Generation and characterization of genetically-altered mice lacking a novel vitamin K2 synthesis enzyme Ubiad1

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It was demonstrated that tissue vitamin K2 originates from oral vitamin K1 by a mechanism that involves the release of vitamin K3 from vitamin K1 in the intestine followed by delivery of vitamin K3 through the mesenteric lymphatic system and blood circulation to tissues, and then reduced by an unknown redox enzyme in the tissues and converted into vitamin K2 by the prenylating enzyme Ubiad1. To investigate the function of ubiad1, we attempted to generate mice lacking Ubiad1 by gene targeting, but it was found that Ubiad1-deficient mouse embryos failed to survive beyond embryonic day 7.5. We have succeeded in generating hematopoietic and nerve tissue -specific, bone specific- or neuron-specific Ubiad1-deficient mice by intercrossing Ubiad1 flox/flox mice with Nestin-Cre expressing mice, Osterix-Cre expressing mice or Synapsin-Cre expressing mice.