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The four-cell C. elegans embryo contains two sister cells called ABa and ABp that initially have equivalent abilities to produce ectodermal cell types. Multiple Notch-mediated interactions occur during the early cell divisions that diversify the ABa and ABp descendants. The first interaction determines the pattern of ectodermal cell types produced by ABp. The second interaction induces two ABa granddaughters to become mesodermal precursors. We show that T-box transcription factors called TBX-37 and TBX-38 are essential for mesodermal induction, and that these factors are expressed in ABa, but not ABp, descendants. We provide evidence that the first Notch interaction functions largely, if not entirely, to prevent TBX-37, TBX-38 expression in ABp descendants. Neither the second Notch interaction nor TBX-37, TBX-38 alone are sufficient for mesodermal induction, indicating that both must function together. We conclude that TBX-37, TBX-38 play a key role in distinguishing the outcomes of two sequential Notch-mediated interactions. [ABSTRACT FROM AUTHOR]

The Notch signaling pathway is involved in a wide variety of cell-fate decisions during development. The diverse behavior of Notch-activated cells is thought to depend on tissue- or cell-type-specific transcription factors, yet the identities of such factors and the mechanism of cooperation with the Notch pathway are largely unknown. We identify here an enhancer in the promoter of ref-1, a C. elegans Notch target, which promotes Notch-dependent expression in mesodermal and endodermal cells. The enhancer contains predicted binding sites for the Notch transcriptional effector LAG-1/CSL that are essential for expression, a non-CSL site required for mesodermal expression, and four predicted binding sites for GATA transcription factors that are required for endodermal expression. We show that endodermal expression involves the GATA transcription factor ELT-2, and that ELT-2 can bind LAG-1/CSL in vitro. In many types of Notch-activated embryonic cells, ectopic ELT-2 is sufficient to drive expression of reporters containing the enhancer. [ABSTRACT FROM AUTHOR]