Differentiated cells acquire their identities by a combination of intrinsic and extrinsic factors acting on intermediates in the cell lineage and the terminal descendants they produce. In the ventral uterus, a
lin-12 -mediated signal from the AC induces adjacent VU intermediate precursor cells to adopt the p cell fate and produce daughters that connect to the vulva. One set of p daughters, called utse, forms the thin laminar process dorsal to the vulva, while the other p daughters, called
uv1 cells, attach the vulva to the utse [1]. p daughters become
uv1 in response to LIN-3 EGF signaling from the vulva and utse in the absence of this signal [2]. In screens for egg-laying-defective mutants with uterine defects, we have isolated alleles of
sel-12 (which encodes a presenilin [3]) and
cog-2 (which encodes a SOX domain transcription factor [4]) with p cell lineage defects. Specifically, an additional round of cell division indicative of failure to properly specify or maintain the p cell fate was observed in 46/60
sel-12 (
ty11 ) and 48/60
cog-2 (
ty3 ,
ty8 ) p cell daughters followed. Differences in pattern formation suggest that
sel-12 (
ty11 ) gives a partial loss of function in p cell induction (consistent with the previously demonstrated role of SEL-12 in LIN-12/Notch signaling [3]) whereas
cog-2 (
ty3 ,
ty8 ) mutants are defective in maintenance of the p cell fate and differentiation of its daughters. The LIN-11 LIM domain transcription factor is required for p daughter differentiation and responds to
lin-12 activity. We propose that
lin-12 activity in the p cells leads to the following genetically separable events: specification of the p cell fate, maintenance of this fate, and production of daughters that connect to the vulva. The LIN-11 and COG-2 transcription factors may have related functions in the latter events. The activity of the
lin-11 and
cog-2 genes might help to make p daughters competent to differentiate as
uv1 in response to LIN-3 signaling and as utse in its absence. [1] Newman, White, and Sternberg (1995, 1996). Development 121: 263-271; 122: 3617-3626. [2] Chang, Newman, and Sternberg (1999). Current Biology 9: 237-246. [3] Levitan and Greenwald (1995). Nature 377: 351-354. [4] Hanna-Rose and Han (1999). Development 126: 169-179.