Recovery.gov - Track the Money

SOUTHERN ILLINOIS UNIVERSITY

Neural tube defects (such as anencephaly and Spina bifida) result from the embryonic failure of the neural tube to close followed by the outward expansion of the neural tissue. It is estimated that neural tube defects occur in 1 in 1,000 births in humans, and both environmental and genetic factors contribute to these complex disorders. We propose to study how a deficiency in a transcriptional regulator called DEAF-1 results in neural tube defects using a mouse model. We hypothesize that DEAF-1 protein is essential for neural tube closure through the transcriptional regulation of target genes and by interactions with protein partners controlling cell proliferation and cell death. To test this hypothesis, we will evaluate cellular proliferation, cell death, and potential alteration of DEAF-1 protein interactions or signaling partners during neural tube closure in the mouse embryo. We will also examine the effects of genotoxic stress on mouse embryo fibroblasts isolated from mouse embryos deficient in DEAF-1. The results of this study will give insight into how dysregulation and mutations in DEAF-1 may contribute to neural tube defects in humans.

Clarification of Codes