Establishing Caenorhabditis elegans as a model for neural tube defects
Chelle King Porter♦
Dr. Timothy Walston, Dr. Jon Beck, and Dr. Brent Buckner, Faculty Mentors
In C. elegans, one of the major morphogenetic events is the development of the hypodermis of the embryo. In vertebrates, failure of similar cell migrations often results in neural tube defects (NTDs), such as spina bifida. NTDs increase when a pregnant woman is exposed to ethanol or valproic acid early in pregnancy. NTDs decrease when pregnant women have high levels of folic acid. The effects of folic acid, valproic acid, and ethanol on embryonic lethality and hypodermal morphogenesis in C. elegans were examined to establiC. elegans as a model for NTDs using axenic media, a folate transporter mutant, RNA interference, and folate-deficient E. coli. Removal of folic acid has been challenging and unsuccessful, despite various experimental techniques. Results from this study suggest that valproic acid and ethanol cause an increase in embryonic lethality and that C. elegans embryos are susceptible to similar environmental toxins as human embryos. These results will help us explore and better understand how NTDs arise in human embryos.
Keywords: C. elegans, valproic acid, folate, ethanol, spina bifida, NTD, model, axenic
Topic(s):Biology
Presentation Type: Oral Paper
Session: 47-1
Location: MG 2001
Time: 1:15