Long before you were aware of anything or anyone even realized you were under construction, things were happening that determined critical features of your life.
In the earliest hours of your embryonic status, cells were developing and multiplying, critical processes were starting up, networks were connecting and genetic codes — for better or worse — were directing the whole project.
That early development is the focus of the research University of Delaware biologist Shuo Wei pursues. Wei, associate professor of biological sciences, looks specifically at how problems in cellular signal relays affect these processes and cause birth defects.
Now Wei’s research has won more than $1.8 million in support from the National Institutes of Health for his study of genetic mutations that can disrupt proper development of neural crest stem cells in embryos.
Neural crest stem cells are “multipotent” stem cells, which means several kinds of tissues develop from these cells, including skull and facial structures, heart tissue, pigment cells and the peripheral nervous system.
When something goes wrong with the neural crest, birth defects are the result, including some of the most common known in humans.
Wei’s lab is focusing on the DDX3X gene and related genes and the roles they play in neural crest development.
The significance of the DDX3X gene in developmental disorders is relatively new science, Wei said. One of his former doctoral students, Mark Perfetto, brought the gene to Wei’s attention about seven years ago when he saw a report in Science Magazine. He urged Wei to look into it because the authors described the influence of DDX3X on a cell signaling pathway known as “Wnt signaling,” a focus of Wei’s research. Many researchers are investigating Wnt (pronounced “wint”) signaling because of its critical role in embryonic development.
“Because Wnt signaling is critical for neural crest development, we hypothesized that mutating the DDX3X gene may cause neural crest defects,” Wei said.
They studied this mutation in frogs and found that all tadpoles that had this genetic mutation had severe neural crest defects, such as underdeveloped facial structures.