Seven independent srf mutants that express an L1 -specificcuticle antigen at inappropriate stages (referred to as srf heterochronic mutants for convenience) have been characterized genetically. In immunofluorescence tests, L1 -specificmonoclonal antibody M37 binds to the surface of live wild-type L1 'sand heterochronic srf mutant L1 -L4larval stages but not to adults. The expression of an antigenic O-linked glycoprotein is altered in these mutants [Hemmer, et al, J. Cell Biol. 5, 1237-1247 (1991)]. Five of the mutations show linkage to chromosome II visible markers, and three of these map near
dpy-10 in three-factor crosses with
dpy-10 and
unc-4 .Four of these,
yj15 ,
yj41 ,
yj43 and
yj5 fail to complement the reference mutation
yj13 ,suggesting that they are all alleles of the same gene, now referred to as
srf-6 .These five mutants show no distinct phenotype besides the srf heterochronic phenotype. In contrast, the remaining two mutations show linkage to
dpy-1 III and have a temperature-sensitive dauer-constitutive (daf-c) phenotype in addition to the srf heterochronic phenotype. Like other known daf-c mutants,
yj11 and
yj12 grow normally at 16 , but form dauers when grown at 25 .
yj11 fails to complement
daf-7 III for the daf-c phenotype (Patrice Albert and Don Riddle, personal communication). Based on these results, we tested the reference allele of each of the previously characterized daf-c genes
daf-1 ,
daf-2 ,
daf-4 ,
daf-7 ,
daf-8 ,
daf-11 ,and
daf-14 for the srf heterochronic phenotype. Mutant stocks were grown at the permissive temperature, 16 , to prevent constitutive dauer formation and permit examination of all other post-embryonic stages. Surprisingly, in immunofluorescence tests, all of these daf-c mutants, with the exception of
daf-2 (
e1370),bound monoclonal antibody M37 at larval stages L1 -L4but not as adults, just as the
srf-6 mutants did. These experiments suggest that the pathways for dauer formation and temporal control of surface marker expression have some steps in common. Interestingly, the temperature-sensitive period for dauer formation brackets the L1 molt [Swanson and Riddle, Dev. Biol 86, 27-40 (1981)], the same time at which switching of L1 -specificsurface marker expression appears to occur. However, none of the five
srf-6 alleles shows a ts daf-c phenotype, suggesting that the srf phenotype can be altered without affecting dauer formation. Conversely,
daf-2 (
e1370)mutants only bind M37 at the L1 stage, indicating that at least one daf-c gene can be altered without affecting surface marker expression. Lastly, the daf-c mutants show the srf heterochronic phenotype when grown at 16 , even though the daf-c phenotype is not expressed at this temperature. The daf-c genes have been proposed to be involved in a signal transduction process that evaluates environmental signals and leads to dauer formation under appropriate conditions; indeed,
daf-1 encodes a putative receptor transmembrane serine/threonine protein kinase [Georgi, Albert, and Riddle, Cell 61, 635-645 (1990)]. The evidence described above suggests that these same daf-c genes are also involved in a distinct process, timing of stage-specific surface marker expression.