| First Author | Ito T | Year | 2006 |
| Journal | Mol Cell Biol | Volume | 26 |
| Issue | 8 | Pages | 3194-203 |
| PubMed ID | 16581793 | Mgi Jnum | J:107421 |
| Mgi Id | MGI:3621109 | Doi | 10.1128/MCB.26.8.3194-3203.2006 |
| Citation | Ito T, et al. (2006) Transcription elongation factor S-II is required for definitive hematopoiesis. Mol Cell Biol 26(8):3194-203 |
| abstractText | Transcription elongation factor S-II/TFIIS promotes readthrough of transcriptional blocks by stimulating nascent RNA cleavage activity of RNA polymerase II in vitro. The biologic significance of S-II function in higher eukaryotes, however, remains unclear. To determine its role in mammalian development, we generated S-II-deficient mice through targeted gene disruption. Homozygous null mutants died at midgestation with marked pallor, suggesting severe anemia. S-II(-/-) embryos had a decreased number of definitive erythrocytes in the peripheral blood and disturbed erythroblast differentiation in fetal liver. There was a dramatic increase in apoptotic cells in S-II(-/-) fetal liver, which was consistent with a reduction in Bcl-x(L) gene expression. The presence of phenotypically defined hematopoietic stem cells and in vitro colony-forming hematopoietic progenitors in S-II(-/-) fetal liver indicates that S-II is dispensable for the generation and differentiation of hematopoietic stem cells. S-II-deficient fetal liver cells, however, exhibited a loss of long-term repopulating potential when transplanted into lethally irradiated adult mice, indicating that S-II deficiency causes an intrinsic defect in the self-renewal of hematopoietic stem cells. Thus, S-II has critical and nonredundant roles in definitive hematopoiesis. |
