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Bone marrow-induced Mef2c deficiency delays B cell development and alters the expression of key B cell regulatory proteins

ABSTRACT: The Mef2 family transcriptional regulator Mef2c is highly expressed in maturing bone marrow and peripheral mature B cells. To evaluate the role of this transcription factor in B cell development, we generated a B cell specific conditional deletion of Mef2c using the Mb-1-Cre transgene that is expressed during the early stages of immunoglobulin rearrangement. Young mice possessing this defect demonstrated a significant impairment in B cell numbers in bone marrow and spleen. This phenotype was evident in all B cell subsets; however, as the animals mature, the deficit in the peripheral mature B cell compartments was overcome. The absence of Mef2c in mature B cells led to unique CD23+ and CD23- subsets that were evident in Mef2c KO primary samples as well as cultured, differentiated B cells but not in WT cell populations. Genome wide expression analysis of immature and mature B cells lacking Mef2c indicated altered expression for a number of key regulatory proteins for B cell function including Ciita, CD23, Cr1/Cr2, and Tnfsf4. Chromatin immunoprecipitation analysis confirmed Mef2c binding to the promoters of these genes indicating a direct link between the presence (or absence) of Mef2c and altered transcriptional control in mature B cells. Four samples are submitted.

ORGANISM(S): Mus musculus

SUBMITTER: John Weis

PROVIDER: E-GEOD-34210 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Bone marrow-induced Mef2c deficiency delays B cell development and alters the expression of key B cell regulatory proteins

Project description:The Mef2 family transcriptional regulator Mef2c is highly expressed in maturing bone marrow and peripheral mature B cells. To evaluate the role of this transcription factor in B cell development, we generated a B cell specific conditional deletion of Mef2c using the Mb-1-Cre transgene that is expressed during the early stages of immunoglobulin rearrangement. Young mice possessing this defect demonstrated a significant impairment in B cell numbers in bone marrow and spleen. This phenotype was evident in all B cell subsets; however, as the animals mature, the deficit in the peripheral mature B cell compartments was overcome. The absence of Mef2c in mature B cells led to unique CD23+ and CD23- subsets that were evident in Mef2c KO primary samples as well as cultured, differentiated B cells but not in WT cell populations. Genome wide expression analysis of immature and mature B cells lacking Mef2c indicated altered expression for a number of key regulatory proteins for B cell function including Ciita, CD23, Cr1/Cr2, and Tnfsf4. Chromatin immunoprecipitation analysis confirmed Mef2c binding to the promoters of these genes indicating a direct link between the presence (or absence) of Mef2c and altered transcriptional control in mature B cells.

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