Chromosomes and Hormones

Chromosomes, Hormones and the SRY Gene

The biological basis of sex involves an interacting cascade of genetic, gonadal, and hormonal factors. Understanding how chromosomes, the SRY gene, and sex hormones interact to produce typical male and female development is foundational to the psychology of gender — and provides the biological baseline against which psychological and social influences can be evaluated.

Sex Determination Pathway Conception: 23rd chromosome pair XY — SRY gene present (on short arm of Y chromosome) XX — no SRY gene (default developmental pathway) Indifferent gonads → Testes Indifferent gonads → Ovaries Testosterone + DHT + MIF androgens masculinise genitalia and organise male-typical brain Oestrogen + progesterone support female internal structures and organise female-typical brain Typical male development Typical female development Female development is the default pathway — active SRY expression is required for male differentiation

Chromosomal Sex

Human somatic cells contain 46 chromosomes in 23 pairs. The 23rd pair are the sex chromosomes: typically XX in females and XY in males. Eggs always carry an X chromosome; sperm carry either X or Y — so the sperm determines the chromosomal sex of the offspring. Chromosomal sex establishes the genetic blueprint but does not directly produce sex differentiation — the critical step involves gene expression and subsequent hormonal action.

The SRY Gene and Gonadal Development

The SRY gene (Sex-determining Region Y), located on the short arm of the Y chromosome, is the master switch for male sex determination. In a foetus with XY chromosomes, SRY is expressed around weeks 6–7 of gestation, triggering the indifferent (bipotential) gonads to develop into testes rather than ovaries. The absence of SRY — in XX foetuses, or in XY foetuses with non-functional SRY — allows the indifferent gonads to develop into ovaries by default. This is why female development is described as the default developmental pathway: it does not require active female-specific gene expression in the same way that male development requires SRY.

Sex Hormones and Differentiation

Once gonadal sex is established, the gonads produce sex hormones that drive the differentiation of internal reproductive structures, external genitalia, and — crucially for psychology — brain organisation.

In males: the testes produce testosterone, which promotes development of the Wolffian ducts into male internal structures (vas deferens, seminal vesicles, epididymis), and dihydrotestosterone (DHT), produced by 5-alpha reductase conversion of testosterone, which masculinises the external genitalia. The testes also produce Müllerian inhibiting factor (MIF), which causes regression of the Müllerian ducts (otherwise the default female internal reproductive structures). In females: without androgens, the Müllerian ducts develop into uterus, fallopian tubes, and upper vagina; without DHT, female external genitalia develop.

Organisational and Activational Effects

Hormones exert two fundamentally different types of effect on the brain and behaviour:

  • Organisational effects: occur prenatally (and perinatally), when sex hormones permanently organise neural circuits — setting up the brain's architecture in a sex-typical direction. These effects are largely irreversible. Prenatal testosterone exposure, for example, is thought to organise the brain towards male-typical patterns of cognition, social behaviour, and later hormonal responses.
  • Activational effects: occur from puberty onwards, when rising sex hormone levels activate the already-organised circuits. These effects are largely reversible — they depend on continued hormonal exposure. Testosterone at puberty activates sex drive, aggression, and muscle development; oestrogen activates female-typical pubertal changes. The distinction explains why prenatal hormone exposure (organisational) has lasting effects even before the person reaches puberty (when activational hormones begin).

Evidence for organisational effects comes from studies of congenital adrenal hyperplasia (CAH — see B1535), where prenatal androgen excess in XX individuals produces masculinised behaviour, and from animal studies where prenatal hormone manipulation produces persistent, dose-dependent changes in sex-typical behaviour.

 Key Takeaways

  • Sex chromosomes: XX (typically female), XY (typically male). Sperm determines chromosomal sex.
  • SRY gene (on Y chromosome short arm): triggers testes development from indifferent gonads at ~6–7 weeks gestation. Without SRY → ovaries develop by default.
  • Female development is the default pathway — active SRY expression required for male differentiation.
  • Testes produce: testosterone (male internal structures), DHT via 5-alpha reductase (male external genitalia), MIF (suppresses female internal structures).
  • Organisational effects: prenatal hormones permanently organise brain architecture (irreversible). Activational effects: puberty onwards hormones activate already-organised circuits (reversible).
  • Prenatal testosterone exposure organises the brain towards male-typical patterns — evidenced by CAH studies (see B1535) and animal research.