Natural and hormonally induced incubation patch development was studied in the California quail, Lophortyx californicus. Defeathering of the patch in wild females began during late egg laying and reached a maximum level, as did histological aspects of patch formation (vascularization, epidermal hyperplasia, edema) during early incubation. The quail patch was not as edematous as is that of passerine birds. Caged females not allowed to incubate failed to develop fully defeathered patches. The skin of males with incubating mates exhibited some signs of patch development, and two out of the seven males collected with regressing testes had fully developed patches. In reproductively inactive quail of both sexes, neither diethylstilbestrol, estradiol-17β, nor progesterone had an effect on the ventral abdominal skin. Diethylstilbestrol plus progesterone caused defeathering in two of eight birds. Bioassay of the pituitaries of diethylstilbestrol-treated birds indicated that this hormone failed to cause patch formation, in contrast to the effectiveness of estrogen in passerine birds, either because it did not release prolactin from the pituitary or because endogenous prolactin levels were low at the time of the experiment. Prolactin alone caused epidermal hyperplasia, and when administered either with estrogen, testosterone or progesterone produced defeathering, epidermal hyperplasia, vascularization and edema. In breeding birds, progesterone caused defeathering but no histological responses, whereas prolactin caused complete incubation patch formation. It was concluded that the California quail is intermediate between most passerine birds and phalaropes in both incubation behavior and incubation patch physiology. © 1969.