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Embryology · Urogenital system

Sex determination: SRY, anti-Müllerian hormone and testosterone !

  • Process

One gene on the Y chromosome decides whether the gonad becomes a testis; three testicular hormones then shape the rest of the genital tract.

Updated 2026-11-01

See it in 3D: Ovaries · Body of uterus · Ductus deferens · Epididymis · Prostate

What it is

Until week 7 the gonad and ducts look the same in both sexes. The SRY gene on the Y chromosome switches on SOX9 and turns the gonad into a testis; without SRY, ovarian genes such as WNT4, RSPO1 and FOXL2 take over. From then on the phenotype depends on three testicular signals: anti-Müllerian hormone, testosterone and dihydrotestosterone (DHT).

Key facts

  • Weeks 4–6: primordial germ cells migrate from the yolk sac wall to the gonadal ridges.
  • Week 7: the indifferent gonad begins to become a testis if SRY is present.
  • Weeks 8–10: AMH and testosterone act on the ducts.
  • By about week 12 the external genitalia can be told apart; male genitalia are complete around week 14.
  • The ovary expresses WNT4 and RSPO1 and represses the SOX9 pathway.

Structure

  • Chromosomal level: XX or XY.
  • Gonadal level: testis or ovary, decided by SRY and SOX9 against WNT4, RSPO1 and FOXL2.
  • Phenotypic level: ducts and external genitalia, decided by AMH, testosterone, DHT and their receptors.

Step by step

  1. The karyotype is set at fertilization (XX or XY).
  2. Germ cells reach the indifferent gonad.
  3. With SRY, SOX9 makes Sertoli cells and a testis forms; without it, an ovary forms.
  4. Sertoli cells secrete AMH and the Müllerian ducts regress.
  5. Leydig cells secrete testosterone and the Wolffian ducts are kept.
  6. DHT masculinizes the external genitalia and forms the prostate.
  7. Without AMH or androgens, the uterus, tubes, upper vagina and female external genitalia develop.

Markers

  • SRY
  • SOX9
  • AMH
  • WNT4
  • RSPO1
  • FOXL2
  • DHT
  • SRD5A2
  • AR

Clinical notes

  • Congenital adrenal hyperplasia from 21-hydroxylase deficiency: excess adrenal androgens virilize the external genitalia of a 46,XX fetus.
  • Androgen insensitivity (AR gene): 46,XY with testes, no uterus (AMH works) and female external genitalia.
  • 5α-reductase deficiency: 46,XY with normal Wolffian ducts but atypical external genitalia at birth.
  • Translocation of SRY onto the X chromosome: 46,XX male.
  • Turner syndrome (45,X): ovaries that become fibrous streaks; Klinefelter syndrome (47,XXY): small testes.

Test yourself

Think of the answer, then tap the question to see it.

Which hormone makes the Müllerian ducts regress, and which cell makes it?

Anti-Müllerian hormone, made by the Sertoli cells of the fetal testis.

Which structures depend on testosterone and which on DHT?

Testosterone keeps the Wolffian ducts (epididymis, ductus deferens, seminal vesicle); DHT forms the male external genitalia and the prostate.

Which gene starts testis differentiation, and where is it?

SRY, on the short arm of the Y chromosome; it switches on SOX9, which makes Sertoli cells.

Why does a 46,XY person with complete androgen insensitivity have no uterus?

Their testes make AMH normally, so the Müllerian ducts regress even though androgens cannot act.

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See it in 3D

The structures of Durgical's 3D anatomy where it is found.

← All of embryology

Educational content on embryonic development; not a guide to prenatal diagnosis or to medicines in pregnancy and no substitute for a health professional's advice. No doses are given.

Sources: Embryology, Sexual Development - StatPearls - NCBI Bookshelf (StatPearls Publishing (NCBI Bookshelf), 2023); Embryology, Genitourinary - StatPearls - NCBI Bookshelf (StatPearls Publishing (NCBI Bookshelf), 2023).

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