Familial hypertrophic cardiomyopathy related E180G mutation increases flexibility of human cardiac α-tropomyosin

► First direct probe AFM imaging of single molecules of E180G mutant tropomyosin. ► E180G mutation markedly reduces persistence length, implying increased flexibility. ► Mutant persistence length is less than the length of a tropomyosin molecule. ► Flexibility implies spatial gradient of partial activation within one regulatory unit. ► Increased flexibility explains many aspects of altered cardiac dysfunction.