Effects of the flexed‐tailed gene on the development of the house mouse

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Abstract
The flexures in the flexed‐tailed mouse consist of unilateral fusions of adjacent vertebrae. Fusions, if complete, produce straight stiff segments.In normal mouse embryogeny, the precartilage cells surrounding the developing nucleus pulposus of the embryonic intervertebral disk in the proximal tail region begin to elongate and become fiber‐like at about 14 days after fertilization. In the flexed mouse, such differentiation fails to take place on one side of an affected disk, and these cells develop through cartilage to bone. At such a point there is frequently a bend in the notochordal axis. Other abnormalities of the notochord have been observed. These are not the cause of the flexures.The gene for flexed tail also produces two effects more general in their expression. First, it slows the growth of the vertebral column as indicated by the shorter vertebrae of the proximal tail region. This is observable 13 days after fertilization. Second, it produces an embryonic anemia which is already in existence at 14 days after fertilization. It is postulated that the flexures are due to the retardation of growth at a time which is critical for the intervertebral disks. Whether this retardation is the primary effect of the gene and produces the anemia, or whether the anemia is primary and produces the retardation, the data do not show.