Overactive EGF signaling suppresses a egg-laying phenotype independent of known signaling mediators.

Nicotinamide recycling is critical to the development and function of . Excess nicotinamide in a nicotinamidase mutant causes the necrosis of uv1 and OLQ cells and a highly penetrant egg laying defect. An EGF receptor () gain-of-function mutation suppresses the Egl phenotype in animals. However, gain-of-function mutations in either of the known downstream mediators, or , are not sufficient. Phosphatidylcholine synthesis is neither required nor sufficient, in contrast to its role in the rescue of uv1 necrosis. The mechanism behind the suppression of the Egl phenotype is unknown.