treatment did not measurably affect the expression of CK1delta and epsilon, it significantly elevated the specific kinase activity in the retina. Similarly, CK1delta/epsilon specific kinase activity was also elevated in NGF treated PC12 cells compared with untreated controls. Neurite extension in PC12 cells was associated with a change in the activity of CK1delta C-terminal targeting kinases, suggesting that activity of these kinases might be necessary for neurite outgrowth. Pharmacological inactivation of CK1delta and epsilon markedly compromised neurite outgrowth of both, PC12 cells and LI stimulated RGCs in a concentration dependent manner. These data provide evidence for a so far unknown, but essential role of CK1 isoforms in neurite growth.

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CRRD Object Information
CRRD ID: 10059659
Created: 2015-08-24
Species: All species
Last Modified: 2015-08-24
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.