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Regulation of promoter and intron enhancer activity in immunoglobulin heavy-chain genes during B-cell differentiation
1Division of Molecular Immunology, Research Institute for Biological Sciences, Science University of Tokyo, Chiba, Japan.
Chloramphenicol acetyltransferase (CAT) transgenic mice, in which the transgene is regulated by the VH promoter and heavy-chain intron enhancer (E mu), were examined to investigate the variation of activity of these cis-acting elements during the late stage of B-cell development. CAT enzyme activity decreased when resting B cells were stimulated through B-cell receptors (BCR) with goat anti-mouse IgM antibodies in vitro. On the other hand, when these B cells were stimulated by lipopolysaccharide (LPS) in vitro, they showed enhanced CAT activity, accompanied by an increase in the number of CD43+ B220+ cells (pro-plasma and plasma cells). In addition, the CAT activities in CD43+ B220+ and PNAhi B220+ cells from immunized mice were higher than those in CD43- B220+ and PNAlo B220+ cells, respectively. These results suggest that the activity of E mu in the context of VH promoter was transiently down-regulated by stimulation through the BCR but enhanced at the pro-plasma and plasma stages.
Chloramphenicol acetyltransferase (CAT) transgenic mice, in which the transgene is regulated by the VH promoter and heavy-chain intron enhancer (E mu), were examined to investigate the variation of activity of these cis-acting elements during the late stage of B-cell development. CAT enzyme activity decreased when resting B cells were stimulated through B-cell receptors (BCR) with goat anti-mouse IgM antibodies in vitro. On the other hand, when these B cells were stimulated by lipopolysaccharide (LPS) in vitro, they showed enhanced CAT activity, accompanied by an increase in the number of CD43+ B220+ cells (pro-plasma and plasma cells). In addition, the CAT activities in CD43+ B220+ and PNAhi B220+ cells from immunized mice were higher than those in CD43- B220+ and PNAlo B220+ cells, respectively. These results suggest that the activity of E mu in the context of VH promoter was transiently down-regulated by stimulation through the BCR but enhanced at the pro-plasma and plasma stages.