JCB logo
AbD Serotec
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents

Published online
doi:10.1083/jcb.1834iti3
The Journal of Cell Biology, Vol. 183, No. 4, 568-569
The Rockefeller University Press, 0021-9525 $30.00
© Leslie
This Article
Right arrow Full Text (PDF, 729K)
Right arrow PPT slides of all figures
Right arrow Alert me when this article is cited
Services
Right arrow Email this article
Right arrow Similar articles in this journal
Right arrow Alert me to new content in the JCB
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Leslie, M.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Leslie, M.
Social Bookmarking
 Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Facebook   Add to Reddit   Add to Technorati   Add to Twitter  
What's this?

In This Issue

Axons lose their identity



Figure 1
After removal of ankyrinG, this axon (arrows) grew a stubble of dendritic spines.

Inside every axon is a dendrite waiting to get out. Hedstrom et al. converted mature axons into dendrites by banishing a protein crucial for neuron development. The results suggest that this transformation could occur after nerve cell damage.

At the junction between the axon and the cell body is the axon initial segment (AIS), which sparks action potentials. Researchers also suspect that the AIS enables an axon to maintain its identity. Although scientists have teased out some of the molecular events that determine whether a neuron outgrowth will become an axon or a dendrite, they know little about what keeps these structures distinct.

In cultured neurons, Hedstrom et al. used RNAi to cut production of ankyrinG, a protein that helps spur formation of the AIS. Loss of ankyrinG caused the AIS to disappear. For example, sodium channels that normally crowd the AIS's plasma membrane dispersed. When ankyrinG was absent the erstwhile axons began to resemble dendrites, sprouting spines and developing excitatory synapses. Characteristic molecules from the cell body and dendrites, such as the microtubule polymerizing protein MAP2, also infiltrated the axons.

The AIS appears to serve as a filter that screens out dendritic proteins, Hedstrom et al. conclude. How the structure bars some proteins from the axon is still uncertain. Injuries and diseases can transform dendrites into axons. The findings raise the possibility that these insults could cause the reverse transformation by changing the amount of ankyrinG and altering the AIS.

Hedstrom, K.L., et al. 2008. J. Cell Biol. doi:10.1083/jcb.200806112.[Abstract/Free Full Text]



Mitch Leslie

mitchleslie{at}comcast.net


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Facebook Facebook   Add to Reddit Reddit   Add to Technorati Technorati   Add to Twitter Twitter    What's this?



This Article
Right arrow Full Text (PDF, 729K)
Right arrow PPT slides of all figures
Right arrow Alert me when this article is cited
Services
Right arrow Email this article
Right arrow Similar articles in this journal
Right arrow Alert me to new content in the JCB
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Leslie, M.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Leslie, M.
Social Bookmarking
 Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Facebook   Add to Reddit   Add to Technorati   Add to Twitter  
What's this?


  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents