International Immunology, Vol. 11, No. 10, 1663-1671,
October 1999
© 1999 Japanese Society for Immunology
The CH1 and transmembrane domains of µ in the context of a 
2b transgene do not suffice to promote B cell maturation
1 Department of Molecular Genetics and Cell Biology, University of Chicago, Chicago, IL 60637, USA
2 Department of Comparative Medicine, University of Alabama at Birmingham, Birmingham, AL 35294-0019, USA
Correspondence to: U. Storb
Mice carrying a 
2b transgene have been shown previously to be deficient in B cell development. In particular, a developmental block exists at the pre-B cell stage. The few B cells that develop all express endogenous µ heavy chains. The phenotype suggests that 2b exerts a strong feedback inhibition on endogenous Ig gene rearrangement, but, unlike µ, cannot support further B cell development. In this study we have created hybrid transgenes between 2b and µ. Transgenic mice with a CH1 domain of µ, or both a CH1 and transmembrane/cytoplasmic domain of µ replacing the respective domains of a 2b transgene, have the same B cell defect as 2b transgenic mice. Interestingly, the severity of the defect is correlated with the level of expression of the transgene, suggesting that the degree of feedback inhibition of Ig gene rearrangement depends on the level and timing of Ig production. Crossing the 2b/µ transgenes into a Bcl-xL transgenic line allows immature 2b B cells to survive, but not to develop to maturity. Therefore, the missing function of µ is not simply an anti-apoptotic effect.
Keywords: B lymphocytes, bone marrow, gene rearrangement, mRNA, transgenic mice
3 Present address: Department of Comparative Medicine, University of Alabama at Birmingham, Birmingham, AL 35294-0019, USA