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MEF2C protects bone marrow B-lymphoid progenitors during stress haematopoiesis. | LitMetric

AI Article Synopsis

  • DNA double strand break (DSB) repair is vital for B-cell receptor formation, essential for B-cell survival, and MEF2C plays a key role in enhancing the expression of genes necessary for this repair process.
  • Mice lacking the Mef2c gene show a poor recovery of B-lymphoid cells after stress from radiation or chemotherapy, despite having normal B-cell levels under normal conditions.
  • MEF2C binds to active regions of the DNA that regulate DNA repair and B-cell development genes, and its absence leads to reduced accessibility of these regions, highlighting its protective role during stressful situations.

Article Abstract

DNA double strand break (DSB) repair is critical for generation of B-cell receptors, which are pre-requisite for B-cell progenitor survival. However, the transcription factors that promote DSB repair in B cells are not known. Here we show that MEF2C enhances the expression of DNA repair and recombination factors in B-cell progenitors, promoting DSB repair, V(D)J recombination and cell survival. Although Mef2c-deficient mice maintain relatively intact peripheral B-lymphoid cellularity during homeostasis, they exhibit poor B-lymphoid recovery after sub-lethal irradiation and 5-fluorouracil injection. MEF2C binds active regulatory regions with high-chromatin accessibility in DNA repair and V(D)J genes in both mouse B-cell progenitors and human B lymphoblasts. Loss of Mef2c in pre-B cells reduces chromatin accessibility in multiple regulatory regions of the MEF2C-activated genes. MEF2C therefore protects B lymphopoiesis during stress by ensuring proper expression of genes that encode DNA repair and B-cell factors.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4987520PMC
http://dx.doi.org/10.1038/ncomms12376DOI Listing

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