The mutants
lin-4(
e912) II and
unc-86(
e1416,
e1507,
n306) III display cell lineage reiterations, in which certain cells appear to adopt the lineage potential of one of their ancestors (Chalfie, Horvitz, and Sulston, Cold Spring Harbor Abstracts, p. 6, 1979). As a result, some cell types are overproduced and others are not generated at all. We hope to determine how
lin-4 and
unc-86 control cell lineages. As a first step, we plan to identify the null phenotypes of these genes and to establish the nature of the existing mutations. Toward this end, we have begun genetic studies of
lin-4 and
unc-86.The three existing alleles of
unc-86 III result in similar phenotypes: mutant animals are mechanosensory defective (Mec), egg- laying defective, and Him (producing about 2.5% males). Surprisingly, by both complementation tests and map position, the him defect of
e1507 is distinct from that of
e1416 and
n306, i.e. heterozygotes of
e1416 or
n306 with
e1507 are non-Him, and the him defect of
e1507 has been separated by recombination from the other traits of the original
e1507 isolate, CB1507. Perhaps the Him phenotype of CB1507 was fortuitous. None of the three
unc-86 alleles is suppressed by the null allele-specific suppressor
sup-7(
st5) X. We have sought revertants of
e1416: following EMS mutagenesis, 15,000 F1's and their progeny were screened for increased motility (
unc-86 animals, like other Mec mutants, are lethargic). An extragenic suppressor was isolated and mapped to LGI. The suppressed animals were active but still Mec, and the isolated suppressor appeared to be hyperactive; we suspect that this mutant bypasses the Mec-induced lethargy. We have obtained a deficiency by mutagenizing males with gamma-rays, mating them with appropriately marked
unc-86 hermaphrodites, and seeking Unc- 86 Fl cross progeny. This deficiency fails to complement for the Mec phenotype of CB1507 and for both the Mec and Him phenotypes of
e1416; it also fails to complement
unc-36(
e251) and at least two lethal mutations we have generated that are closely linked to
unc-86.The only allele of
lin-4 is
e912, which was isolated by Babu after P-32 mutagenesis. Two independent partial revertants of
e912 have been obtained; one (
n179) appeared spontaneously and the other (
n360) was isolated after gamma-ray mutagenesis.
n179 and
n360 are alleles and define a new locus about 4% to the right of
dpy-7 X. The isolated suppressor is itself a cell lineage mutant, affecting many of the same lineages as
e912 (e.g. vulva, lateral hypodermis, male tail), although not as severely.
e912 complements
let-22(
mn22) and
let-30(
mn30), the two most closely linked recessive lethal mutations isolated by Bob Herman.
let-30 is to the left of
lin-4, and
let-22 is to the right of
lin-4 and to the left of
dpy-10; these loci should help identify a deficiency spanning
lin-4.
e912 is dauer-defective and blocks dauer formation by the dauer constitutive mutation
daf-4(
e1364). We hope that reversion of
daf-4 will yield additional
lin-4 alleles; the isolation of dauer larvae from mutagenized populations of
lin-4; rate suppressors of
e912. A new cell lineage mutant,
n355, has been isolated after gamma-ray mutagenesis.
n355 appears phenotypically similar to
e912; however, in contrast to
e912, this new mutation is dominant and unlinked to the cluster of LGII. We have compared the SDS gel protein profiles of whole extracts prepared from N2,
e912, and
n355. Both
e912 and
n355 are missing an adult- specific doublet of about 190,000 daltons; the suppressed strain
e912;
n179 has this doublet. These proteins might be localized in adult- specific cells that are missing in
e912 and
n355; alternatively, adult- specific gene expression may be defective in cells that are present in both adults and younger animals.