Christopher Yengo, MS, PhD

Chris Yengo’s laboratory is focused on investigating mechanisms of actomyosin-based motility including muscle contraction, intracellular transport, and cytoskeletal dynamics. The Yengo lab strives to understand how impairments in actomyosin based contractility/motility play a role in the pathogenesis of disease and design therapies that directly mediate actomyosin function.

There are currently three areas of focus in the lab.

Examining the conserved mechanism of actomyosin-based force generation. The lab has contributed significantly to our understanding of the conserved fundamental mechanisms underlying mechanical and biochemical coupling in myosin, a long-standing question in the field. We plan to utilize our biophysical approaches to develop novel small molecule allosteric regulators of myosin function.

Investigating the impact of disease mutations associated with contractile defects in cardiac, skeletal, and smooth muscle. A main focus of our work over the past 10 years has been on defining the molecular basis of inherited cardiomyopathies which is a major cause of heart failure and the leading cause of sudden death in young athletes. Our work has provided crucial information about the molecular basis of disease pathogenesis and the impact of therapeutic drugs. We have plans to extend our approach to studies of skeletal and smooth muscle myosin mutations associated with skeletal myopathies and aortic aneurysm, respectively.

Examining the role of class III myosins in progressive hearing loss. The stereocilia of inner ear hair cells function as mechanosensors of the auditory and vestibular system. Class III myosins (MYO3A and MYO3B) are critical for determining the length, width, and stability of stereocilia and mutations in MYO3A are associated with non-syndromic deafness. Our long-term goals are to determine role of myosins in the stereocilia and develop specific allosteric regulators that can serve as therapies for progressive hearing loss.