Fig 6. Most genes expressed in multiple posterior lineages are either activated or repressed by pop-1.

A) Expression driven by the end-1 promoter in the EMS lineage is high in the posterior E descendants and absent from the anterior MS descendants. Depleting pop-1 by RNAi increases end-1 promoter activity in the MS lineage and decreases it in the E lineage, equalizing expression as previously demonstrated. B) nob-1 expression in posterior daughter-derived lineages is lost after both pop-1/TCF and sys-1/β-catenin RNAi (green boxes) in the ABp lineage, but expression is unchanged in the E lineage. C) Expression of ceh-36 in ABp is expanded into previously unexpressing cells with pop-1 RNAi (purple boxes) but unchanged in response to sys-1 RNAi. Expression of ceh-36 in ABalpa is decreased in response to pop-1 and sys-1 by RNAi (green boxes). D) In response to pop-1 RNAi, expression of pal-1 in AB lineage (ABpr shown) is greatly decreased, but expression in the C lineage becomes equalized. E) A known anterior to posterior fate transformation (blue underline, arrow) caused by pop-1 RNAi causes ectopic expression of nhr-67, while normal expression is decreased. The loss of expression from the nhr-67 promoter in response to sys-1 RNAi suggests that nhr-67 depends on pop-1/sys-1 for activation. F) Table showing the number of genes expressed in each sub-lineage and the response to pop-1 RNAi in each. See full lineage diagram in Fig 1E.