| First Author | Hong H | Year | 2022 |
| Journal | Cell Rep | Volume | 38 |
| Issue | 7 | Pages | 110386 |
| PubMed ID | 35172136 | Mgi Jnum | J:324794 |
| Mgi Id | MGI:6874535 | Doi | 10.1016/j.celrep.2022.110386 |
| Citation | Hong H, et al. (2022) Postnatal regulation of B-1a cell development and survival by the CIC-PER2-BHLHE41 axis. Cell Rep 38(7):110386 |
| abstractText | B-1 cell development mainly occurs via fetal and neonatal hematopoiesis and is suppressed in adult bone marrow hematopoiesis. However, little is known about the factors inhibiting B-1 cell development at the adult stage. We report that capicua (CIC) suppresses postnatal B-1a cell development and survival. CIC levels are high in B-1a cells and gradually increase in transitional B-1a (TrB-1a) cells with age. B-cell-specific Cic-null mice exhibit expansion of the B-1a cell population and a gradual increase in TrB-1a cell frequency with age but attenuated B-2 cell development. CIC deficiency enhances B cell receptor (BCR) signaling in transitional B cells and B-1a cell viability. Mechanistically, CIC-deficiency-mediated Per2 derepression upregulates Bhlhe41 levels by inhibiting CRY-mediated transcriptional repression for Bhlhe41, consequently promoting B-1a cell formation in Cic-null mice. Taken together, CIC is a key transcription factor that limits the B-1a cell population at the adult stage and balances B-1 versus B-2 cell formation. |
