Perspective: embedded molecular switches, anticancer selection, and effects on ontogenetic rates: a hypothesis of developmental constraint on morphogenesis and evolution.

The switch between the cell cycle and the progress of differentiation in developmental pathways is prevalent throughout the eukaryotes in all major cell lineages. Disruptions to the molecular signals regulating the switch between proliferative and differentiating states are severe, often resulting in cancer formation (uncontrolled proliferation) or major developmental disorders. Uncontrolled proliferation and developmental disorders are potentially lethal defects in the developing animal. Therefore, natural selection would likely favor a tightly controlled regulatory mechanism to help prevent these fundamental defects. Although selection is usually thought of as a consequence of environmental or ecological influences, in this case the selective force to maintain this molecular switch is internal, manifested as a potentially lethal developmental defect. The morphogenetic consequences of this prevalent, deeply embedded, and tightly controlled mechanistic switch are currently unexplored, however experimental and correlative evidence from several sources suggest that there are important consequences on the control of growth rates and developmental rates in organs and in the whole animal. These observations lead one to consider the possibility of a developmental constraint on ontogenetic rates and morphological evolution maintained by natural selection against cancer and other embryonic lethal defects.