期刊
CELL REPORTS
卷 38, 期 7, 页码 -出版社
CELL PRESS
DOI: 10.1016/j.celrep.2022.110386
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资金
- Samsung Science and Technology Foundation [SSTF-BA1502-14]
- National Research Foundation (NRF) of Korea [NRF-2021R1A2C3004006, NRF-2021R1A6A1A10042944, NRF-2017R1A5A1015366]
- Korea Basic Science Institute (National Research Facilities and Equipment Center) - Ministry of Education [2021R1A6C101A390]
- Global PhD Fellowship [NRF-2017H1A2A1042705, NRF-2018H1A2A1059794]
- BK21 Program
- National Research Foundation of Korea [2021R1A6C101A390] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
CIC is a key transcription factor that limits the population of B-1a cells in the adult stage and balances the formation of B-1 and B-2 cells.
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.
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