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Postnatal tissue-specific disruption of transcription factor FoxN1 triggers acute thymic atrophy.

The transcription factor FoxN1 is essential for differentiation of thymic epithelial cell (TEC) progenitors during thymic organogenesis. However, limited information is available on the postnatal contribution of FoxN1 to thymic maintenance. To address this question, we generated a loxP-floxed FoxN1 (fx) mouse with three different promoter-driven inducible CreER(T) transgenes. Postnatal ubiquitous deletion of FoxN1 caused dramatic thymic atrophy in 5 days and more severe deterioration in medullary TECs (mTECs) than in cortical TECs (cTECs). Induction of FoxN1 deletion selectively in K5 promoter-driven somatic epithelial cells (mostly mTECs and possibly some adult epithelial stem cells) was sufficient to cause significant thymic atrophy, whereas FoxN1 deletion in K18 promoter-driven somatic epithelial cells (mostly cTECs) was not. Thymic atrophy resulted from increased apoptosis and was associated with activation of the p53 gene in mature mTECs. Although FoxN1 is required for the development of both mTECs and cTECs in thymic organogenesis, it is most important for the maintenance of mTECs in the postnatal thymus, which are in turn necessary to prevent thymic atrophy.

Pubmed ID: 19955175 RIS Download

Mesh terms: Animals | Apoptosis | Atrophy | Epithelial Cells | Forkhead Transcription Factors | Gene Knockdown Techniques | Mice | Mice, Transgenic | Promoter Regions, Genetic | Stem Cells | Thymus Gland | Time Factors | Transgenes | Tumor Suppressor Protein p53

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Associated grants

  • Agency: NIAID NIH HHS, Id: R01AI081995
  • Agency: NIAID NIH HHS, Id: R21 AI079747
  • Agency: NIAID NIH HHS, Id: R01 AI081995
  • Agency: NIAID NIH HHS, Id: R21 AI064939
  • Agency: NIAID NIH HHS, Id: R21AI064939
  • Agency: NIAID NIH HHS, Id: R21AI079747

Mouse Genome Informatics (Data, Gene Annotation)

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