Loss of sphingomyelin synthase-1 does not cause egg retention or locomotion defects in Caenorhabditis elegans

Abstract

Sphingomyelin is a critical sphingolipid found in plasma membranes of metazoa that provides structural and communicative functions. Sphingomyelin synthases are key enzymes that generate sphingomyelin but their precise functions in animal development and function are not fully understood. The Caenorhabditis elegans model encodes five sphingomyelin synthases (sms-1-5). Previously, egg-laying and locomotion phenotypes were observed in an sms-1(ok2399) deletion mutant. In this study, we attempted to replicate these findings to enable mechanistic dissection of sphingomyelin function. We indeed found that the sms-1(ok2399) mutant exhibited egg-laying and locomotion defects, however, we were unable to rescue this phenotype. Further, we generated two additional sms-1 deletion mutants (rp398 and rp399) and found that their egg-laying and locomotion behavior is not different to wild-type animals. We suggest that the sms-1(ok2399) contains a background mutation that causes behavioral deficits, and that SMS-1 loss does not overtly affect C. elegans egg-laying or locomotion.