Transcription factors AP-2α and AP-2β regulate distinct segments of the distal nephron in the mammalian kidney

Joseph O. Lamontagne, Hui Zhang, Alia M. Zeid, Karin Strittmatter, Alicia D. Rocha, Trevor Williams, Sheryl Zhang and Alexander G. Marneros ()
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Joseph O. Lamontagne: Massachusetts General Hospital and Harvard Medical School
Hui Zhang: Massachusetts General Hospital and Harvard Medical School
Alia M. Zeid: Massachusetts General Hospital and Harvard Medical School
Karin Strittmatter: Massachusetts General Hospital and Harvard Medical School
Alicia D. Rocha: Massachusetts General Hospital and Harvard Medical School
Trevor Williams: University of Colorado, Anschutz Medical Campus
Sheryl Zhang: Massachusetts General Hospital and Harvard Medical School
Alexander G. Marneros: Massachusetts General Hospital and Harvard Medical School

Nature Communications, 2022, vol. 13, issue 1, 1-18

Abstract: Abstract Transcription factors AP-2α and AP-2β have been suggested to regulate the differentiation of nephron precursor populations towards distal nephron segments. Here, we show that in the adult mammalian kidney AP-2α is found in medullary collecting ducts, whereas AP-2β is found in distal nephron segments except for medullary collecting ducts. Inactivation of AP-2α in nephron progenitor cells does not affect mammalian nephrogenesis, whereas its inactivation in collecting ducts leads to defects in medullary collecting ducts in the adult. Heterozygosity for AP-2β in nephron progenitor cells leads to progressive distal convoluted tubule abnormalities and β-catenin/mTOR hyperactivation that is associated with renal fibrosis and cysts. Complete loss of AP-2β in nephron progenitor cells caused an absence of distal convoluted tubules, renal cysts, and fibrosis with β-catenin/mTOR hyperactivation, and early postnatal death. Thus, AP-2α and AP-2β have non-redundant distinct spatiotemporal functions in separate segments of the distal nephron in the mammalian kidney.

Date: 2022
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DOI: 10.1038/s41467-022-29644-3

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