Reggies/flotillins regulate cytoskeletal remodeling during neuronal differentiation via CAP/ponsin and Rho GTPases

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2008
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Langhorst, Matthias F.
Jaeger, Friederike A.
Mueller, Stephanie
Hartmann, L. Sven
Luxenhofer, Georg
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European Journal of Cell Biology ; 87 (2008), 12. - pp. 921-931. - ISSN 0171-9335. - eISSN 1618-1298
Abstract
The reggies/flotillins were discovered as proteins upregulated during axon regeneration. Here, we show that expression of a trans-negative reggie-1/flotillin-2 deletion mutant, R1EA, which interferes with oligomerization of the reggies/flotillins, inhibited insulin-like growth factor (IGF)-induced neurite outgrowth in N2a neuroblastoma cells and impaired in vitro differentiation of primary rat hippocampal neurons. Cells expressing R1EA formed only short and broad membrane protrusions often with abnormally large growth cones. R1EA expression strongly perturbed the balanced activation of the Rho-family GTPases Rac1 and cdc42. Furthermore, focal adhesion kinase (FAK) activity was also enhanced by R1EA expression, while other signaling pathways like ERK1/2, PKC or PKB signaling were unaffected. These severe signaling defects were caused by an impaired recruitment of the reggie/flotillin-associated adaptor molecule CAP/ponsin to focal contacts at the plasma membrane. Thus, the reggies/flotillins are crucial for coordinated assembly of signaling complexes regulating cytoskeletal remodeling.
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570 Biosciences, Biology
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ISO 690LANGHORST, Matthias F., Friederike A. JAEGER, Stephanie MUELLER, L. Sven HARTMANN, Georg LUXENHOFER, Claudia STÜRMER, 2008. Reggies/flotillins regulate cytoskeletal remodeling during neuronal differentiation via CAP/ponsin and Rho GTPases. In: European Journal of Cell Biology. 87(12), pp. 921-931. ISSN 0171-9335. eISSN 1618-1298. Available under: doi: 10.1016/j.ejcb.2008.07.001
BibTex
@article{Langhorst2008Reggi-1279,
  year={2008},
  doi={10.1016/j.ejcb.2008.07.001},
  title={Reggies/flotillins  regulate cytoskeletal remodeling during neuronal differentiation via CAP/ponsin and Rho GTPases},
  number={12},
  volume={87},
  issn={0171-9335},
  journal={European Journal of Cell Biology},
  pages={921--931},
  author={Langhorst, Matthias F. and Jaeger, Friederike A. and Mueller, Stephanie and Hartmann, L. Sven and Luxenhofer, Georg and Stürmer, Claudia}
}
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    <dcterms:abstract xml:lang="eng">The reggies/flotillins were discovered as proteins upregulated during axon regeneration. Here, we show that expression of a trans-negative reggie-1/flotillin-2  deletion mutant, R1EA, which interferes with oligomerization of the reggies/flotillins, inhibited insulin-like growth factor (IGF)-induced neurite outgrowth in N2a neuroblastoma cells and impaired in vitro differentiation of primary rat hippocampal neurons. Cells expressing R1EA formed only short and broad membrane protrusions often with abnormally large growth cones. R1EA expression strongly perturbed the balanced activation of the Rho-family GTPases Rac1 and cdc42. Furthermore, focal adhesion kinase (FAK) activity was also enhanced by R1EA expression, while other signaling pathways like ERK1/2, PKC  or PKB signaling were unaffected. These severe signaling defects were caused by an impaired recruitment of the reggie/flotillin-associated adaptor molecule CAP/ponsin to focal contacts at the plasma membrane. Thus, the reggies/flotillins are crucial for coordinated assembly of signaling complexes regulating cytoskeletal remodeling.</dcterms:abstract>
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