Overview

Also Known As:ERα KO

This Esr1 mutant strain is a functional knock out of ERα. Female mice homozygous for this mutation are infertile, exhibit cystic ovaries that lack corpora lutea and hypoplastic uteri that are unresponsive to estrogen. Homozygous males show reduced testis weight associated with diminished sperm count. These mice may be suitable for use in studies related to estrogen signaling, estrous cycle, obesity, metabolic syndrome and hormonal regulation of a variety of organ systems.

Please note: Mice carrying this Esr1^tm1Ksk allele (Stock No. 004744), express a low level of a truncated form of ERα, the result of alternate splicing of the transcript. In contrast, mice carrying the Esr1^tm4.2Ksk allele (Stock No. 026176) have no tissue responses to estrogen and no estrogen receptor alpha activity.

Donating Investigator

Kenneth Korach, LRDT, NIEHS, NIH

Genetic overview

Genetic Background	Generation

Esr1^tm1Ksk

Allele Type	Gene Symbol	Gene Name
Targeted (Null/Knockout)	Esr1	estrogen receptor 1 (alpha)

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Research Applications

Reproductive Biology Research
Internal/Organ Research
Developmental Biology Research
Neurobiology Research

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Base Price

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Details

Detailed Description

The targeted Esr1 gene encodes a ligand-activated transcription factor and nuclear estradiol hormone receptor. In the ERKO line (Stock #004744) multiple transcript variants may form due to alternative cryptic splicing of the endogenous mouse Esr1 gene. These mice carry an insertional disruption mutation of the Esr1 gene in which exon 2 has been deleted and a series of stop codons have been inserted. Two truncated mutant transcripts and a truncated protein (approximately 61kDa in size) having a deleted N-terminus are detected in uterine tissue from homozygous female mice by RT-PCR and Western blot analysis.
At birth, mice homozygous for the targeted allele are viable and normal in size and appearance. Female homozygous mice are infertile, exhibit cystic ovaries that lack corpora lutea and have hypoplastic uteri that are unresponsive to estrogen. Homozygous males are infertile, low normal testis weight as adults and diminished sperm count (10% of normal.
Homozygous females have more than 4-fold higher level of serum estradiol and elevated androgen levels compared to wildtype controls, indicative of estrogen insensitivity. There is approximately 3% of the Estradiol binding in uterine tissue from homozygotes compared to levels observed in wildtype controls; no estradiol binding is detected in other tissues (brain, kidney, and liver) from homozygotes. Female neuroendocrine estrogen negative feedback is disrupted with highly elevated LH, normal FSH levels but no prolactin.

Please note: Mice carrying this Esr1^tm1Ksk allele (Stock No. 004744), express a low level of a truncated form of ERα, the result of alternate splicing of the transcript. In contrast, mice carrying the Esr1^tm4.2Ksk allele (Stock No. 026176) have no tissue responses to estrogen and no estrogen receptor alpha activity.

Development

A targeting vector containing a neomycin resistance gene driven by the mouse phosphoglycerate kinase promoter, and polyA signal sequence, was used to disrupt the second exon of the targeted gene. A herpes simplex virus thymidine kinase was used for negative selection. The construct was electroporated into 129P2/OlaHsd-derived E14TG2a embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6 blastocysts. Correctly targeted ES cells were injected into C57BL/6J blastocysts to obtain chimeric animals. This strain originated on a B6;129P2 background and has been backcrossed to C57BL/6 for ten generations.

Control Suggestions

Wild-type from the colony
000664 C57BL/6J

Additional Information

Considerations for Choosing Controls

Selected References

Lubahn DB; Moyer JS; Golding TS; Couse JF; Korach KS; Smithies O. 1993. Alteration of reproductive function but not prenatal sexual development after insertional disruption of the mouse estrogen receptor gene. Proc Natl Acad Sci U S A 90(23):11162-6PubMed: 8248223 MGI: J:16338

