| First Author | Tian L | Year | 2021 |
| Journal | Immunity | PubMed ID | 33862015 |
| Mgi Jnum | J:305836 | Mgi Id | MGI:6706589 |
| Doi | 10.1016/j.immuni.2021.03.012 | Citation | Tian L, et al. (2021) Clonal multi-omics reveals Bcor as a negative regulator of emergency dendritic cell development. Immunity 54(6) |
| abstractText | Despite advances in single-cell multi-omics, a single stem or progenitor cell can only be tested once. We developed clonal multi-omics, in which daughters of a clone act as surrogates of the founder, thereby allowing multiple independent assays per clone. With SIS-seq, clonal siblings in parallel "sister" assays are examined either for gene expression by RNA sequencing (RNA-seq) or for fate in culture. We identified, and then validated using CRISPR, genes that controlled fate bias for different dendritic cell (DC) subtypes. This included Bcor as a suppressor of plasmacytoid DC (pDC) and conventional DC type 2 (cDC2) numbers during Flt3 ligand-mediated emergency DC development. We then developed SIS-skew to examine development of wild-type and Bcor-deficient siblings of the same clone in parallel. We found Bcor restricted clonal expansion, especially for cDC2s, and suppressed clonal fate potential, especially for pDCs. Therefore, SIS-seq and SIS-skew can reveal the molecular and cellular mechanisms governing clonal fate. |
