Parturition at term, the end stage of a successful pregnancy, occurs as a result of powerful, co-ordinated and periodic contractions of uterine smooth muscle (myometrium). To occur in a propitious manner, a high degree of control over the activation of a myometrial cell is required. We review the molecular mechanisms and structural composition of myometrial cells that may contribute to their increased contractile capacity at term. We focus attention on pathways that lead to the activation of filamentous networks traditionally labeled 'contractile' or 'cytoskeletal' yet draw attention to the fact that functional discrimination between these systems is not absolute.