Sex Determination/Development

ASCI 442

chromosomal sex

genotype

mammals (XX, XY)

birds (ZW, ZZ)

some lizards and tortoises have no heteromorphic pair of chromosomes, sex is determined by temperature and steroids

in mammals one X is inactivated → barr body in female somatic cells

Klinefelter’s Syndrome 

XXY

sterile

testicular hypoplasia

Turner’s Syndrome

XO

sterile

inactive “streak” ovaries

male gene expression allowing for bipotential gonad to differentiate

thermosensitive period

hot (30C) - female

28.5 C - ovotestis

cold (25C) - male

sertoli cells in differentiation

express SRY, SOX-9, AMH, seminiferous cords

female gene expression allowing for bipotential gonad to differentiate

gonadal sex (differentiation of gonad)

undifferentiated gonad nezt to mesonephros

primordial germ cells migrate from yolk sac to mesonephros

chemostatic agent stimulates movement to the mesonephros and into indifferent gonad

primordial germ cell migration

morphological changes during gonadal differentiation

female vs male events 

phenotypic sex

differentiation of reproductive tract and external genitalia

Mullerian duct → female tract → oviduct, uterus, cervix, vagina

Wolffian duct → male tract → epididymis, vas deferens, accesory sez glands

male gonade produces

• AMH (Sertoli cells) blocks development of female tract

• hormones: testosterone (maintain Wolffian ducts) and 5a-dihdrytestosterone (Leydig cells)

routes of testosterone metabolism in developing tissues

differentiation of external genitalia

testis decent

caused by INSUL3 from the Leydig cells, tyrosine kinase receptor

hermaphrodite

congenital malformation in sexual development

true hermaphrodite

male and female structures

mosaic, ovotestis with XX AND XY

male psuedohermaphrodite

externally female, internally have testis

5a-reductase deficiency (Dominican Republic) prevents testosterone conversion to 5aDHT

can also be caused by lack of androgen receptor

testicular feminization

female psuedohermaphrodite

congenital adrenal hyperplasia

ACTH stimulates the adrenals to produce cortisol or aldosterone but lack of enzyme for the converson of P4 → cortisol increase enzyme for conversion of testosterone, causing masculinization

free martin

female born twin to a fale

fusion of placenta

female tract does not develop due to AMH/androgen exposure

sexual differentiation of the brain

testicular hormones: testosterone from testis of fetus results in male behavior. medial preoptic nucleus in brain is larger in males

• rats castrated on day of birth have a female brian 

• give females testosterone at birth they develop a male brain

role of aromatization and a-fetaprotein

aromatization and a-fetoprotein

brain converts testosterone to estrogen (aromatization) estrogen causes changes in brain neurons

a-fetoprotein produced by fetal liver increase during late gestation, it binds to estrogen and inactivates its affect in females, does not bind testosterone (free in blood)

female has low levels of testosterone

animals that are exceptions to the rule

spotted hyenas

elephants

tammar wallabies