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#AMH

6 public questions tagged with this topic.

Sex determination-l

Sertoli cells secrete which hormone to prevent female duct development?

During male embryogenesis newly formed testis cords contain Sertoli cells that secrete Anti-Müllerian Hormone glycoprotein belonging to TGF-β family. AMH acts via type II receptor on Müllerian duct mesenchyme activating Smad signaling leading to apoptosis and epithelial-mesenchymal transformation causing regression from cranial to caudal direction, eliminating primordia of uterus and oviducts. Sertoli cells also support germ cell survival, create blood-testis barrier and secrete inhibin. Their endocrine secretion of AMH provides crucial anti-female signal complementing testosterone pro-male signal for proper reproductive tract patterning and sexual dimorphism.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 17: Sertoli cell AMH prevents female duct development.

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sex determination-ll

AMH function in male mammals:

Anti-Müllerian Hormone performs male-specific function of eliminating female reproductive duct anlage. Secreted shortly after testis cords form by Sertoli cells, AMH binds Amhr2 receptor serine-threonine kinase on mesenchyme of Müllerian ducts leading to phosphorylation of Smad1/5/8, induction of matrix metalloproteinases, inhibition of Wnt7a and apoptosis of duct epithelium. Resulting regression prevents formation of uterus, oviducts and upper vagina in males ensuring only Wolffian derivatives develop. Mutations in AMH or receptor cause Persistent Müllerian Duct Syndrome where males retain uterus alongside normal testes.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 17: AMH function in Müllerian regression.

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sex determination-ll

AMH is produced by:

Anti-Müllerian Hormone in fetal testes originates from Sertoli cells forming testis cords. After Sry upregulates Sox9 in pre-Sertoli cells, Sox9 together with Sf1/Nr5a1, Wt1 and Gata4 binds Amh promoter activating transcription shortly before testosterone synthesis. Secreted dimeric glycoprotein acts locally on Müllerian duct mesenchyme inducing regression and preventing uterus development. Sertoli cells also establish blood-testis barrier and nurture germ cells. Leydig cells produce testosterone, theca cells produce androgens, granulosa cells produce low AMH postnatally for follicle regulation, distinct from embryonic Sertoli-derived surge driving duct regression.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 17: Sertoli cells secrete AMH to regress Müllerian ducts.

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Fertilization in mammals-lll

AMH primarily induces:

Anti-Müllerian hormone is dimeric glycoprotein of TGF-beta family secreted by Sertoli cells of fetal testis under SOX9 activation soon after SRY determination. AMH binds AMHR2 receptors on mesenchyme surrounding Müllerian ducts, triggering apoptosis and extracellular matrix remodeling causing duct regression in male embryos between weeks 8-10. This prevents development of uterus, fallopian tubes and upper vagina, allowing Wolffian duct differentiation toward male tract under testosterone. In females absence of AMH permits Müllerian duct persistence forming female reproductive tract. Mutations cause persistent Müllerian duct syndrome. AMH does not induce spermatogenesis or Leydig differentiation directly.

Ref: Behringer et al., Cell 1994: Anti-Müllerian hormone signaling in Müllerian duct regression and male sexual differentiation.

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