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. 2017 Apr 1;144(7):1273–1282. doi: 10.1242/dev.145722

Fig. 1.

Fig. 1.

SET-4 promotes dauer arrest. (A) Schematic of the set-4 locus and three mutant alleles. Exons are indicated as boxes, separated by introns. Gray, green and yellow denote untranslated regions, coding sequence and SET domain coding sequence, respectively. Deletions are indicated by black bars. (B) set-4 mutations suppress the dauer-constitutive phenotype of eak-7;akt-1 mutants [n (left to right)=236, 627, 389, 521, 638]. (C) set-4(n4600) suppresses the dauer-constitutive phenotype of daf-2(e1368) mutants and is rescued by the single-copy set-4 transgene dpSi5 (n=913, 1668, 1568, 1785). (D,E) set-4 is dispensable for dauer arrest in (D) daf-1(m40) (n=2215, 2189, 1816, 1899) and (E) daf-9(dh6) mutants (n=1753, 1561, 2188, 2486). (F) set-4 and dpy-21 mutations suppress dauer arrest in XX hermaphrodites but not in XO males (n=567, 1330, 579, 1003, 1012, 700). (G) set-4 and dpy-21 mutations attenuate the response of wild-type animals to dauer pheromone [n (0 μl, 2 μl, 10 μl): wild type=542, 461, 544; set-4=413, 246, 387; dpy-21=334, 220, 275]. set-4 versus wild type: P<0.01 by two-way ANOVA.