| First Author | Min S | Year | 2020 |
| Journal | iScience | Volume | 23 |
| Issue | 9 | Pages | 101524 |
| PubMed ID | 32932139 | Mgi Jnum | J:306971 |
| Mgi Id | MGI:6717589 | Doi | 10.1016/j.isci.2020.101524 |
| Citation | Min S, et al. (2020) p63 and Its Target Follistatin Maintain Salivary Gland Stem/Progenitor Cell Function through TGF-beta/Activin Signaling. iScience 23(9):101524 |
| abstractText | Multipotent DeltaNp63-positive cells maintain all epithelial cell lineages of the embryonic and adult salivary gland (SG). However, the molecular mechanisms by which DeltaNp63 regulates stem/progenitor (SP) cell populations in the SG remains elusive. To understand the role of DeltaNp63 in directing cell fate choices in this gland, we have generated DeltaNp63-deleted adult mice and primary salivary cell cultures to probe alterations in SP cell differentiation and function. In parallel, we have leveraged RNA-seq and ChIP-seq-based characterization of the DeltaNp63-driven cistrome and scRNA-seq analysis to molecularly interrogate altered SG cellular identities and differentiation states dependent on DeltaNp63. Our studies reveal that ablation of DeltaNp63 results in a loss of the SP cell population and skewed differentiation that is mediated by Follistatin-dependent dysregulated TGF-beta/Activin signaling. These findings offer new revelations into the SP cell gene regulatory networks that are likely to be relevant for normal or diseased SG states. |
