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Limits to in vivo fate changes of epithelia in thymus and parathyroid by ectopic expression of transcription factors Gcm2 and Foxn1

MPS-Authors

Nagakubo,  Daisuke
Department of Developmental Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Hirakawa,  Mayumi
Department of Developmental Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Iwanami,  Norimasa
Department of Developmental Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Boehm,  Thomas
Department of Developmental Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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10.1038_s41598-022-17844-2.pdf
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Citation

Nagakubo, D., Hirakawa, M., Iwanami, N., & Boehm, T. (2022). Limits to in vivo fate changes of epithelia in thymus and parathyroid by ectopic expression of transcription factors Gcm2 and Foxn1. Scientific Reports, 12: 13554. doi:10.1038/s41598-022-17844-2.


Cite as: https://hdl.handle.net/21.11116/0000-000B-C6CA-2
Abstract
The development of the parathyroid and the thymus from the third pharyngeal pouch depends on the activities of the Gcm2 and Foxn1 transcription factors, respectively, whose expression domains sharply demarcate two regions in the developing third pharyngeal pouch. Here, we have generated novel mouse models to examine whether ectopic co-expression of Gcm2 in the thymic epithelium and of Foxn1 in the parathyroid perturbs the establishment of organ fates in vivo. Expression of Gcm2 in the thymic rudiment does not activate a parathyroid-specific expression programme, even in the absence of Foxn1 activity. Co-expression of Foxn1 in the parathyroid fails to impose thymopoietic capacity. We conclude that the actions of Foxn1 and Gcm2 transcription factors are cell context-dependent and that they each require permissive transcription factor landscapes in order to successfully interfere with organ-specific cell fate.