Abstract
Inherited quantitative aspects of the Rh blood-group system and susceptibility of Rh to the effects of independently segregating suppressor genes can be accounted for with a conjugated operon model. This assumes the existence of four operator or promotor (control) genes for these functions, while closely linked structural regions determine the qualitative characteristics of Rh antigens. Observed restriction of antigenic crossreactivity to the products of adjacent genetic regions and data from blood typing of nonhuman primates both suggest that Rh complexity arose from a series of gene duplications and independent mutations.