pmr-1 encodes a Secretory Protein Calcium ATPase required for migration of cells on the embryo surface in C. elegans (Praitis, et al 2013). To identify other genes involved in cell migration, we carried out an RNAi suppressor screen. We found that
bli-4(RNAi) significantly suppresses embryonic lethality in pmr-(
ru5) mutant lines. BLI-4 is a calcium-dependent proprotein convertase gene that functions in cuticle development (Thacker, et al 2000). While we found neither
bli-4(
e937) nor
bli-4(RNAi) had embryonic phenotypes, Thacker, et al (2000), showed that
bli-4(
h520), which carries a genetic change that disrupts a predicted substrate binding site, is an embryonic lethal allele. When we examined
bli-4(
h520) embryos, we found phenotypes, including displaced cells, that were similar to
pmr-1(
ru5) embryos. To further explore the genetic interaction between the genes, we crossed the
pmr-1(
ru5) into an sDp2 balanced
bli-4(
h520) line. The sDp2 balanced
bli-4(
h520) and
pmr-1(
ru5) double mutant line showed slight, but not significantly increased viability compared to the single mutant lines. While both
pmr-1(
ru5) and
bli-4(
h520) are embryonic lethal alleles, we obtained sick but viable individuals homozygous for both alleles that had lost sDp2, confirming an interaction between the two genes. To better understand how the two genes interact, we examined
bli-4 expression patterns in embryos. Fluorescence studies showed
bli-4::GFP is expressed in leading cells during enclosure and in several other unidentified cells. We utilized the Packer, et al (2019) embryonic transcriptome database to examine the endogenous expression of
bli-4 RNA in developing embryos. While we did not observe significant changes in gene expression in cells undergoing surface migrations, we discovered that
bli-4 is upregulated in many of these lineages once migration events are complete. Our current model is that
pmr-1 activity is critical for migratory behavior and that
bli-4 expression may be important for the transition of cells from migratory to epithelial. Because defects in
pmr-1 reduce migration rates, delays in the migratory-to-epithelial transition caused by disruption of
bli-4 could permit additional time for cells to be properly positioned during embryogenesis resulting in restored viability.