Sexual differentiation in humans is genetically and hormonally controlled.
In response to a signal from a dominant-acting gene on the Y chromosome, pr
imordial cells in the embryonic gonad ridge differentiate into Sertoli cell
s and affect newly migrated germ cells to differentiate as spermatogonia, t
hus creating a testis. The cells of the embryonic testis secrete hormones t
hat lead to the development of most, it not all, male secondary sexual char
acteristics. The Sertoli cells secrete mullerian inhibitory factor (MIF), c
ausing regression of the mullerian ducts and of stray oogonia. The Leydig c
ells secrete testosterone, causing differentiation and growth of the wolffi
an duct structures. Dihydrotestosterone, created by metabolism of testoster
one, causes growth of the prostate and phallus and fusion of the labioscrot
al folds. In the absence of SRY, Sertoli cell differentiation does not occu
r. Rather germ cells migrating into the primordial gonad differentiate as o
ogonia and cause interstitial cells to differentiate as granulosa cells. In
the absence of MIF and testosterone, the mullerian ducts differentiate and
grow as female internal genitalia and the external genitalia are feminized
. Several genes have been identified that control testis determination. The
se include SRY, WT1, SOX9, SF1, XH2, and DAX1. Most of these genes were dis
covered by analysis of rare cases of sex reversal (genetic sex of one type,
gonadal sex of the other type) .