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. 2002 Dec 15;16(24):3136–3141. doi: 10.1101/gad.251202

Figure 4.

Figure 4

A model of lin-39 activity during vulva formation. (A) lin-39 inhibits cell fusion in the VPCs by repressing the fusogen eff-1. This model of interactions among lin-39, eff-1, and cell fusion predicts the fusion pattern of the VPCs in wild-type, single, and double mutants. In all diagrams, dashed lines represent fusing cells, and solid lines represent nonfusing cells. Cells that express LIN-39 have black nuclei. (BE) Structural fates of the vulval cells in different genotypes. (B) In wild-type worms, lin-39 acts in P(3–8).p at L1 and in P(5–7).p at L3, preventing these cells from fusion. The result is a 22-cell primordium that forms the seven vulval rings. (C) In lin-39(−) single mutants, eff-1 is not repressed and at L1, all cells fuse and contribute their nuclei to the surrounding hypodermis. (D) In eff-1(−) single mutants, none of the cells are able to fuse with the hypodermis, resulting in ectopic cells that migrate along with the vulva precursors. (E) In eff-1(−);lin-39(−) double mutants, despite the lack of the inhibitory activity of lin-39, the Pn.p cells are not able to fuse at L1 and at L3 in the absence of eff-1 activity. In the absence of lin-39, the cells fail to proliferate. They do succeed in forming rings (three in this example), but these rings are structurally abnormal and nonfunctional.