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. 2017 Feb 15;144(4):698–707. doi: 10.1242/dev.146001

Fig. 5.

Fig. 5.

Ectopic expression of UNC-44L causes epidermal defects in dapk-1 mutants. (A) DAPK-1 negatively regulates UNC-44L. Images show head morphology in wild type and mutants. unc-44(tm349), which contains a deletion in the large isoform-specific exon and causes an open reading frame shift, suppresses the Mor phenotypes of dapk-1(ju4) (arrows). (B) Dysregulation of UNC-44L does not enhance the Mor phenotype of dapk-1(ju4). Quantification shows the fraction of animals with epidermal defects in genotypes indicated at L4 and 1-day-old adult stages. The fraction of animals displaying Mor defects in ssup-72(0); dapk-1(ju4) or unc-44(ju1378 ju1412); dapk-1(ju4) is comparable with dapk-1 single mutants. (C) Dysregulated UNC-44L exacerbates lethality of dapk-1(ju4). Percentage of living animals in genotypes indicated at 1-day-old and 2-day-old adult stages. In ssup-72(0); dapk-1(ju4) or unc-44(ju1378 ju1412); dapk-1(ju4), fewer worms survive to early adulthood compared with dapk-1(ju4) single mutants. (D) Exclusion of UNC-44L in larval epidermis is required for maintaining epidermal integrity in dapk-1(ju4). Expression of SSUP-72 in larval epidermis driven by Pcol-10 or Pdpy-7 strongly reduces Mor phenotypes in dapk-1(ju4); sydn-1(0); ssup-72(0); unc-44(ju1412). Expression of SSUP-72 in adult epidermis driven by Pcol-19 modestly reduces Mor phenotypes in dapk-1(ju4); sydn-1(0); ssup-72(0); unc-44(ju1412). Expression of SSUP-72 in neurons driven by Prgef-1 does not reduce Mor phenotypes in dapk-1(ju4); sydn-1(0); ssup-72(0); unc-44(ju1412). Transgenic worms were picked and animals with epidermal defects were counted. Data are average ratio±s.e.m. from three independent experiments. Numbers of animals analyzed are indicated. *P<0.05, ***P<0.001 (one-way ANOVA and Bonferroni's multiple comparison post-test).