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Genetics

Esr1^tm1Ksk

Allele Symbol: Esr1^tm1Ksk

Allele Name	targeted mutation 1, Kenneth S Korach
Allele Type	Targeted (Null/Knockout)
Allele Synonym(s)	AERKO; alphaERKO; alpha-ERKO; ER1KO; ERalpha-; ER-alpha^-; ERalphaKO; ERalpha-KO; ERalphaKOCH; ERa-Neo; ERKO; Esr1^tm1Unc; Esr1tm1Ksk
Gene Symbol and Name	Esr1, estrogen receptor 1 (alpha)
Gene Synonym(s)
Strain of Origin	129P2/OlaHsd
Chromosome	10
Molecular Note	Insertion of a PGK-neomycin resistance cassette into exon 2 disrupted the reading frame downstream of the ATG start site. ELISA studies using antibodies to the carboxy terminus detected low concentrations of endogenous protein in uterine tissue from homozygous mutant mice. RT-PCR analysis detected two truncated mutant transcripts in uterine tissue from homozygous mice. Western blot analysis detected a 61 kDa protein in uterine tissue from homozygotes. Transient transfection assays confirmed that this protein retains some transactivation activity in the presence of estradiol.
Mutations Made By	Kenneth Korach, LRDT, NIEHS, NIH

Disease/Phenotype

Disease Terms

Research Areas By Phenotype

This mouse can be used to support research in many areas including:

Genotype: Esr1^tm1Ksk related

Reproductive Biology Research
- Developmental Defects Affecting Gonads
  - germ cell deficient
- Fertility Defects
Internal/Organ Research
- Other Organ Defects
Developmental Biology Research
- Internal/Organ Defects
  - ovary; uterus

Neurobiology Research
- Parkinson's Disease
  - increased vulnerability to MPTP

Mammalian Phenotype Terms by Genotype

The following phenotype information is associated with a similar, but not exact match to this JAX^® Mice strain

Genotype: Esr1^tm1Ksk/Esr1^tm1Ksk
involves: 129P2/OlaHsd * C57BL/6J

adipose tissue phenotype

increased gonadal fat pad weight
- in males at 4 months of age

increased retroperitoneal fat pad weight
- in males at 4 months of age

increased total body fat amount
- in males at 4 months of age but not at 1 or 2 months of age

mammalian phenotype

skeleton phenotype
- Normal - unlike for the appendicular skeleton, no difference in the length of the axial skeleton is detected

nervous system phenotype

abnormal hypothalamus morphology
- in the anteroventral periventricular nucleus the number of TH positive neurons is increased in males compared to wild-type males

abnormal innervation
- the percentage area of the uterus innervated by PGP 9.5 and DBH immunoreactive nerves is increased even when normalized for the decrease in uterine size

renal/urinary system phenotype

abnormal kidney physiology
- display plasmacytosis of the kidney

cortical renal glomerulopathies
- show some degree of mesangial sclerosis at 1 year of age

glomerulonephritis
- seen in males and females by 1 year of age

increased urine protein level
- in males and females at 1 year of age

renal glomerular immunoglobulin deposits
- deposits of IgG are detected in the glomeruli

reproductive system phenotype

abnormal endometrium morphology
- endometrial stroma is less dense, approaching a mesh like morphology in extreme cases

abnormal epididymis morphology
- by 20-24 weeks of age, epididymides were often hypospermic esp. in the caput and corpus regions

abnormal female reproductive system physiology
- females fail to respond to estrogen treatment

abnormal ovary morphology
- containing few granulosa cells
- hyperemic cystic ovaries

abnormal seminiferous tubule epithelium morphology
- at 20 days after birth, the seminiferous epithelium is thinner than normal

abnormal seminiferous tubule morphology
- by 20-24 weeks of age, seminiferous tubules either had a dilated lumen and a thin layer of Sertoli cells or a disorganized epithelium with few spermatogonia or lacked a lumen and contained mostly Sertoli cells

abnormal spermatogenesis
- disruption of spermatogenesis evident after 10 weeks of age
- spermatogenesis occurs in the seminiferous tubules of some mutants at 3-5 months of age

abnormal uterus morphology
- the percentage area of the uterus innervated by PGP 9.5 and DBH immunoreactive nerves is increased even when normalized for the decrease in uterine size

absent corpus luteum

asthenozoospermia
- mutant sperm beat less vigorously and display less forward progression than wild-type sperm
- the sperm motility of 8-16-wk-old males declines from 20% to less than 1% during a 90-min period of in vitro capacitation

