PUBLICATION

Lipids, Rafts and Traffic: Chapter 11 - The 'lipid raft' microdomain proteins reggie-1 and reggie-2 (flotillins) are scaffolds for protein interaction and signalling

Authors
Stürmer, C.A., and Plattner, H.
ID
ZDB-PUB-050119-5
Date
2005
Source
Biochemical Society symposium   72: 109-118 (Journal)
Registered Authors
Stuermer, Claudia
Keywords
none
MeSH Terms
  • Animals
  • Drosophila
  • Humans
  • Membrane Microdomains/chemistry
  • Membrane Microdomains/metabolism*
  • Membrane Proteins/chemistry
  • Membrane Proteins/genetics
  • Membrane Proteins/metabolism*
  • Models, Biological
  • Multiprotein Complexes
  • PrPC Proteins/metabolism
  • RNA, Small Interfering/genetics
  • Signal Transduction
  • T-Lymphocytes/metabolism
  • Zebrafish
PubMed
15649135 Full text @ Biochem. Soc. Symp.
Abstract
Reggie-1 and reggie-2 are two evolutionarily highly conserved proteins which are up-regulated in retinal ganglion cells during regeneration of lesioned axons in the goldfish optic nerve. They are located at the cytoplasmic face of the plasma membrane and are considered to be 'lipid raft' constituents due to their insolubility in Triton X-100 and presence in the 'floating fractions'; hence they were independently named flotillins. According to our current view, the reggies subserve functions as protein scaffolds which form microdomains in neurons, lymphocytes and many other cell types across species as distant as flies and humans. These microdomains are of a surprisingly constant size of less than or equal to 0.1 mm in all cell types, whereas the distance between them is variable. The microdomains co-ordinate signal transduction of specific cell-surface proteins and especially of GPI (glycosylphosphatidylinositol)-anchored proteins into the cell, as is demonstrated for PrP(c) (cellular prion protein) in T-lymphocytes. These cells possess a pre-formed reggie cap scaffold consisting of densely packed reggie microdomains. PrP(c) is targeted to the lymphocyte reggie cap when activated by antibody cross-linking, and induces a distinct Ca(2+) signal. In developing zebrafish, reggies become concentrated in neurons and axon tracts, and their absence, after morpholino antisense RNA-knockdown, results in deformed embryos with reduced brains. Likewise, defects in Drosophila eye morphogenesis occur upon reggie overexpression in mutant flies. The defects observed in the organism, as well as in single cells in culture, indicate a morphogenetic function of the reggies, with emphasis on the nervous system. This complies with their role as scaffolds for the formation of multiprotein complexes involved in signalling across the plasma membrane.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping