Fig. 8. A model for specification of the MS blastomere. A gene cascade that begins with maternal SKN-1 progresses through activation of med-1,2 in EMS, which in turn activate tbx-35 in MS. POP-1 represses endoderm specification in MS. In E, the sister of MS, a Wnt/MAPK-dependent mechanism represses tbx-35 through an unknown effector (not shown). TBX-35 acts upstream of genes that specify pharynx and muscle fates, through regulators such as pha-4 and hlh-1, respectively (Gaudet and Mango, 2002; Krause et al., 1990). TBX-35 also represses targets of maternal PAL-1, blocking C fates. Activation of med-1,2 by SKN-1 is direct (Maduro et al., 2001), as is activation of tbx-35 by MED-1,2 (this work). In addition to med-1,2, SKN-1 also activates the expression of one or more Delta/Serrate/Lag (DSL) proteins that enable the MS cell to signal the AB lineage to make anterior pharynx (Priess et al., 1987).