Abstract
The importance of c-myc as a target of the Blimp-1 repressor has been studied in BCL-1 cells, in which Blimp-1 is sufficient to trigger terminal B-cell differentiation. Our data show that Blimp-1-dependent repression of c-myc is required for BCL-1 differentiation, since constitutive expression of c-Myc blocked differentiation. Furthermore, ectopic expression of cyclin E mimicked the effects of c-Myc on both proliferation and differentiation, indicating that the ability of c-Myc to drive proliferation is responsible for blocking BCL-1 differentiation. However, inhibition of c-Myc by a dominant negative form was not sufficient to drive BCL-1 differentiation. Thus, during Blimp-1-dependent plasma cell differentiation, repression of c-myc is necessary but not sufficient, demonstrating the existence of additional Blimp-1 target genes.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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B-Lymphocytes / cytology*
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Cell Differentiation
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Cyclin E / metabolism
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Cytokines / pharmacology
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Gene Expression Regulation
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Histocompatibility Antigens Class II / metabolism
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Immunoglobulin M / metabolism
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Membrane Glycoproteins / metabolism
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Models, Biological
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Mutation
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Plasma Cells / cytology
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Proteoglycans / metabolism
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Proto-Oncogene Proteins c-myc / genetics
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Proto-Oncogene Proteins c-myc / metabolism*
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RNA, Messenger / biosynthesis
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Repressor Proteins / metabolism*
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Syndecans
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Transcription Factors / genetics
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Transcription Factors / metabolism*
Substances
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Cyclin E
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Cytokines
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Histocompatibility Antigens Class II
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Immunoglobulin M
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Membrane Glycoproteins
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Proteoglycans
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Proto-Oncogene Proteins c-myc
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RNA, Messenger
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Repressor Proteins
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Syndecans
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Transcription Factors