Studies on the mechanisms of histidase development in rat skin and liver. I. Basis for tissue specific developmental changes in catalytic activity.

Skin and liver histidases of the rat follow markedly differing developmental courses. In skin, the enzyme activity emerges in late fetal life, rises to a maximum during the first postnatal week and then declines; in liver, histidase activity initially appears in the neonatal period and progressively rises thereafter. The enzymes in both tissues, however, are immunologically identical, as demonstrated by Ouchterlony double diffusion, immunoelectrophoresis, and immunotitration analyses of histidase in adult animals. Furthermore, although crude preparations of skin and liver histidase differ slightly in electrophoretic mobility on acrylamide gels, the isoelectric points and Michaelis constants of the enzyme from both skin and liver are the same. During development neither dissociable activators nor inhibitors of the enzyme are evident, which might account for the divergent developmental patterns, nor are enzyme inhibitors found in tissues devoid of histidase activity. No immunologically cross-reacting materials are detectable in skin and liver at developmental stages prior to the emergence of enzyme activity, nor in tissues not expressing histidase catalytic activity. Furthermore, there is no evidence of elaboration of immunological variants of histidase in skin and liver during development. These data are compatible with the view that all developmental changes in catalytic activity are due to altered amounts of the same enzyme antigen.