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Journal Article

The BTG2-PRMT1 module limits pre-B cell expansion by regulating the CDK4-Cyclin-D3 complex

MPS-Authors

Börsig,  Theresa
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Reth,  Michael
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;
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Citation

Dolezal, E., Infantino, S., Drepper, F., Börsig, T., Singh, A., Wossning, T., et al. (2017). The BTG2-PRMT1 module limits pre-B cell expansion by regulating the CDK4-Cyclin-D3 complex. Nature Immunology, 18, 911-920. doi:10.1038/ni.3774.


Cite as: https://hdl.handle.net/11858/00-001M-0000-002E-85AA-B
Abstract
Developing pre-B cells in the bone marrow alternate between proliferation and differentiation phases. We found that protein arginine methyl transferase 1 (PRMT1) and B cell translocation gene 2 (BTG2) are critical components of the pre-B cell differentiation program. The BTG2-PRMT1 module induced a cell-cycle arrest of pre-B cells that was accompanied by re-expression of Rag1 and Rag2 and the onset of immunoglobulin light chain gene rearrangements. We found that PRMT1 methylated cyclin-dependent kinase 4 (CDK4), thereby preventing the formation of a CDK4-Cyclin-D3 complex and cell cycle progression. Moreover, BTG2 in concert with PRMT1 efficiently blocked the proliferation of BCR-ABL1-transformed pre-B cells in vitro and in vivo. Our results identify a key molecular mechanism by which the BTG2-PRMT1 module regulates pre-B cell differ-entiation and inhibits pre-B cell leuke-mogenesis.