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. 2023 Dec 19;14:8452. doi: 10.1038/s41467-023-44184-0

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© The Author(s) 2023

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 9 — AEP can differentiate to AT1 cells via either the AT1tr or Krt8⁺ states during homeostasis, with Nkx2-1 release from AT2 genes during transition through a Krt8⁺ state²⁴. Nkx2-1 activity and expression are lowest in Krt8⁺ cells²¹, and Nkx2-1 must re-engage chromatin to complete the AT1 transition from the Krt8⁺ state²⁴. Permanent Nkx2-1 loss in AEPs causes transition to proliferative, stressed, Krt8⁺-like state characterized by unconstrained growth in vitro and in vivo. Nkx2-1 is therefore required for the progenitor activity of AEPs.