Research Interests

Congenital anomalies affect about 1% of all live births, with nearly one‑third involving the craniofacial complex. Central to forming these structures are neural crest cells (NCCs), a migratory, multipotent population that gives rise to craniofacial bone, cartilage, connective tissue, pigment cells, and components of the peripheral nervous system. Disruptions in NCC induction, migration, or differentiation can lead to a broad range of craniofacial, cardiac, and enteric nervous system defects, making it essential to understand the mechanisms that guide their development.

During embryogenesis and early childhood, the craniofacial skeleton changes rapidly to accommodate the growth of the brain, eyes, and airway. At The Dash Lab, we investigate the cellular, molecular, and genetic pathways that shape craniofacial development. By integrating developmental biology, genetics, and advanced imaging, we aim to uncover how the face forms, and why it sometimes goes awry.

Neural crest cells are multipotent population responsible for building much of the face and skull, including neurons of the peripheral nervous system and cartilage and bone of the head and face the . By uncovering how these cells form, migrate, and interact with surrounding tissues, and how their disruption leads to congenital anomalies, we aim to illuminate the biological pathways that underlie pediatric craniofacial disorders.

Disease Context - Craniofacial Anomalies

Craniofacial anomalies are among the most visible and medically complex congenital conditions, affecting a child’s breathing, feeding, speech, vision, and neurological development from the earliest stages of life. Beyond the immediate medical concerns, these conditions often require multiple surgeries, long-term therapies, and continuous monitoring throughout childhood. The physical, emotional, and social challenges can be profound, for both children and their families, making early diagnosis, improved treatment strategies, and a deeper understanding of the root causes essential.

At The Dash Lab, we work to address these challenges at their foundation. Our research focuses on the cellular, molecular, and genetic mechanisms that guide craniofacial development. Through developmental biology, advanced imaging, and genetic approaches, our work strives to inform the next generation of diagnostic and therapeutic strategies. Ultimately, our goal is to contribute scientific insights that help reduce the burden on affected children and improve long-term clinical outcomes.

Cellular Context - Neural Crest Cells and their Distinct Lineages

Neural Crest cells are multipotent population responsible for building much of the face and skull, including neurons and glia of the peripheral nervous system as well as cartilage and bone in the head and face. By uncovering how these cells form, migrate, and interact with surrounding tissues, and how their disruption leads to congenital anomalies, we aim to illuminate the biological pathways that underlie pediatric craniofacial disorders.

Tissue Context - How Neural Crest Cells Interact with their surrounding Cells?

Neural crest cells do not develop in isolation, they rely on constant communication with the tissues they encounter as they migrate and differentiate. Signals from the neuroepithelium, mesoderm, endoderm, vasculature, and extracellular matrix guide their movement, shape their fate decisions, and ensure the coordinated formation of craniofacial structures. Disruptions to any of these interactions can profoundly alter development, leading to congenital craniofacial anomalies.

In The Dash Lab, we investigate these critical tissue–tissue interactions to understand how neural crest cells interpret and respond to cues from their environment. By examining how neighboring tissues influence neural crest behavior—at cellular, molecular, and genetic levels—we aim to uncover the mechanisms that drive normal craniofacial development and how breakdowns in these communication systems contribute to disease.

Molecular Context - The Mediator Complex

The Mediator complex is a highly conserved, multi‑subunit regulator that serves as a critical bridge between transcription factors and RNA polymerase II, ensuring that genes are activated at the right time and place during development. Its modular structure, comprising head, middle, tail, and kinase domains, allows different subunits to fine‑tune transcriptional responses in a cell‑type– and context‑specific manner. Disruptions to individual Mediator subunits have been increasingly linked to human developmental disorders, including craniofacial anomalies, highlighting its essential role in coordinating gene expression programs during embryogenesis.

In The Dash Lab, we investigate how specific Mediator subunits, such as Med23 and Med24, regulate neural crest cell behavior and craniofacial development. By integrating genetics, imaging, and functional assays in model organisms, we aim to uncover how perturbations in Mediator‑dependent transcription lead to defects in cell fate, migration, and tissue–tissue interactions. Our goal is to define the transcriptional networks governed by Mediator that are fundamental to building the face.