Submitted by Administrator on Thu, 18/05/2017 - 14:19
Dr Folma Buss and others have identified a new role for myosin VI in the construction and maintenance of gap junctions between cardiomyocytes.
Cardiac function depends on the precise transmission of electrical activity throughout the heart muscle, and disturbances to this highly coordinated process are the hallmark of acquired heart disease. Gap junctions are cell membrane -spanning channels that aid the coordinated transmission of action potential by coupling neighboring cardiomyocytes electrochemically. The basic subunit of the gap junction is the connexin, and connexin 43 is the primary gap junction-forming protein in the ventricular myocardium.
Disturbance of connexin 43 and the gap junctions has been observed in pathological states, including idiopathic dilated cardiomyopathy, hypertrophy and acute cardiac ischemia.
This study has confirmed that myosin VI localises to the gap junctions in cardiomyocytes. The study also found that the loss of myosin VI leads to the reduction in gap junction size, which in turn results in reduced intercellular communication. The reduction in gap junction size was due to impaired gap junction plaque growth.
This work was published by the Journal of Cell Science and can be read here.
