A 3-week-old knockout mouse has shorter leg bones than a wild-type mouse. What deficiency likely caused this?

The deficiency that likely caused the shorter leg bones in the knockout mouse is related to Insulin-like growth factor I (IGF-I). IGF-I plays a crucial role in promoting growth and development during childhood and adolescence. It is primarily produced in the liver and is stimulated by growth hormone, and it functions by stimulating the growth of various tissues, including bone.

In the context of bone development, IGF-I promotes chondrocyte activity in the growth plates of bones, encouraging the proliferation and maturation of these cells, which are essential for longitudinal bone growth. A deficiency in IGF-I can lead to inadequate stimulation of these processes, resulting in shorter bones and dwarfism.

In knockout models where IGF-I is specifically absent or diminished, the growth plates may not function normally, leading to decreased longitudinal growth of the bones. This results in the observation of shorter leg bones, as described in the scenario.

The other options, while they play roles in body processes, do not directly correlate with this specific defect in bone growth as closely as IGF-I does. For example, calcitonin is involved in calcium homeostasis and bone remodeling but is not the primary regulator of growth. Cortisol has effects on metabolism and can influence bone density but would not