JCB logo
PeproTech: Your source for Cell Biology Research Reagents
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents
Published online 17 April 2006. doi:10.1083/jcb.200511055
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 173, Number 2, 265-277
This Article
Right arrow Full Text
Right arrow PDF (Full Text)
Right arrow PPT slides of all figures
Right arrow Supplemental Material Index
Right arrow Correction (v173,p821)
Right arrow Alert me when this article is cited
Right arrow Citation Map
Services
Right arrow Email this article
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new content in the JCB
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Tararuk, T.
Right arrow Articles by Coffey, E. T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Tararuk, T.
Right arrow Articles by Coffey, E. T.
Social Bookmarking
Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

Article

 JNK1 phosphorylation of SCG10 determines microtubule dynamics and axodendritic length

Tatsiana Tararuk1, Nina Östman1, Wenrui Li1, Benny Björkblom1, Artur Padzik1, Justyna Zdrojewska1, Vesa Hongisto1, Thomas Herdegen2, Witold Konopka3, Michael J. Courtney4, and Eleanor T. Coffey1

1 Turku Centre for Biotechnology, Turku, FIN-20521, Finland
2 Institute of Pharmacology, University of Kiel, 24105 Kiel, Germany
3 The Nencki Institute, 02-093 Warsaw, Poland
4 A.I. Virtanen Institute, University of Kuopio, Kuopio, FIN-70211, Finland

Correspondence to Eleanor T. Coffey:ecoffey{at}btk.fi

c-Jun NH2-terminal kinases (JNKs) are essential during brain development, when they regulate morphogenic changes involving cell movement and migration. In the adult, JNK determines neuronal cytoarchitecture. To help uncover the molecular effectors for JNKs in these events, we affinity purified JNK-interacting proteins from brain. This revealed that the stathmin family microtubule-destabilizing proteins SCG10, SCLIP, RB3, and RB3' interact tightly with JNK. Furthermore, SCG10 is also phosphorylated by JNK in vivo on sites that regulate its microtubule depolymerizing activity, serines 62 and 73. SCG10-S73 phosphorylation is significantly decreased in JNK1–/– cortex, indicating that JNK1 phosphorylates SCG10 in developing forebrain. JNK phosphorylation of SCG10 determines axodendritic length in cerebrocortical cultures, and JNK site–phosphorylated SCG10 colocalizes with active JNK in embryonic brain regions undergoing neurite elongation and migration. We demonstrate that inhibition of cytoplasmic JNK and expression of SCG10-62A/73A both inhibited fluorescent tubulin recovery after photobleaching. These data suggest that JNK1 is responsible for regulation of SCG10 depolymerizing activity and neurite elongation during brain development.

N. Östman and W. Li contributed equally to this paper.

Abbreviations used in this paper: DCX, doublecortin; GFAP, glial cell intermediate filament protein; JBD, JNK binding domain; JIP, JNK-interacting protein; PJNK, phospho-JNK; WT, wild type.


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 Reddit Reddit   Add to Technorati Technorati    What's this?


This article has been cited by other articles:



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