AnkyrinG is required for maintenance of the axon initial segment and neuronal polarity

  • Hedstrom K
  • Ogawa Y
  • Rasband M
  • 7


    Mendeley users who have this article in their library.
  • N/A


    Citations of this article.


The axon initial segment (AIS) functions as both a physiological and physical bridge between somatodendritic and axonal domains. Given its unique molecular composition, location, and physiology, the AIS is thought to maintain neuronal polarity. To identify the molecular basis of this AIS property, we used adenovirus-mediated RNA interference to silence AIS protein expression in polarized neurons. Some AIS proteins are remarkably stable with half-lives of at least 2 wk. However, silencing the expression of the cytoskeletal scaffold ankyrinG (ankG) dismantles the AIS and causes axons to acquire the molecular characteristics of dendrites. Both cytoplasmic- and membrane-associated proteins, which are normally restricted to somatodendritic domains, redistribute into the former axon. Furthermore, spines and postsynaptic densities of excitatory synapses assemble on former axons. Our results demonstrate that the loss of ankG causes axons to acquire the molecular characteristics of dendrites; thus, ankG is required for the maintenance of neuronal polarity and molecular organization of the AIS.

Author-supplied keywords

  • Adenoviridae
  • Animals
  • Ankyrins
  • Axons
  • Cell Polarity
  • Cells: Cultured
  • Dendrites
  • Gene Expression Regulation
  • Mice
  • Nerve Tissue Proteins
  • RNA Interference
  • Time Factors

Get free article suggestions today

Mendeley saves you time finding and organizing research

Sign up here
Already have an account ?Sign in

Find this document


  • K L Hedstrom

  • Y Ogawa

  • M N Rasband

Cite this document

Choose a citation style from the tabs below

Save time finding and organizing research with Mendeley

Sign up for free