The L14 lectin is a 14 × 10(3) M(r) carbohydrate binding protein belonging to the family of S-type lectins. The pattern of expression of this protein during mouse embryogenesis suggests that it may have multiple roles during pre- and post-implantation development. Using the technique of homologous recombination in embryonic stem cells, we have introduced a null mutation in the gene encoding the L14 lectin and generated a strain of mice carrying the mutant allele. We report here that homozygous mutant animals that lack the L14 lectin develop normally and are viable and fertile. The absence of any major phenotypic abnormalities in these mutant animals suggests that other protein(s) potentially compensate for the absence of the L14 lectin. Here we show that a related protein termed L30, a lectin that has carbohydrate binding specificity similar to that of L14, is present in the same embryonic cell populations as L14 at the time of implantation, suggesting that the two S-type lectins may be capable of functional substitution at this early stage of embryogenesis.