Abstract
Endogenous induction of the galactose operon in galactokinaseless mutants of E. coli K12 has been examined. It has been found that this pleiotropic phenomenon depends not only on a defective galactoklnase, but also on additional factors. An unimpaired UDP-glucose/UDP-galactose pathway is a prerequisite for the formation of endogenous inducer. This is borne out by the fact that galactokln-aseless mutants with an additional defect of either UDPG pyrophosphorylase or UDPGal-4-epimerase lose their constitutivity of the galactose operon. An efficient retention mechanism for the endogenous inducer seems also to be of importance in the manifestation of endogenous induction.