NR2F2 regulation of interstitial cell fate in the embryonic mouse testis and its impact on differences of sex development DOI Creative Commons
Martin A. Estermann, Sara A. Grimm,

Abigail S Kitakule

et al.

Nature Communications, Journal Year: 2025, Volume and Issue: 16(1)

Published: April 28, 2025

Abstract Testicular fetal Leydig cells produce androgens essential for male reproductive development. Impaired cell differentiation leads to differences of sex development including hypospadias, cryptorchidism, and infertility. Despite are thought originate from proliferating progenitor in the testis interstitium, precise mechanisms governing interstitial transition remain elusive. Using mouse models single-nucleus multiomics, we find that arise a Nr2f2 -positive population. Embryonic deletion testes results development, dysgenic testes, hypoplasia, hypospadias. By combining multiomics NR2F2 ChIP-seq promotes fate while suppresses by modulating key transcription factors downstream genes. Our findings establish as crucial regulator provide molecular insights into linked mutations.

Language: Английский

NR2F2 regulation of interstitial cell fate in the embryonic mouse testis and its impact on differences of sex development DOI Creative Commons
Martin A. Estermann, Sara A. Grimm,

Abigail S Kitakule

et al.

Nature Communications, Journal Year: 2025, Volume and Issue: 16(1)

Published: April 28, 2025

Abstract Testicular fetal Leydig cells produce androgens essential for male reproductive development. Impaired cell differentiation leads to differences of sex development including hypospadias, cryptorchidism, and infertility. Despite are thought originate from proliferating progenitor in the testis interstitium, precise mechanisms governing interstitial transition remain elusive. Using mouse models single-nucleus multiomics, we find that arise a Nr2f2 -positive population. Embryonic deletion testes results development, dysgenic testes, hypoplasia, hypospadias. By combining multiomics NR2F2 ChIP-seq promotes fate while suppresses by modulating key transcription factors downstream genes. Our findings establish as crucial regulator provide molecular insights into linked mutations.

Language: Английский

Citations

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