The Journal of Experimental Medicine
Fluorescence In Vivo Endomicroscopy
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents
Published 19 December 2005. doi:10.1084/jem.20051190
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 202, Number 12, 1669-1677
This Article
Right arrow Full Text
Right arrow Full Text (PDF, 801K)
Right arrow PPT slides of all figures
Right arrow Supplemental Material Index
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 JEM
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 Borghesi, L.
Right arrow Articles by Gerstein, R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Borghesi, L.
Right arrow Articles by Gerstein, R.
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

 E47 is required for V(D)J recombinase activity in common lymphoid progenitors

Lisa Borghesi1, Jennifer Aites1, Shakira Nelson1, Preslav Lefterov1, Pamela James2, and Rachel Gerstein3

1 Department of Immunology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261
2 Graduate Program in Immunology and Virology, University of Massachusetts Medical School, Worcester, MA 01655
3 Department of Molecular Genetics and Microbiology, University of Massachusetts Medical School, Worcester, MA 01655

CORRESPONDENCE Lisa Borghesi: borghesi{at}pitt.edu

Common lymphoid progenitors (CLPs) are the first bone marrow precursors in which V(D)J recombinase activity is up-regulated. Here, we show that loss of the transcription factor E47 produces a reduced CLP population that lacks V(D)J recombinase activity and D-JH rearrangements in vivo. Apart from a profound arrest before the pro–B cell stage, other downstream lymphoid progeny of CLPs are still intact in these mice albeit at reduced numbers. In contrast to the inhibition of recombinase activity in early B lineage precursors in E47-deficient animals, loss of either E47 or its cis-acting target Erag (enhancer of rag transcription) has little effect on recombinase activity in thymic T lineage precursors. Taken together, this work defines a role for E47 in regulating lineage progression at the CLP stage in vivo and describes the first transcription factor required for lineage-specific recombinase activity.

Abbreviations used: CLP, common lymphoid progenitor; EBF, early B cell factor; ETP, early thymic progenitor; LSK, lin– scahi kithi; TN, triple negative.


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