Mechanism of the pleiotropic effects of the short‐ear mutant gene in the mouse

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Abstract
The recessive mutant gene short‐ear (se) reduces the rate of proliferation of precartilage cells, producing a skeleton of reduced size with numerous small defects. It also reduces the rate of proliferation of callus cells in healing bone fractures. In this study se was shown not to affect rate of regeneration of liver, thymus, or connective tissue.Short‐eared mice have many anatomical abnormalities of the soft tissues including medial displacement of the left gonad, ventral displacement of the right renal artery, hydroureter and hydronephrosis, giant cell granulomas on the ventral surface of the liver, and on some genetic backgrounds an increased frequency of cysts of the lungs. Young se/se mice often have neuromuscular waviness of the tail. In the heterozygous condition (+/se) the gene causes a slight reduction in skeletal size and a slight increase in frequency of hydroureter, liver lesions, lung cysts, and wavy tail. It was shown that the viscera appear to be crowded from the 11‐day stage of gestation and that crowding is probably responsible for the abnormalities of the left gonad, the right renal artery, and the ureter, and is possibly a contributing cause of the granulomas of the liver. The probable cause of the crowding is the slower growth of the skeleton, resulting in a body cavity too small to accommodate the visceral mass of normal size. It is not clear that crowding is a sufficient explanation of the liver lesions or that it explains the effect of se on frequency of lung cysts or on waviness of the tail.