The LIM homeobox gene Lhx9 is essential for mouse gonad formation

Ohad S. Birk, Delane E. Casiano, Christopher A. Wassif, Tiziana Cogliati, Liping Zhao, Yangu Zhao, Alexander Grinberg, SingPing Huang, Jordan A. Kreidberg, Keith L. Parker, Forbes D. Porter and Heiner Westphal ()
Additional contact information
Ohad S. Birk: Laboratory of Mammalian Genes and Development and
Delane E. Casiano: Laboratory of Mammalian Genes and Development and
Christopher A. Wassif: Heritable Disorders Branch, National Institute of Child Health and Human Development, NIH
Tiziana Cogliati: Medicine Branch National Cancer Institute, NIH
Liping Zhao: Department of Internal Medicine University of Texas Southwestern Medical Center
Yangu Zhao: Laboratory of Mammalian Genes and Development and
Alexander Grinberg: Laboratory of Mammalian Genes and Development and
SingPing Huang: Laboratory of Mammalian Genes and Development and
Jordan A. Kreidberg: Department of Medicine Children's Hospital
Keith L. Parker: Department of Internal Medicine University of Texas Southwestern Medical Center
Forbes D. Porter: Heritable Disorders Branch, National Institute of Child Health and Human Development, NIH
Heiner Westphal: Laboratory of Mammalian Genes and Development and

Nature, 2000, vol. 403, issue 6772, 909-913

Abstract: Abstract During mammalian embryonic development, the ovaries and testes develop from somatic cells of the urogenital ridges as indifferent gonads, harbouring primordial germ cells that have migrated there. After sex determination of the gonads, the testes produce testosterone and anti-Mullerian hormone which mediate male sexual differentiation, and the female developmental pathway ensues in their absence1,2,3. Here we show that transcripts of the LIM homeobox gene Lhx9 are present in urogenital ridges of mice at embryonic day 9.5; later they localize to the interstitial region as morphological differentiation occurs. In mice lacking Lhx9 function, germ cells migrate normally, but somatic cells of the genital ridge fail to proliferate and a discrete gonad fails to form. In the absence of testosterone and anti-Mullerian hormone, genetically male mice are phenotypically female. The expression of steroidogenic factor 1 (Sf1), a nuclear receptor essential for gonadogenesis2, is reduced to minimal levels in the Lhx9-deficient genital ridge, indicating that Lhx9 may lie upstream of Sf1 in a developmental cascade. Unlike mice lacking other genes that mediate early stages of gonadogenesis4,5,6, Lhx9 mutants do not exhibit additional major developmental defects. Thus, LHX9 mutations may underlie certain forms of isolated gonadal agenesis in humans.

Date: 2000
References: Add references at CitEc
Citations:

Downloads: (external link)
https://www.nature.com/articles/35002622 Abstract (text/html)
Access to the full text of the articles in this series is restricted.

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:nature:v:403:y:2000:i:6772:d:10.1038_35002622

Ordering information: This journal article can be ordered from
https://www.nature.com/

DOI: 10.1038/35002622

Access Statistics for this article

Nature is currently edited by Magdalena Skipper

More articles in Nature from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().