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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Lhcgrtm1Zmlei
targeted mutation 1, Zhenmin Lei
MGI:2181998
Summary 2 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Lhcgrtm1Zmlei/Lhcgrtm1Zmlei either: 129X1/SvJ-Lhcgrtm1Zmlei or (involves: 129X1/SvJ * C57BL/6) MGI:2182004
ht2
Lhcgrtm1Zmlei/Lhcgr+ either: 129X1/SvJ-Lhcgrtm1Zmlei or (involves: 129X1/SvJ * C57BL/6) MGI:3813871


Genotype
MGI:2182004
hm1
Allelic
Composition
Lhcgrtm1Zmlei/Lhcgrtm1Zmlei
Genetic
Background
either: 129X1/SvJ-Lhcgrtm1Zmlei or (involves: 129X1/SvJ * C57BL/6)
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lhcgrtm1Zmlei mutation (1 available); any Lhcgr mutation (27 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
reproductive system
• at 7-8 weeks of age, spermatocyte apoptosis is dramatically increased in mutant testes relative to wild-type testes
• at 60 days of age, mutant males display a shorter anogenital distance relative to wild-type
• at 60 days of age, the mutant prostate is so hypoplastic that is barely recognizable and difficult to dissect from underlying tissue
• fewer acini are observed
• a 21-day testosterone replacement therapy of 30-day-old mutant males restores prostate morphology and increases size and number of acini
• severely reduced at 60 days of age
• marked hypoplasia with fewer acini at 60 days of age
• a 21-day testosterone replacement therapy of 30-day-old mutant males restores seminal vesicle morphology and increases size and number of acini
• seminiferous tubules are disarrayed and devoid of sperm at 60 days of ahe
• mutant testes contain mostly fetal-type and few, if any, adult-type Leydig cells
• a drastic reduction in Leydig cell number and hypotrophy are observed at 60 days of age
• a 21-day testosterone replacement therapy of 30-day-old mutant males fails to restore Leydig cell number or improve hypotrophy
• significantly reduced seminiferous tubule diameters at 60 days of age
• a 21-day testosterone replacement therapy of 30-day-old mutant males increases seminiferous tubule diameters
• severely reduced at 60 days of age
• no scrotal testes are detected at 60 days of age
• a 21-day testosterone replacement therapy of 30-day-old mutant males restores scrotal descent of testes
• a micropenis is observed at 60 days of age
• a 21-day testosterone replacement therapy of 30-day-old mutant males improves penis growth; however, mutant penuses remain small
• at 60 days of age, the female reproductive tract is very thin and exhibits a severely reduced wet weight
• at 60 days of age, mutant ovaries are very small and pale
• a 21-day estradiol and progesterone replacement therapy of 30-day-old female mutants has no effect on ovarian morphology
• at 60 days of age
• at 60 days of age, mutant ovaries contain preantral and antral but no preovulatory follicles or corpora lutea
• treatment with PMSG increases the number of small antral follicles with no other obvious changes in the ovaries or the reproductive tract
• ovarian folliculogenesis is arrested beyond the antral stage
• at 60 days of age, the wet weight of mutant ovaries is severely reduced
• at 60 days of age, only a few glands are present in endometrium
• a 21-day estradiol and progesterone replacement therapy of 30-day-old female mutants fails to restore endometrial gland number
• at 60 days of age, the thickness of all uterine layers is decreased
• a 21-day estradiol and progesterone replacement therapy of 30-day-old female mutants increases uterine thickness but fails to restore the number of endometrial glands
• at 60 days of age, the mutant vagina appears underdeveloped relative to wild-type
• a 21-day estradiol and progesterone replacement therapy of 30-day-old female mutants restores vaginal development and improves cytology; however, the number of leukocytes remains significantly low
• at 60 days of age, the vaginal orifice is ambiguous and difficult to detect
• spermatogenesis is arrested beyond round spermatid stage
• a 21-day testosterone replacement therapy of 30-day-old mutant males causes a resumption of spermatogenesis but sperm numbers remain low
• at 7-8 weeks of age, mutant epididymal tubules are much smaller and lumens are completely devoid of spermatozoa
• secretion of glycogen and glycoproteins is quite weak in epithelial cells and in lumen of epididymal tubules as shown by PAS staining
• a 21-day testosterone replacement therapy of 30-day-old mutant males results in a lumen containing polynucleated epithelial cells mixed with spermatozoa and restores the secretory activity of the epididymis
• semiquantitative RT-PCR and Western blot analysis of epididymal steroid hormone receptor levels revealed that while androgen receptor (AR) and estrogen receptor (ER)-beta levels decreased, ER-alpha levels increased in mutant epididymis relative to wild-type
• testosterone replacement therapy reverses the AR, ER-alpha, and ER-beta changes; however, AR immunostaining remains diffuse cytoplasmic rather than nuclear
• at 7-8 weeks of age, the luminal diameters of tubules and height of principal cells in proximal and distal caput epididymis are dramatically reduced
• in addition, the percentage of ciliated epithelial cells and their cilia height is decreased
• a 21-day testosterone replacement therapy of 30-day-old mutant males fails to completely restore the luminal diameters in proximal and distal caput and principal cell heights in caput epididymis
• at 7-8 weeks of age, the luminal diameters of tubules and height of principal cells in proximal and distal cauda epididymis are dramatically reduced
• in addition, the percentage of ciliated epithelial cells and their cilia height is decreased
• a 21-day testosterone replacement therapy of 30-day-old mutant males fails to completely restore the luminal diameters in proximal and distal cauda epididymis
• at 7-8 weeks of age, no clear or halo cells, which represent minor cell populations in the epithelial cell lining, are observed
• the number of principal cells is reduced and they become cubic with centrally located nuclei
• only a few of the principal cells contain cilia, and the length of stereocilia is decreased
• a 21-day testosterone replacement therapy of 30-day-old mutant males causes principal cells to become columnar with nuclei returned to the basal part of the cells, restores the number of ciliated cells and cilia lengths, and reverses the absence of clear and halo cells
• at 60 days of age, mutant epididymal tubule diameters are much smaller than wild-type
• a 21-day testosterone replacement therapy of 30-day-old mutant males causes an enlargement of epididymal tubules and restores sperm content
• severely reduced at 60 days of age
• marked hypoplasia at 60 days of age
• mutant females are acyclic at 60 days of age
• female mutants are completely infertile
• a 21-day estradiol and progesterone replacement therapy of 30-day-old female mutants fails to restore fertility
• mutant males are completely infertile
• a 21-day testosterone replacement therapy of 30-day-old mutant males restores the size and weight of epididymides, seminal vesicles, and prostate but males remain infertile
• a marked decrease in cell proliferation is observed with less than 10% of principal cell nuclei staining PCNA positive in mutant epididymi vs ~98% in wild-type and heterozygous epididymi
• a 21-day testosterone replacement therapy of 30-day-old mutant males restores epididymal growth to a wild-type size; increased growth appears to reflect an increase in cell proliferation as shown by PCNA staining

