| Abstract |
In the 4-cell C. elegans embryo, a signal from P2 to its anterior sister, EMS, specifies the posterior daughter of EMS, E, as the sole founder cell for intestine. The P2-to-EMS signal restricts high level zygotic expression of the redundant GATA transcription factors, END-1 and END-3, to only the E lineage. Expression of END-1 or END-3 in early blastomeres is sufficient to drive intestinal differentiation. We show here that a number of E lineage characteristics, which are also regulated through P2-EMS signaling, can be uncoupled from intestine development, and each with a different sensitivity to specific perturbations of the P2-EMS signal. For example, we show that the extended cell cycle in Ea and Ep depends on the P2-induced high level expression of the cell cycle regulator, WEE-1.1, in E. A mutation in wee-1.1 results in shortened Ea and Ep cell cycles, but has no effect upon intestinal differentiation or embryogenesis. Furthermore, it has been shown previously that the total number of E lineage cell divisions is regulated by a mechanism dependent upon E being specified as the intestinal founder cell. We now show, however, that cell division counting can be uncoupled from intestine differentiation in the E lineage. Many mutations in P2-EMS signal genes exhibit nonfully-penetrant defects in intestinal differentiation. When embryos with those mutations generate intestinal cells, they often make too many intestinal cells. In addition, at the level of individual embryos, expression of end-1 and end-3, and another very early E-specific zygotic gene, sdz-23, exhibit stochastic and discordant defects in P2-EMS signaling mutants. We show here that sdz-23 is expressed close to wildtype levels in embryos deleted of both end-1 and end-3. sdz-23 does not appear to function in intestine development, raising the intriguing possibility that the P2-EMS interaction has downstream molecular consequences within the E lineage independent of end-1/3 and intestinal development.
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