Cellular & Molecular Medicine

Working at the nexus of functional genomics, computational biology, and cellular biology, our group is both experimental and computational. We develop novel single-cell genomic technologies and apply them to better understand lung development and disease.

I am investigating a human connective tissue disorder in mice. I am also investigating the role of gut bacteria in colon cancer risk in both a mouse model of colon cancer and in humans with colon cancer.

Our research is focused on elucidating the structure and function of titin and nebulin, two large filamentous proteins found in muscle. We use a range of model systems with a major focus on KO and TG mouse models. The techniques that we use range from single molecule mechanics, (immuno) electron microscopy, exon microarray analysis, in vitro motility assays, low angle X-ray diffraction, cell physiology (including calcium imaging), muscle mechanics, and isolated heart physiology.

The research in my laboratory is focused on identifying the components and molecular mechanisms regulating actin architecture in cardiac and skeletal muscle during normal development and disease. Control of actin filament lengths and dynamics is important for cell motility and architecture and is regulated in part by capping proteins that block elongation and depolymerization at both the fast-growing (barbed) and slow-growing (pointed) ends of the filaments.

The long-term goal of research in my lab is to understand the molecular mechanisms of muscle contraction. I am especially interested in how contractile proteins of muscle sarcomeres regulate the force and speed of contraction in the heart. The question is important from both basic science and clinical perspectives because mutations in sarcomere proteins of muscle are a leading cause of hypertrophic cardiomyopathy (HCM), the most common cause of sudden cardiac death in the young and a prevalent cause of heart failure in adults. Myosin binding protein-C (MyBP-C) is a muscle regulatory protein that speeds actomyosin cycling kinetics in response to adrenaline (b-adrenergic stimuli) and is one of the two most commonly affected proteins linked to HCM. Currently, the major research focus in my lab is understanding the mechanisms by which cMyBP-C regulates contractile speed and mechanisms by which mutations in cMyBP-C cause disease.

We are interested in the effects of early life exposures to environmental toxicants on lung growth and development. We determine if the early life exposures leads to adult disease.

Julie Ledford's research focuses on respiratory disease, and genetic and molecular mechanisms of allergic airway diseases in children.

My laboratory aims to identify the genetic and environmental reasons that certain individuals are predisposed to develop complex diseases like heart disease. We use new technologies, experimental, and computational approaches to identify molecular patterns indicative of disease predisposition.

We combine chemical and computer vision approaches to discover how regenerative tissues process environmental information to promote accurate cell fate decisions and prevent uncontrolled cell growth.