Calcium signaling is known to play a critical role in cell migration (Ridley et al., 2003; Wei et al., 2012). In C. elegans, embryos with disruptions in the secretory pathway calcium ATPase gene
pmr-1 show defects in cell migration that result in lethal phenotypes. Previous work has shown that
pmr-1(lof) phenotypes can be suppressed by changes in the activity of the calcium channels IP3-receptor/ITR-1 and ryanodine receptor/UNC-68, indicating that cell migration defects are the results of changes in calcium homeostasis (Praitis et al., 2013). To identify additional genes important for cell migration during embryogenesis, we performed a genetic screen to isolate additional suppressors of the
pmr-1(
ru5) strain, reasoning that disruption of cell migration due to changes in
pmr-1 activity could be suppressed by commensurate changes in other genes that regulate calcium levels or signaling. In this screen, we identified the
kez8 allele. We confirmed that the
kez8 allele suppresses the
pmr-1(
ru5) mutant phenotype by examining the percentage of viable progeny produced by
pmr-1(
ru5);
kez8 strains when grown under restrictive conditions. The viability of the
pmr-1(
ru5);
kez8 strain is 67%, significantly higher than the 3.9% viability observed in the
pmr-1(
ru5) control strain at 25C (Table 1; p<0.01).