ABSTRACT
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.
Subject(s)
Body Patterning/genetics , Caenorhabditis elegans Proteins/physiology , Caenorhabditis elegans/embryology , Caenorhabditis elegans/genetics , Membrane Proteins/physiology , Myoblasts, Smooth Muscle/physiology , Proto-Oncogene Proteins c-fos/physiology , Receptor, Notch1/physiology , Transcription Factors/physiology , Uterus/embryology , Animals , Binding Sites , Caenorhabditis elegans Proteins/genetics , Caenorhabditis elegans Proteins/metabolism , Cell Differentiation/genetics , DNA-Binding Proteins/metabolism , Disorders of Sex Development/embryology , Disorders of Sex Development/genetics , Enhancer Elements, Genetic , Female , Gene Expression Regulation , Models, Biological , Myoblasts, Smooth Muscle/metabolism , Oncogene Protein p65(gag-jun)/metabolism , Proto-Oncogene Proteins c-fos/metabolism , Receptors, Notch , Transcription Factors/genetics , Transcription Factors/metabolism , Uterus/metabolismABSTRACT
We isolated egl-13 mutants in which the pi cells of the Caenorhabditis elegans uterus initially appeared to develop normally but then underwent an extra round of cell division. The data suggest that egl-13 is required for maintenance of the pi cell fate.
