Worm Breeder's Gazette 5(1): 23
These abstracts should not be cited in bibliographies. Material contained herein should be treated as personal communication and should be cited as such only with the consent of the author.
A major question in the analysis of dauer larva formation is: 'How do the genes work together to specify the developmental sequence?' The epistatic relationships between genes were determined by constructing double mutants, homozygous for both a constitutive and a defective mutation. On the basis of the suppression patterns, a pathway was constructed with individual genes assigned to the control of various steps (Figure 1). A summary of the complete battery of cross- suppression tests is given in Table 1. The pathway includes some mutants which exhibit pleiotrophic sensory defects correlated with abnormal neural ultrastructure. We proposed that the genetic pathway corresponds to a pathway of neurotransmission involving reception of an environmental signal associated with starvation, and the conversion of that signal into a neuro-endocrine response. [See Figure 1] Figure 1. An updated genetic pathway for dauer larva formation based on epistatic relationships between dauer-constitutive mutations and dauer-defective mutations. Gene names of dauer-constitutives are given in the pathway itself to represent points where false signals can be initiated. Dauer-defective genes block the pathway at the positions shown by dashed lines. The designation, daf, for dauer formation, is applied to both constitutive and defective mutants. Dauer-defective mutants which block only the upper pathway in Figure 1 (e.g. daf-18 and daf-6) do not form dauers on starved plates. Therefore, we conclude that the lower pathway specified by daf-2 must not function under these specific conditions. This second pathway may represent the response to different environmental signals, or it may function only in daf-2 mutants. All the epistatic relationships are based on tests with ts dauer- constitutive alleles because the ts property facilitates the construction of multiple mutants containing these mutations. However, a few lethal dauer-constitutive alleles have been collected. Animals homozygous for the 'lethal' alleles always form dauers and the dauers never recover. Stocks are maintained as balanced heterozygotes. The ability of a dauer-defective daf-16 mutation to suppress a lethal daf- 2 mutation was tested by constructing a homozygous daf-16 The daf-16 mutation is completely epistatic; the strain does not form dauers even when starved. The presence of the daf-2 allele in this strain as confirmed by complementation testing. Suppression in this case shows that (1) daf-16 provides an absolute block to the most extreme constitutive mutations, although it does not suppress alleles of certain other constitutive genes, (2) the effects of the 'lethal' mutations on development subsequent to the dauer stage can be examined, and (3) suppression provides a means to maintain homozygous stocks of the lethal constitutive alleles. Table 1. Suppression of dauer-constitutive mutations by dauer- [See Table 1] a (+) indicates that, in a particular constitutive-defective double mutant, the constitutive phenotype is suppressed (the defective is epistatic). A (-) indicates gene pairs in which the constitutive is epistatic (no suppression of the constitutive phenotype). In cases where suppression is not complete the fraction of the double-mutant population which escapes dauer formation is given in parentheses as percent suppression. Dauer-defective strains are all single mutants with allele numbers corresponding to the strain numbers. Corresponding gene names and lineage groups are given in parentheses. The multiply-marked constitutives have the following genotypes, where allele numbers are given in parentheses after the corresponding gene name: DR194. dpy-11(e224)daf-11(m47) 57); DR189, dpy-5(e61)daf-8(e1393)unc-29(e1O72); DR133, dpy-1(e1)daf-7(e1372)unc- 32(e189);DR202, 38)daf-14(m77); DR204, daf-1(m40) dpy-4(e1166); D446,daf-4(e1364)unc-32(e189); DR130, dpy1(e1)daf-2( e1370)unc-32(e189).
