All neurons in C. elegans are produced from asymmetric cell divisions in which a mother cell divides to produce daughters that differ in cell fate. Our lab has previously identified two genes,
ham-1 and
pig-1 , that regulate the asymmetric divisions of many neuroblasts in the worm including the HSN/PHB neuroblast. In wild-type animals, the HSN/PHB neuroblast divides to produce a smaller anterior daughter that undergoes programmed cell death and a larger posterior daughter that subsequently divides to produce an HSN motor neuron and a PHB sensory neuron. Mutations in either
ham-1 or
pig-1 transform the anterior daughter of the HSN/PHB neuroblast into its sister, resulting in the production of extra HSNs and PHBs. These mutations also perturb the normal asymmetries in daughter cell size, presumably by altering the position of the HSN/PHB neuroblast cleavage plane. The molecular mechanisms by which
ham-1 and
pig-1 regulate asymmetric division in the HSN/PHB lineage are not understood. Here we describe two new mutants, ham
(gm345) and
snc-1(
gm350) [ s uper n umerary c ells] that alter the normal number of neurons in lineages also perturbed by mutations in
ham-1 and/or
pig-1 . The ham
(gm345) mutation results in sterile and uncoordinated phenotypes and maps in the gene cluster on LG III to the right of
unc-32 . These mutants are missing PHBs, display the HSN abnormal migration (Ham) phenotype, and have ectopic serotonin-expressing neurons, some of which may be additional HSNs. In our assay for PHBs,
gm345 appears to be epistatic to a
ham-1 null allele: the double mutant is missing PHBs and only rarely has extra PHBs. Conversely,
gm345 enhances the penetrance of extra PHBs of
pig-1 mutants. Current efforts are focused on cloning
gm345 and determining whether
gm345 mutations perturb the position of the HSN/PHB neuroblast cleavage plane. In addition to the HSN/PHB neuroblast lineage,
ham-1 and
pig-1 mutations also disrupt asymmetric division in two touch neuron lineages:
ham-1 and
pig-1 mutants both have extra PLMs, and
pig-1 mutants have extra AVMs and PVMs.
snc-1(
gm350) was isolated in a sensitized screen for mutants with extra touch neurons (see abstract by Gutierrez, Cordes, and Garriga).
snc-1 mutants have extra AVMs, PVMs, PLMs, HSNs and other phenotypes characteristic of
pig-1 mutants. Further phenotypic characterization of
snc-1 will be presented.