The laboratory of Dr. Christopher Yengo studies molecular motor and cytoskeletal proteins and their role in human disease. The lab is currently focused on myosin motors and the actin cytoskeleton. Biochemical, biophysical, and cell biological approaches are utilized to investigate basic molecular mechanisms of motor-based transport, contraction and organization of the actin cytoskeleton. In the long term, the Yengo lab hopes to develop therapeutic strategies for diseases that impact actomyosin-based functions.

The Yengo lab is studying inherited forms of heart disease caused by mutations in human beta-cardiac myosin, the molecular motor that drives contraction in the heart. The lab examines the impact of mutations and therapeutic drugs on the myosin ATPase mechanism, force generating properties and key structure-function relationships. A site-specific fluorescence labeling strategy was initially designed in myosin V and has allowed examination of how mutations disrupt important structural changes in the cardiac myosin ATPase cycle and how therapeutic drugs can reverse these effects. Other forms of heart failure are also being investigated, including diabetic and alcohol cardiomyopathy. 

The Yengo lab is investigating the role of class III myosins in the formation and maintenance of actin based protrusions, such as filopodia, microvilli and stereocilia. There are two isoforms of class III myosins, Myo3A and Myo3B, encoded by separate genes. Class III myosins are unique in that they contain an N-terminal kinase domain, and Myo3A harbors point mutations associated with delayed onset deafness. The Yengo lab is investigating the role of class III myosins in the length maintenance of inner ear hair cell stereocilia as well motor transport within the stereocilia. The impact of the disease mutations on the regulation and function of Myo3A and the ability of Myo3B to compensate for the lack of Myo3A function is under investigation.