The Caenorhabditis elegans
rol-3(
e754) mutation is a member of a general class of mutations affecting gross morphology, presumably through disruption of the nematode cuticle. Adult worms homozygous for
rol-3(
e754) exhibit rotation about their long axis associated with a left-hand twisted cuticle, musculature, gut and ventral nerve cord. Our laboratory previously isolated 12 recessive lethal alleles of
rol-3. All these lethal alleles cause an arrest in development at either early or mid-larval stages, suggesting that the
rol-3 gene product performs an essential developmental function. Furthermore, through the use of the heterochronic mutants
lin-14 and
lin-29, we have established that the expression of
rol-3(
e754)'s adult specific visible function is not dependent on the presence of an adult cuticle. In an attempt to understand
rol-3's developmental role we sought to identify other genes whose products interact with that of
rol-3. Toward this end, we generated eight EMS induced and two gamma irradiation-induced recessive suppressors of the temperature sensitive (ts) mid-larval lethal phenotype of
rol-3(
s1040ts). These suppressors define two complementation groups
srl-1 II and
srl-2 III; and, while they suppress the
rol-3(
s1040) lethality, they do not suppress the adult specific visible rolling phenotype. Furthermore, there is a complex genetic interaction between
srl-2 and
srl-1 such that
srl-2(
s2506) fails to complement all srl alleles tested. These results suggest that
srl-1 and
srl-2 may share a common function and, thus, possibly constitute members of the same gene family. Mutations in both
srl-1 and
srl-2 produce no obvious hermaphrodite phenotypes in the absence of
rol-3(
s1040ts); however, males homozygous for either
srl-1 or
srl-2 display aberrant tail morphology. We present evidence suggesting that the members of
srl-2 are not allele specific with respect to their suppression of
rol-3 lethality, and that
rol-3 may act in some way to influence proper posterior morphogenesis. Finally, based on our genetic analysis of
rol-3 and the srl mutations, we present a model whereby the wild-type products of the srl loci act in a concerted manner to negatively regulate the
rol-3 gene.