| First Author | Solanki A | Year | 2017 |
| Journal | J Exp Med | Volume | 214 |
| Issue | 7 | Pages | 2041-2058 |
| PubMed ID | 28533268 | Mgi Jnum | J:243893 |
| Mgi Id | MGI:5912672 | Doi | 10.1084/jem.20160852 |
| Citation | Solanki A, et al. (2017) The transcription factor Gli3 promotes B cell development in fetal liver through repression of Shh. J Exp Med 214(7):2041-2058 |
| abstractText | Before birth, B cells develop in the fetal liver (FL). In this study, we show that Gli3 activity in the FL stroma is required for B cell development. In the Gli3-deficient FL, B cell development was reduced at multiple stages, whereas the Sonic hedgehog (Hh [Shh])-deficient FL showed increased B cell development, and Gli3 functioned to repress Shh transcription. Use of a transgenic Hh-reporter mouse showed that Shh signals directly to developing B cells and that Hh pathway activation was increased in developing B cells from Gli3-deficient FLs. RNA sequencing confirmed that Hh-mediated transcription is increased in B-lineage cells from Gli3-deficient FL and showed that these cells expressed reduced levels of B-lineage transcription factors and B cell receptor (BCR)/pre-BCR-signaling genes. Expression of the master regulators of B cell development Ebf1 and Pax5 was reduced in developing B cells from Gli3-deficient FL but increased in Shh-deficient FL, and in vitro Shh treatment or neutralization reduced or increased their expression, respectively. |