endocrine/exocrine glands
• at 60 days of age, the mutant prostate is so hypoplastic that is barely recognizable and difficult to dissect from underlying tissue
• fewer acini are observed
• a 21-day testosterone replacement therapy of 30-day-old mutant males restores prostate morphology and increases size and number of acini
• severely reduced at 60 days of age
• marked hypoplasia with fewer acini at 60 days of age
• a 21-day testosterone replacement therapy of 30-day-old mutant males restores seminal vesicle morphology and increases size and number of acini
• at 60 days of age, only a few glands are present in endometrium
• a 21-day estradiol and progesterone replacement therapy of 30-day-old female mutants fails to restore endometrial gland number
• at 60 days of age, mutant ovaries are very small and pale
• a 21-day estradiol and progesterone replacement therapy of 30-day-old female mutants has no effect on ovarian morphology
• at 60 days of age
• at 60 days of age, mutant ovaries contain preantral and antral but no preovulatory follicles or corpora lutea
• treatment with PMSG increases the number of small antral follicles with no other obvious changes in the ovaries or the reproductive tract
• ovarian folliculogenesis is arrested beyond the antral stage
• at 60 days of age, the wet weight of mutant ovaries is severely reduced
• seminiferous tubules are disarrayed and devoid of sperm at 60 days of ahe
• mutant testes contain mostly fetal-type and few, if any, adult-type Leydig cells
• a drastic reduction in Leydig cell number and hypotrophy are observed at 60 days of age
• a 21-day testosterone replacement therapy of 30-day-old mutant males fails to restore Leydig cell number or improve hypotrophy
• significantly reduced seminiferous tubule diameters at 60 days of age
• a 21-day testosterone replacement therapy of 30-day-old mutant males increases seminiferous tubule diameters
• severely reduced at 60 days of age
• no scrotal testes are detected at 60 days of age
• a 21-day testosterone replacement therapy of 30-day-old mutant males restores scrotal descent of testes

homeostasis/metabolism
• dramatically decreased serum testosterone levels in mutant males
• significantly decreased, but not totally suppressed, serum estradiol levels in mutant females
• moderately increased serum estradiol levels in mutant males
• moderately increased serum FSH levels in both mutant female and male animals
• dramatically increased serum LH levels in both mutant female and male animals
• significantly decreased, but not totally suppressed, serum progesterone levels in mutant females

growth/size/body
• mutant females are ~50% heavier than controls with accumulated visceral fat at 60 days of age
• mutant males accumulate visceral fat at a later age (~ 120 days), but remain lighter possibly due to reduced muscle mass and bone density

adipose tissue
• mutant males display accumulated visceral fat at a later age than females (at ~120 days versus at ~60 days of age, respectively)

digestive/alimentary system
• at 60 days of age, mutant males display a shorter anogenital distance relative to wild-type

renal/urinary system
• a micropenis is observed at 60 days of age
• a 21-day testosterone replacement therapy of 30-day-old mutant males improves penis growth; however, mutant penuses remain small

cellular
• at 7-8 weeks of age, spermatocyte apoptosis is dramatically increased in mutant testes relative to wild-type testes




Genotype
MGI:3813871
ht2
Allelic
Composition
Lhcgrtm1Zmlei/Lhcgr+
Genetic
Background
either: 129X1/SvJ-Lhcgrtm1Zmlei or (involves: 129X1/SvJ * C57BL/6)
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lhcgrtm1Zmlei mutation (1 available); any Lhcgr mutation (27 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• at 60 days of age, moderately reduced serum testosterone levels in heterozygous males relative to wild-type levels
• at 60 days of age, modestly increased serum FSH levels in both heterozygous male and female animals relative to wild-type levels





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last database update
01/18/2022
MGI 6.17
The Jackson Laboratory