Table 1.

Phenotypes in knockout and transgenic mice.

Model	Gender	Reproductive phenotype
Disrupted pituitary glycoprotein hormone α-subunit [56]	Female	Prepubertal external genitalia, underdeveloped ovaries and uterus, limited follicle development, absence of ovulation, failure of vaginal orifice opening, infertility
	Male	Prepubertal external genitalia, reduced testes size, impaired spermatogenesis, testosterone deficiency, infertility
LH receptor null [57,58]	Female	Underdeveloped genitalia, ambiguous vaginal opening, arrested follicular growth, decreased estradiol and progesterone levels, infertility
	Male	Underdeveloped genitalia, abdominal testes, micropenis, Leydig cell hypotrophy, disarray of seminiferous tubules, spermatogenic arrest, modestly elevated estradiol levels, infertility
LH β-subunit null [59]	Female	Hypogonadism, decreased serum estradiol and progesterone levels, defects in folliculogenesis, gene expression abnormalities, uterine hypoplasia, infertility
	Male	Decreased testicular size, Leydig cell hypoplasia, gene expression abnormalities, reduced testosterone levels, impaired spermatogenesis, infertility
hCG α-subunit overexpression [60]	Female and male	Normal and fertile*
hCG β-subunit overexpression [60–62]	Female	Precocious puberty, enhanced ovarian steroidogenesis, abnormal uterine structure, hyperprolactinemia, infertility†
	Male	Mild hypogonadism, fertile† Infertility*
hCG α- and β-subunit overexpression [60,61]	Female	Elevated levels of serum estradiol, hemorrhagic and cystic ovaries, thecal layer enlargement, stromal cell proliferation, infertility*, tumorigenesis*
	Male	Increased testicular androgen production, focal Leydig cell hypertrophy, progressive seminiferous tubule degeneration, urethral obstruction, infertility† Leydig cell hyperplasia, very high serum testosterone levels, reduced testis size, enlarged seminal vesicles, infertility*

LH, luteinizing hormone; hCG, human chorionic gonadotropin.

^*Transgene expression was driven by the ubiquitin promoter.

^†Mice expressing high levels of hCG, with transgene expression driven by the metallothionein 1 promoter.