The gene
unc-86 III is known to affect specific developmental decisions involving cell division:
unc-86 mutants undergo posterior parental reiterations in the postembryonic cell lineages of three neuroblasts (Chalfie, Horvitz and Sulston, Cell, 24, 59, 1981). We have continued genetic studies of
unc-86, including the generation of new
unc-86 alleles and the characterization of the
unc-86 region. A revised map of a portion of LGIII is shown below. We have isolated five new
unc-86 alleles by complementation screening: EMS-mutagenized
dpy-19 males were mated with marked
unc-86 hermaphrodites and F1 Unc- 86 cross progeny were picked. None of these nine alleles was suppressed by the amber suppressor
sup-7 X. In addition, an EMS-induced temperature-sensitive (ts)
unc-86 allele,
n848, was isolated by Nancy Tsung in a screen for animals abnormal in dopaminergic or serotonergic neurons. At 20 C,
n848 animals have the supernumerary dopaminergic neurons characteristic of
unc-86 mutants, but appear wild-type in the dissecting microscope; at 25 C,
n848 animals are Mec and Egl. We have investigated the temperature- sensitive period (tsp) for the Mec and Egl phenotypes of
n848. The tsp for Mec is embryonic, as is the generation of the mechanosensory neurons. In contrast, the tsp for Egl is in the L4, considerably after all neurons in the hermaphrodite have been generated. Thus, the Egl phenotype of
unc-86 does not result from a lineage defect. Several lines of evidence indicate that
unc-86 animals are Egl because they fail in the differentiation of the hermaphrodite-specific neurons (HSN's). 1)
unc-86 animals have the Egl phenotype characteristic of HSN-deficient animals (see Trent, Tsung and Horvitz, this Newsletter). 2)
unc-86 adults have missing, displaced or abnormal HSN's. 3)
unc-86 L1 hermaphrodites contain undifferentiated HSN's that are normal by three criteria: first, they are capable of forming a functional HSN in
n848 animals grown at 25 C if the temperature is shifted down in the L4, the normal time of HSN differentiation; second,
egl-1(
n487), which appears to induce specifically the programmed deaths of the HSN's in wild type (see Ellis and Horvitz, this Newsletter), also induces the deaths of these putative HSN's in
unc-86 animals; third, these putative HSN's are normal in lineage history, migration and appearance (John Sulston, personal communication). Thus, the wild-type function of
unc-86, which is necessary for the correct execution of several developmental decisions involving cell division, is also necessary for the execution of a developmental decision not involving cell division. This observation indicates that developmental decisions can occur independently of cell division and that
unc-86 controls at least one such decision. [See Figure 1] Approximate length of region shown is 0.6 map units. EMS-induced lethals were generated linked to
dpy-19. deficiencies were generated with gamma rays. lin
(n758) and lin
(n766) , which are synthetic multivulva mutations (see Ferguson and Horvitz, this Newsletter), were mapped by Chip Ferguson.
n709, which causes VC neurons to undergo programmed cell death, was generated and mapped by Hilary Ellis (see Newsletter, Vol. 7, Mo. 1). Alleles of
sup-18, which are suppressors of
unc-93(
e1500), were isolated and mapped by Iva Greenwald.