Foxn1 is not essential for T‐cell development in teleosts

Author:

Schorpp Michael1,Swann Jeremy B.1,Hess Isabell1,Ho Hsuan‐Ching23,Pietsch Theodore W.4,Boehm Thomas15

Affiliation:

1. Max Planck Institute of Immunobiology Freiburg Germany

2. National Museum of Marine Biology & Aquarium Pingtung Taiwan

3. Department and Graduate Institution of Aquaculture National Kaohsiung University of Science and Technology Kaohsiung Taiwan

4. School of Aquatic and Fishery Sciences and Burke Museum of Natural History and Culture University of Washington Seattle Washington USA

5. Faculty of Medicine University of Freiburg Freiburg Germany

Abstract

AbstractIn 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.

Funder

FP7 Ideas: European Research Council

Max-Planck-Gesellschaft

Publisher

Wiley

Subject

Immunology,Immunology and Allergy

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