Document Detail


Loss of Wnt5a Disrupts Primordial Germ Cell Migration and Male Sexual Development in Mice.
MedLine Citation:
PMID:  21900680     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
Disruptions in the regulatory pathways controlling sex determination and differentiation can cause disorders of sex development (DSD), often compromising reproductive function. Although extensive efforts have been channeled into elucidating the regulatory mechanisms controlling the many aspects of sexual differentiation, the majority of DSD phenotypes are still unexplained at the molecular level. In this study, we have analyzed the potential involvement of Wnt5a in sexual development and show in mice that Wnt5a is male-specifically up-regulated within testicular interstitial cells at the onset of gonad differentiation. Homozygous deletion of Wnt5a affected sexual development in male mice, causing testicular hypoplasia and bilateral cryptorchidism despite the Leydig cells producing factors such as Hsd3b1 and Insl3. Additionally, Wnt5a-null embryos of both sexes showed a significant reduction in gonadal germ cell numbers, which was caused by aberrant primordial germ cell migration along the hindgut endoderm prior to gonadal colonization. Our results indicate multiple roles for Wnt5a during mammalian reproductive development, and help to clarify further the aetiology of Robinow syndrome (OMIM 268310), a disease previously linked to the WNT5A pathway.
Authors:
Kallayanee Chawengsaksophak; Terje Svingen; Ee Ting Ng; Trevor Epp; Cassy M Spiller; Charlotte Clark; Helen Cooper; Peter Koopman
Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2011-9-7
Journal Detail:
Title:  Biology of reproduction     Volume:  -     ISSN:  1529-7268     ISO Abbreviation:  -     Publication Date:  2011 Sep 
Date Detail:
Created Date:  2011-9-8     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0207224     Medline TA:  Biol Reprod     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
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