Calbindin D 9k knockout mice are indistinguishable from wild-type mice in phenotype and serum calcium level

Abstract
Since the discovery of calbindin D9k, its role in intestinal calcium absorption has remained unsettled. Further, a wide distribution of calbindin D9k among tissues has argued for its biological importance. We discovered a frameshift deletion in the calbindin D9k gene in an ES cell line, E14.1, that originated from 129/OlaHsd mice. We produced mice with the mutant calbindin D9k gene by injecting the E14.1 ES cell subline into the C57BL/6 host blastocysts and proved that these mice lack calbindin D9k protein. Calbindin D9k knockout mice were indistinguishable from wild-type mice in phenotype, were able to reproduce, and had normal serum calcium levels. Thus, calbindin D9k is not required for viability, reproduction, or calcium homeostasis.