decreased testis weight
- at 20-23 weeks of age, the weight of mutant testis was significantly lower than that of wild-type or heterozygous males
- Normal - in contrast, the weights of the seminal glands, coagulating glands, and epididymi remained normal at 5-6 months of age

decreased uterus weight
- at 118 days of age

detached sperm flagellum
- sperm heads were commonly detached from the flagellum

dilated rete testis
- Normal - however, the efferent ductules and epididymides showed no signs of dilation or dysmorphology in young or adult mice
- the lumen of the rete testis became significantly dilated at 60 days after birth

dilated seminiferous tubules
- at 20 days after birth, the lumen of seminiferous tubules was significantly dilated
- tubule dilation progressed with age and became more pronounced at 60 days after birth

failure of ejaculation
- ejaculations were never observed in mutants
- when place with a receptive female for 90 min, males display mounts and intromissions but fail to ejaculate

female infertility

impaired fertilization
- sperm from 8-16-wk-old male mutants display a significantly reduced in vitro fertilization capacity relative to wild-type sperm

male infertility
- males sired no offspring during a 2-month mating period

oligozoospermia
- a reduced concentration of epididymal sperm was noted in the caput region at 10 weeks of age, and in more distal regions at 20 weeks of age
- sperm count was 10% that of wild-type
- sperm counts declined and became significantly lower than those of wild-type controls by 12-13 weeks of age

ovarian follicular cyst
- hemorrhagic ovarian cysts

reduced male fertility
- 3 of 15 males sired offspring
- males that did not sire offspring also did not produce vaginal plugs

seminiferous tubule degeneration
- degenerating seminiferous tubules were observed beginning at 10 to 12 weeks of age
- degeneration was initiated at the caudal pole of the testis and progressed in a wave to the cranial pole between 3-6 months of age
- only a few partially intact tubules were noted at the cranial pole at 6 months of age

small uterus

teratozoospermia
- Normal - however, no major sperm head abnormalities were found to occur
- sperm with retroflexed bending in the midpiece region were commonly observed

uterus hypoplasia
- Normal - however, all major cell types are present
- stromal, epithelial, and myometrial tissue compartments are all reduced

respiratory system phenotype

decreased lung weight

skeleton phenotype

decreased bone mineral content
- bone mineral content normalized to body weight is decreased in the total body, femur and spine

decreased bone mineral density
- total areal bone mineral density is slightly decreased and femur bone mineral density is decreased in adults

decreased bone mineralization
- load-induced endosteal mineral apposition rate is 50% lower than in similarly treated wild-type mice
- load-induced increase in periosteal mineralization is decreased 40% compared to in similarly treated wild-type mice
- under non-loading condition, mice exhibit reduced endosteal mineralizing surface compared with wild-type mice

decreased bone ossification
- load-induced periosteal and endosteal bone formation rates are 60% lower than in similarly treated wild-type mice
- under non-loading condition, mice exhibit reduced bone formation compared with wild-type mice

decreased bone strength
- decrease in maximal load
- Normal - however, other parameters, such as maximal stress and elastic modulus, are not significantly different from controls

decreased compact bone area
- decrease in mid-diaphyseal bone mineral content in the femur and tibia mainly as a result of a decrease in cross-sectional area associated with a decrease in periosteal and endosteal circumference

decreased length of long bones

decreased osteoblast cell number
- after 10 minutes of mechanical stress, the number of osteoblast-like cells is decreased unlike in similarly treated wild-type mice
- Normal - however, transfection of the endogenous gene restores the increase in load-induced osteoblast cells to levels greater than in similarly treated wild-type mice

increased compact bone area
- load-induced increase in cortical area is reduced 3-fold compared to in similarly treated wild-type mice
- under non-loading condition, cortical area is 12% greater than in wild-type mice
- under non-loading condition, periosteal perimeter is 6% greater than in wild-type mice

short femur
- at 118 days of age but not at 31 or 65 days of age
- in post-pubertal mice

short tibia
- at 118 days of age but not at 31 or 65 days of age

short ulna
- ulnae are 4% shorter and straighter than in wild-type mice

cardiovascular system phenotype

decreased heart weight

cellular phenotype

asthenozoospermia
- mutant sperm beat less vigorously and display less forward progression than wild-type sperm
- the sperm motility of 8-16-wk-old males declines from 20% to less than 1% during a 90-min period of in vitro capacitation

