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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.
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