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

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.

AFF-1, a FOS-1-regulated fusogen, mediates fusion of the anchor cell in C. elegans.

Cell fusion is fundamental for reproduction and organ formation. Fusion between most C. elegans epithelial cells is mediated by the EFF-1 fusogen.

N-ethylmaleimide sensitive factor is required for fusion of the C. elegans uterine anchor cell.

The fusion of the Caenorhabditis elegans uterine anchor cell (AC) with the uterine-seam cell (utse) is an excellent model system for studying cell-cell fusion, which is essential to animal development. We obtained an egg-laying defective (Egl) mutant in which the AC fails to fuse with the utse. This defect is highly specific: other aspects of utse development and other cell fusions appear to occur normally.

A two-promoter system of gene expression in C. elegans.

The development of multicellular organisms requires precise spatiotemporal gene expression and the expression of cell/tissue specific isoforms of some genes. This task may require more efficient genome organization in Caenorhabditis elegans and other organisms with relatively small genome size. The SL1 leader sequence is trans-spliced to many mRNAs in C.

The EGL-13 SOX domain transcription factor affects the uterine pi cell lineages in Caenorhabditis elegans.

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.