detached sperm flagellum
- sperm heads were commonly detached from the flagellum

oligozoospermia
- a reduced concentration of epididymal sperm was noted in the caput region at 10 weeks of age, and in more distal regions at 20 weeks of age
- sperm count was 10% that of wild-type
- sperm counts declined and became significantly lower than those of wild-type controls by 12-13 weeks of age

teratozoospermia
- Normal - however, no major sperm head abnormalities were found to occur
- sperm with retroflexed bending in the midpiece region were commonly observed

embryo phenotype

abnormal mesonephros morphology
- at P23 the efferent ductules are enlarged and dilated in females
- in adult females well developed and enlarged ductules with occasional epididymal-like initial segments are seen

endocrine/exocrine gland phenotype

abnormal ovary morphology
- containing few granulosa cells
- hyperemic cystic ovaries

abnormal seminiferous tubule epithelium morphology
- at 20 days after birth, the seminiferous epithelium is thinner than normal

abnormal seminiferous tubule morphology
- by 20-24 weeks of age, seminiferous tubules either had a dilated lumen and a thin layer of Sertoli cells or a disorganized epithelium with few spermatogonia or lacked a lumen and contained mostly Sertoli cells

absent corpus luteum

decreased testis weight
- at 20-23 weeks of age, the weight of mutant testis was significantly lower than that of wild-type or heterozygous males
- Normal - in contrast, the weights of the seminal glands, coagulating glands, and epididymi remained normal at 5-6 months of age

dilated rete testis
- Normal - however, the efferent ductules and epididymides showed no signs of dilation or dysmorphology in young or adult mice
- the lumen of the rete testis became significantly dilated at 60 days after birth

dilated seminiferous tubules
- at 20 days after birth, the lumen of seminiferous tubules was significantly dilated
- tubule dilation progressed with age and became more pronounced at 60 days after birth

ovarian follicular cyst
- hemorrhagic ovarian cysts

seminiferous tubule degeneration
- degenerating seminiferous tubules were observed beginning at 10 to 12 weeks of age
- degeneration was initiated at the caudal pole of the testis and progressed in a wave to the cranial pole between 3-6 months of age
- only a few partially intact tubules were noted at the cranial pole at 6 months of age

thymus hypoplasia

behavior/neurological phenotype

abnormal maternal nurturing
- gondadally intact and gonadectomized females showed greatly reduced levels of parental behavior toward newborn pups placed in their home cage

abnormal mating receptivity
- estrogen or estrogen plus progesterone-treated gonadectomized females showed prereceptive posture but did not display lordosis behavior
- females fail to show lordosis posture or receptiveness to wild-type males even when treated with estrogen
- gonadectomized females showed rejections toward male sexual behavior about 80% of the time

abnormal pup retrieval
- noninfanticidal female mutants displayed reduced levels of retrieving behavior

decreased aggression
- male mice showed a decrease in aggressive behavior relative to wild-type

decreased aggression towards males
- in a resident intruder assay aggressive behaviors toward the intruder male are greatly reduced
- loss of offensive attacks is also seen when males are tested in a neutral cage

hyperactivity
- male mice exhibited female-type open field behavior including increased activity

increased aggression towards females
- gonadally intact females exhibit higher levels of aggression toward gonadectomized and steroid-primed female intruders, however gonadectomized mutant females do not show increased aggression

increased vertical activity
- male mice exhibited female-type open field behavior including increased rearing

pup cannibalization
- about 40% of mutant females displayed infanticidal behavior

reduced male mating frequency
- males housed overnight with hormone-primed wild-type females produced significantly fewer copulatory plugs than heterozygous or wild-type males
- males mounted females but made fewer intromissions

growth/size/body region phenotype

decreased body weight
- late pubertal and young adult body weight is decreased compared to controls

increased body weight
- in adult mice (over 44 days of age)

obese
- males at 4 months of age are obese

hematopoietic system phenotype

abnormal B cell number
- 17beta-estradiol-treated castrated mice exhibit a reduced decrease in the frequency of B cells compared with similarly treated wild-type mice
- 17beta-estradiol-treated castrated mice fail to exhibit a decrease in pre-B cells and newly formed B cells unlike similarly treated wild-type mice

