Fig. 8. Modeling the HSN/PHB lineage in pig-1 and ham-1 mutants. In wild-type animals, the HSN/PHB neuroblast is polarized along the AP axis, with an anteriorly displaced cleavage plane (vertical dotted line) and posteriorly localized determinants of neural precursor fate (gray circles). The neuroblast divides to produce a small anterior daughter that inherits no determinants and undergoes apoptosis, and a larger posterior daughter that inherits the determinants and becomes a neural precursor. In pig-1 mutants, the neuroblast does not polarize and this results in a symmetrically localized cleavage plane and uniformly distributed determinants. Both neuroblast daughters inherit these determinants resulting in the production of two neural precursors. In ham-1 mutants, neuroblast polarity is partially inverted along the AP axis resulting in a posteriorly displaced cleavage plane and an anteriorly enriched distribution of cell fate determinants. Extra neurons are produced when a sufficient concentration of determinants enters both neuroblast daughters, resulting in the production of two precursors. No neurons are produced when the anterior daughter undergoes apoptosis and the posterior daughter receives an insufficient concentration of determinants to develop as a precursor. The concentration of determinants in the posterior daughter could fall below a threshold required for precursor fate, either because of stochastic differences in cleavage position or determinant distribution. Neuroblasts in pig-1 ham-1 double mutants are defective for polarity, resulting in pig-1 phenotypes and pig-1 epistasis to ham-1.