In the Schock lab, we are developmental biologists with a passion for pursing both basic science and translational research.

My lab uses multiple developmental model organisms (frog and mouse) to investigate:

1) How neural crest cells, the progenitors of the facial skeleton, make cell fate decisions

2) Develop animal models for human craniofacial syndromes

We hope that our discoveries in both of these areas can lead to improved outcomes for patients with craniofacial syndromes. 

Neural crest cells are one of the most fascinating cell types in the embryo. They are an ectodermal cell population that can give rise cell types associated with both the ectoderm (pigment cells, peripheral neurons/glia) and the mesoderm (bone, cartilage, smooth muscle). Due to the vast number of derivatives with diverse functions, neural crest cells are an excellent cell type to study how transcription factors direct cell fate decisions. We are specifically interested in dissecting roles for SoxE factors during this process. 

SoxE transcription factors (Sox 9 and Sox10) are essential for neural crest cell formation and differentiation. While Sox9 and Sox10 function redundantly during neural crest cell formation, they take on distinct roles as neural crest differentiate into different lineages. Sox9 directs neural crest cells to become cartilage cells while Sox10 coordinates the formation of melanocytes (pigment cells) and peripheral glia. The Schock lab is interested in understanding how transcription factors from the same subfamily, with highly similar DNA binding domains, direct differentiation of the same cell type into different lineages. We are pursuing answers to these questions in Xenopus. 

Animal models provide significant insights into human disease, including understanding syndromes with craniofacial abnormalities. A major limitation of traditional applications of model system studies, however, is that they fail to capture the complexity of human disease, as syndromic phenotypes vary from patient-to-patient. Current approaches to understanding disease include gain- and loss-of-function studies for causative genes, but often such studies are too broad, failing to make strong efforts into understanding specific genotype-phenotype correlations.

In the Schock lab, we will utilize multiple model organisms (Xenopusand mice) to investigate patient specific-variants associated with congenital craniofacial syndromes. Xenopus are an excellent and inexpensive model system for rapidly screening genes of interest and for assaying how patient-specific variants impact formation of the face. We use Xenopus to validate genes that recapitulate patient phenotypes and aggressively investigate gene function during development. Once we have validated a patient variant as being causative for a syndrome, we develop a parallel mouse model where we study how amniote-specific aspects of craniofacial development, including facial patterning, signaling center establishment, and development of amniote-specific craniofacial structures (ex. palate) are impacted by a patient variant.