SATB1(Special A-T rich Binding protein 1)is a cell type-specific factor that regulates the genetic network in developing T cells and neurons.In T cells,SATB1 is required for lineage commitment,VDJ recombination,develo...SATB1(Special A-T rich Binding protein 1)is a cell type-specific factor that regulates the genetic network in developing T cells and neurons.In T cells,SATB1 is required for lineage commitment,VDJ recombination,development and maturation.Considering that its expression varies during B-cell differentiation,the involvement of SATB1 needs to be clarified in this lineage.Using a KO mouse model in which SATB1 was deleted from the pro-B-cell stage,we examined the consequences of SATB1 deletion in naive and activated B-cell subsets.Our model indicates first,unlike its essential function in T cells,that SATB1 is dispensable for B-cell development and the establishment of a broad IgH repertoire.Second,we show that SATB1 exhibits an ambivalent function in mature B cells,acting sequentially as a positive and negative regulator of Ig gene transcription in naive and activated cells,respectively.Third,our study indicates that the negative regulatory function of SATB1 in B cells extends to the germinal center response,in which this factor limits somatic hypermutation of Ig genes.展开更多
文摘SATB1(Special A-T rich Binding protein 1)is a cell type-specific factor that regulates the genetic network in developing T cells and neurons.In T cells,SATB1 is required for lineage commitment,VDJ recombination,development and maturation.Considering that its expression varies during B-cell differentiation,the involvement of SATB1 needs to be clarified in this lineage.Using a KO mouse model in which SATB1 was deleted from the pro-B-cell stage,we examined the consequences of SATB1 deletion in naive and activated B-cell subsets.Our model indicates first,unlike its essential function in T cells,that SATB1 is dispensable for B-cell development and the establishment of a broad IgH repertoire.Second,we show that SATB1 exhibits an ambivalent function in mature B cells,acting sequentially as a positive and negative regulator of Ig gene transcription in naive and activated cells,respectively.Third,our study indicates that the negative regulatory function of SATB1 in B cells extends to the germinal center response,in which this factor limits somatic hypermutation of Ig genes.
