| First Author | Peng V | Year | 2020 |
| Journal | J Biol Chem | Volume | 295 |
| Issue | 44 | Pages | 14866-14877 |
| PubMed ID | 32817168 | Mgi Jnum | J:300602 |
| Mgi Id | MGI:6488324 | Doi | 10.1074/jbc.RA120.013806 |
| Citation | Peng V, et al. (2020) E proteins orchestrate dynamic transcriptional cascades implicated in the suppression of the differentiation of group 2 innate lymphoid cells. J Biol Chem 295(44):14866-14877 |
| abstractText | Group 2 innate lymphoid cells (ILC2s) represent a subset of newly discovered immune cells that are involved in immune reactions against microbial pathogens, host allergic reactions, as well as tissue repair. The basic helix-loop-helix transcription factors collectively called E proteins powerfully suppress the differentiation of ILC2s from bone marrow and thymic progenitors while promoting the development of B and T lymphocytes. How E proteins exert the suppression is not well understood. Here we investigated the underlying molecular mechanisms using inducible gain and loss of function approaches in ILC2s and their precursors, respectively. Cross-examination of RNA-seq and ATAC sequencing data obtained at different time points reveals a set of genes that are likely direct targets of E proteins. Consequently, a widespread down-regulation of chromatin accessibility occurs at a later time point, possibly due to the activation of transcriptional repressor genes such as Cbfa2t3 and Jdp2 The large number of genes repressed by gain of E protein function leads to the down-regulation of a transcriptional network important for ILC2 differentiation. |
