1. dex-1 mutants form partial dauers.
dex-1 mutants form partial dauers. (A) dex-1 mutant dauers are defective for dauer-specific radial shrinkage. The radial shrinkage defect can be rescued with dex-1 cDNA driven by its endogenous promoter (n = 60 per genotype pooled from three trials). **** indicates statistical significance at P < Error bars indicate SEM. (B) Dose-response survival assay to SDS. dex-1 dauers are sensitive to SDS compared to wild-type dauers, but are able to survive low levels of SDS exposure. Nondauer animals are sensitive at all tested SDS concentrations (n = 60 per treatment and dose pooled from three independent trials). Error bars indicate SEM from three independent trials. (C) dex-1 gene schematic. DEX-1 contains two nidogen-like domains, a single epidermal growth factor-like domain, a low-complexity domain previously predicted to have similarity to zonadhesin, and a transmembrane domain. The cs201 mutant allele is a point mutation at the exon 4 splice donor. The previously isolated ns42 mutation truncates the DEX-1 protein in its predicted zonadhesin-like domain. Bar, 1 kb. (D) Percent survival of dauers at 0.1% SDS. The dex-1 SDS sensitivity phenotype is partially rescued by the endogenous dex-1 promoter and DEX-1 cDNA (pMH7) (n = 60 per genotype pooled from three independent trials). Error bars indicate 95% confidence intervals. Nonoverlapping confidence intervals were considered significantly different (*).
Kristen M. Flatt et al. Genetics 2018;211:
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