lin-12 and
glp-1 encode homologous transmembrane proteins that probably act as receptors in regulatory cell interactions during development (Yochem and Greenwald, 1987). The absence of zygotic lin- 12 produces a low level of L1 lethality (~10%), whereas zygotic
glp-1 is not required for embryonic development. However,
lin-12 glp-l double mutants invariably arrest as L1s. We interpret this result as indicating a common essential function of
lin-12 and glp-l during mid/late embryogenesis. Iin-12
glp-1 double mutants have several anatomical abnormalities that may result from cell fate transformations, e.g. they are missing several structures (rectum, anus, excretory cell) and have duplications of others (excretory pore). We call this combination of characteristics the Lag phenotype (for
lin-12 and glp-l). In an effort to identify genes that are required for the functioning of both
lin-12 and glp-l, we have isolated 12 recessive mutations that cause a Lag phenotype. These mutations define two loci, lag-l IV, and
lag-2 V. Mutations in
lag-2 had been previously isolated by Johnsen and Baillie (
let-461), and Tax, Thomas and Horvitz (
sel-3). Iag-1 is a newly identified gene. We think that both lag-l and
lag-2 are required for postembryonic functions of glp-l and
lin-12, since certain alleles can cause postembryonic phenotypes diagnostic of
lin-12 and/or glp-l mutations. The larval lethality of Lag animals may be due, in part or whole, to the absence of the excretory cell. Analysis of a temperature sensitive allele of
lag-2,
q420, indicates that the requirement for
lag-2 function occurs during mid-embryogenesis, at approximately the time of birth of the excretory cell. Mosaic analysis using a strain of genotype
ncl-1 unc-36 lin-12 glp-1; qDp3 suggests that
lin-12 and glp- 1 are required in AB.p (from which the excretory cell is descended) for viability;
unc-36 is required in AB.p, and Unc nonLag mosaics are extremely rare. We are currently attempting the molecular isolation of lag-l and
lag2 in the expectation that this will lead to a better understanding of how they function in concert with
lin-12 and
glp-1. E.L. is supported by Damon Runyon-Walter Winchell postdoctoral fellowship DRG-989.