- page settings
- showhide sidebar
- showhide empty fields
- layout
- (too narrow)
- open all
- close all
- Page Content
- Overview
- External Links
- History
- Referenced
- Tools
- Tree Display
- My WormBase
- My Favorites
- My Library
- Recent Activity
- Comments (0)
history logging is off
Tree Display
My Favorites
My Library
Overview
Thurman, Michellie, Sun, Haonan, Kubica, Sam, & Praitis, Vida (2021). The slo-1 BK potassium channel interacts genetically with pmr-1 secretory pathway calcium ATPase during C. elegans embryonic cell migration. MicroPubl Biol. doi:10.17912/micropub.biology.000351
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).
