PUBLICATION
Foxn1 is not essential for T-cell development in teleosts
- Authors
- Schorpp, M., Swann, J.B., Hess, I., Ho, H.C., Pietsch, T.W., Boehm, T.
- ID
- ZDB-PUB-231002-57
- Date
- 2023
- Source
- European journal of immunology 53(12): e2350725 (Journal)
- Registered Authors
- Boehm, Tom, Schorpp, Michael
- Keywords
- Foxn1, Immunodeficiency, Teleost, Thymic epithelium, Thymopoiesis
- MeSH Terms
-
- Animals
- Epithelial Cells
- Forkhead Transcription Factors/genetics
- Gene Regulatory Networks*
- Mammals/genetics
- Mice
- Mice, Transgenic
- T-Lymphocytes
- Thymus Gland
- Transcription Factors/genetics
- Zebrafish*/genetics
- Zebrafish Proteins/genetics
- PubMed
- 37724048 Full text @ Eur. J. Immunol.
Citation
Schorpp, M., Swann, J.B., Hess, I., Ho, H.C., Pietsch, T.W., Boehm, T. (2023) Foxn1 is not essential for T-cell development in teleosts. European journal of immunology. 53(12):e2350725.
Abstract
In mammals, T-cell development depends on the activity of the Foxn1 transcription factor in the thymic epithelium; mutations in the vertebrate-specific Foxn1 gene are associated with profound T-cell lymphopenia and fatal immunodeficiency. Here, we examined the extent of T-cell development in teleosts lacking a functional foxn1 gene. In zebrafish carrying a deleterious internal deletion of foxn1, reduced but robust lymphopoietic activity is maintained in the mutant thymus. Moreover, pseudogenization or loss of foxn1 in the genomes of deep-sea anglerfishes is independent of the presence or absence of the canonical signatures of the T-cell lineage. Thus, in contrast to the situation in mammals, the teleost thymus can support foxn1-independent lymphopoiesis, most likely through the activity of the Foxn4, an ancient metazoan paralog of Foxn1. Our results imply that during the early stages of vertebrate evolution, genetic control of thymopoiesis was functionally redundant and thus robust; in mammals, the genetic network was reorganized to become uniquely dependent on the FOXN1 transcription factor.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping