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

Development 134, 3999-4009 (2007)
Published by The Company of Biologists 2007
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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


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