Notch/Delta signaling constrains reengineering of pro-T cells by PU.1
0301 basic medicine
570
Cell Survival
T-Lymphocytes
T cell development
610
lineage commitment
Mice, Transgenic
Receptors, Interleukin-2
Models, Biological
hematopoiesis
Mice, Inbred C57BL
Mice
03 medical and health sciences
Gene Expression Regulation
Proto-Oncogene Proteins c-bcl-2
transcription factors
Proto-Oncogene Proteins
Trans-Activators
Animals
Cell Lineage
Receptor, Notch1
gene regulation
Caltech Library Services
Signal Transduction
DOI:
10.1073/pnas.0601188103
Publication Date:
2006-08-02T07:50:15Z
AUTHORS (9)
ABSTRACT
PU.1 is essential for early stages of mouse T cell development but antagonizes it if expressed constitutively. Two separable mechanisms are involved: attenuation and diversion. Dysregulated expression inhibits pro-T survival, proliferation, passage through β-selection by blocking transcription factors, signaling molecules, Rag gene expression, which a rearranged antigen receptor transgene cannot rescue. However, Bcl2 transgenic cells protected from this may even undergo β-selection, as shown transduction defined subsets fetal thymocytes with differentiation in OP9-DL1 OP9 control cultures. The outcome these depends on Notch/Delta signaling. can efficiently divert toward myeloid-like state multigene regulatory changes, vetoes Gene analysis distinguishes sets critical lineage genes different combinatorial responses to signals, suggesting particular importance inhibition E proteins, Myb, and/or Gfi1 (growth factor independence 1) Notch only protects against diversion that have undergone specification after Thy-1 CD25 up-regulation. results imply precursors, normally acts modulate channel transcriptional activities during the until commitment.
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