We have isolated a maternal effect mutation that causes animals to arrest normal development in abundant food either as dauers or as late larvae or sterile adults which retain some dauer-like properties. Homozygous
mg44 progeny from heterozygous parents appear completely normal. In addition, the mutant phenotype of progeny from
mg44 homozygotes can be rescued zygotically suggesting that this gene may function relatively late in development. As is characteristic of many genes involved in dauer formation, temperature has a modulatory effect on the mutant phenotype. At 25 C, progeny of homozygous
mg44 hermaphrodites arrest at the "L3" stage either as fully-formed, SDS resistant dauers or as larvae which exhibit features intermediate between a dauer and an L3 (a darkly-staining intestine characteristic of dauers but no dauer alae and the pharynx is variably slimmed-down and occasionally pumps). At 15 C and 20 C,
mg44 homozygotes produce progeny that initially arrest with a phenotype similar to that described above at 25 C, but then continue to develop, arresting as either L4 'sor sterile adults. These adults make adult alae and the arms of the gonad have reflexed but do not elongate to the extent of normal adults and no oocytes are made. And, like dauers, the intestines of these sterile animals remain extremely dark. Also, many of the worms that arrest as adults have a protruding vulva. The mutant,
mg44 ,maps to chromosome II near a previously-identified maternal effect, non-conditional dauer constitutive,
daf-23 (Riddle, 1988, worm book). We are currently testing whether these two genes are allelic. Preliminary data on the phenotype of double mutants of
mg44 and several dauer defective genes are as follows:
daf-3 (
e1376),
daf-12 (
m20),and
che-3 (
e1379)do not suppress
mg44 while
daf-16 (
m27)does suppress
mg44 .These epistasis results together with the unusual arrest phenotype suggest that
mg44 and perhaps
daf-2 (see below), constitute a new class of genes that is required for non-dauer or continuous development for the following reasons. First, while it is known that the conditional dauer constitutives
daf-1 ,
daf-4 ,
daf-7 ,
daf-8 ,
daf-1 l and
daf-14 are suppressed by mutations in
daf-3 and
daf-12 ,
daf-2 and
mg44 are not suppressed. Second, while it has been shown that double mutants between
daf-16 and the conditional dauer constitutives listed above lead to the formation of partial dauers,
daf-16 appears to suppress dauer formation in both
mg44 and
daf-2 mutants as well as the L4 arrest and adult sterile phenotype of
mg44 .However, it is unlikely that
daf-16 is functioning directly downstream of
daf-2 since
daf-16 ;
daf-2 ;
daf-12 triple mutants arrest with a
daf-2 ;
daf-12 phenotype. Interestingly, we had shown previously that
daf-16 has an additional unusual interaction with the dauer constitutive gene
daf-2 .Specifically,
daf-16 ;
daf-2 double mutants form precocious dauers (~4 hours earlier than
daf-2 alone) which then recover. We have not yet determined whether a similar phenomenon is occurring with
mg44 .And finally, as observed by Vowels and Thomas, (Genetics, 130:105, 1992),
daf-2 ;
daf-12 double mutant worms appear to be unable to develop as either dauers or non-dauers. Based on their observation, Vowels and Thomas suggested that
daf-2 may be required for development to L3 .We propose that
mg44 and
daf-2 may act in the same pathway, directing nondauer development.
daf-16 ,which is epistatic to both of these genes, may have the role of insuring that worms maintain dauer under dauer-inducing conditions.