spacer gif spacer gif spacer gif spacer gif ARCHIVE ANNOUNCEMENT! spacer gif
QUICK SEARCH:   [advanced]


spacer gif
     Home     Help     Feedback     Subscriptions     Archive     Search     Table of Contents    

First published online 17 October 2007
doi: 10.1242/dev.002741

Development 134, 3999-4009 (2007)
Published by The Company of Biologists 2007
This Article
Right arrow Figures Only
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
dev.002741v1
134/22/3999    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Oommen, K. S.
Right arrow Articles by Newman, A. P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Oommen, K. S.
Right arrow Articles by Newman, A. P.

Co-regulation by Notch and Fos is required for cell fate specification of intermediate precursors during C. elegans uterine development

Kavita S. Oommen1 and Anna P. Newman1,2,3,*

1 Program in Developmental Biology, Baylor College of Medicine, Houston, TX 77030, USA.
2 Verna and Marrs McLean Department of Biochemistry and Molecular Biology, Baylor College of Medicine, Houston, TX 77030, USA.
3 The Honors College, Department of Biology and Biochemistry, University of Houston, Houston, TX 77204, USA.

* Author for correspondence (e-mail: apnewman{at}uh.edu)

Accepted 22 August 2007

The Notch pathway is the key signal for many cell fate decisions in the nematode Caenorhabditis elegans including the uterine {pi} cell fate, crucial for a proper uterine-vulval connection and egg laying. Expression of the egl-13 SOX domain transcription factor is specifically upregulated upon induction of the {pi} lineage and not in response to other LIN-12/Notch-mediated decisions. We determined that dual regulation by LIN-12 and FOS-1 is required for egl-13 expression at specification and for complete rescue of egl-13 mutants. We found that fos-1 mutants exhibit uterine defects and fail to express {pi} markers. We show that FOS-1 is expressed at {pi} cell specification and can bind in vitro to egl-13 upstream regulatory sequence (URS) as a heterodimer with C. elegans Jun.

Key words: LIN-12, Notch, LAG-1, CSL, FOS-1, Fos, Jun, Specification, Transcription






© The Company of Biologists Ltd 2007