Fromthe ‡ SectionofCardiovascularBiology,DepartmentofBiochemistry,UniversityofCambridge,DowningSite, Cambridge,CB21QW,UnitedKingdom,the § DivisionofCellandMolecularBiology,SirAlexanderFlemmingBuilding,Imperial College,SouthKensingtonCampus,LondonSW72AZ,UnitedKingdom,theDepartmentofPhysiology,DevelopmentandNeuroscience, UniversityofCambridge,DowningSite,CambridgeCB23EG,UnitedKingdom,andthe NationalHeartandLungInstitute, SirAlexanderFlemmingBuilding,ImperialCollege,SouthKensingtonCampus,London, SW7 2AZ, United Kingdom

To study the function of the Kruppel-like transcription factor KLF13 in vivo, we generated mice with a disrupted Klf13 allele. Although Klf13 / mice are viable, fewer mice were present at 3 weeks than predicted by Mendelian inheritance. Viable Klf13 / mice had reduced numbers of circulating erythrocytes and a larger spleen. The spleen contained an increased number of Ter119 med CD71 hi , Ter119 hi CD71 hi , and Ter119 hi CD71 med cells but not Ter119 hi CD71 cells, indicating an increase in less mature erythroblasts. A higher proportion of the Ter119 med CD71 hi cells were proliferating, indicating that the mice were under a degree of erythropoietic stress. These data indicate that KLF13 is involved in the normal control of erythropoiesis.