  Living cells move thanks to assemblies of actin filaments and myosin motors
that range from very organized striated muscle tissue to disordered
intracellular bundles. The mechanisms powering these disordered structures are
debated, and all models studied so far predict that they are contractile. We
reexamine this prediction through a theoretical treatment of the interplay of
three well-characterized internal dynamical processes in actomyosin bundles:
actin treadmilling, the attachement-detachment dynamics of myosin and that of
crosslinking proteins. We show that these processes enable an extensive control
of the bundle's active mechanics, including reversals of the filaments'
apparent velocities and the possibility of generating extension instead of
contraction. These effects offer a new perspective on well-studied in vivo
systems, as well as a robust criterion to experimentally elucidate the
underpinnings of actomyosin activity.