abnormal bone marrow cell number
- 17beta-estradiol-treated castrated mice fail to exhibit a decrease in bone marrow cellularity unlike similarly treated wild-type mice

abnormal class switch recombination
- 17beta-estradiol-treated castrated mice fail to exhibit immunoglobulin switching unlike similarly treated wild-type mice

abnormal immunoglobulin level
- 17beta-estradiol-treated castrated mice fail to exhibit an increase in production of immunoglobulins (IgA, IgG, and IgM) compared with similarly treated wild-type mice

decreased CD4-positive, alpha beta T cell number
- mice have fewer single positive CD4+ and CD8+ thymocytes compared to in wild-type mice

decreased CD8-positive, alpha-beta T cell number
- mice have fewer single positive CD4+ and CD8+ thymocytes compared to in wild-type mice

increased double-positive T cell number
- mice have increased double positive CD4+CD8+ thymocytes compared to in wild-type mice

increased IgG3 level
- in females

increased plasma cell number
- display plasmacytosis of the spleen and kidney
- lymph nodes also display an accumulation of plasma cells

increased spleen germinal center number
- despite being kept in a specific pathogen free environment mice spontaneously develop germinal centers

thymus hypoplasia

homeostasis/metabolism phenotype

abnormal circulating protein level
- decrease in the concentration of osteocalcin, a marker of bone formation, in the serum at 110 days of age

abnormal response/metabolism to endogenous compounds
- 17beta-estradiol-treated castrated mice fail to exhibit a decrease in bone marrow cellularity, immunoglobulin switching, or increased production of immunoglobulins (IgA, IgG, and IgM) and exhibit a reduced decrease in the frequency of B cells unlike similarly treated wild-type mice
- 17beta-estradiol-treated castrated mice fail to exhibit a decrease in pre-B cells and newly formed B cells unlike similarly treated wild-type mice
- arly treated wild-type mice
- Normal - however, 17beta-estradiol-treated castrated mice exhibit a decrease in pro-B cell

decreased circulating insulin-like growth factor I level
- levels are 23% lower than in wild-type controls at 118 days of age

decreased circulating osteocalcin level
- decrease in the concentration of osteocalcin, a marker of bone formation, in the serum at 110 days of age

increased circulating cholesterol level
- in adult males

increased circulating estradiol level
- about a 10 fold increase in 17beta estradiol levels in females

increased circulating HDL cholesterol level
- in adult males

increased circulating leptin level
- in males at 4 months of age but not at 1 or 2 months of age

increased circulating testosterone level
- at 20-23 weeks of age, serum testosterone levels are moderately increased relative to wild-type and heterozygous levels
- Normal - in contrast, serum LH and FSH levels are slightly but not significantly increased

increased urine protein level
- in males and females at 1 year of age

insulin resistance
- in males at 4 months of age the insulin x free fatty acid product is increased suggesting the mice are insulin resistant

immune system phenotype

abnormal B cell number
- 17beta-estradiol-treated castrated mice exhibit a reduced decrease in the frequency of B cells compared with similarly treated wild-type mice
- 17beta-estradiol-treated castrated mice fail to exhibit a decrease in pre-B cells and newly formed B cells unlike similarly treated wild-type mice

abnormal class switch recombination
- 17beta-estradiol-treated castrated mice fail to exhibit immunoglobulin switching unlike similarly treated wild-type mice

abnormal immunoglobulin level
- 17beta-estradiol-treated castrated mice fail to exhibit an increase in production of immunoglobulins (IgA, IgG, and IgM) compared with similarly treated wild-type mice

abnormal lymph node cell ratio
- display an accumulation of plasma cells

abnormal spleen physiology
- display plasmacytosis of the spleen

decreased CD4-positive, alpha beta T cell number
- mice have fewer single positive CD4+ and CD8+ thymocytes compared to in wild-type mice

decreased CD8-positive, alpha-beta T cell number
- mice have fewer single positive CD4+ and CD8+ thymocytes compared to in wild-type mice

glomerulonephritis
- seen in males and females by 1 year of age

increased anti-double stranded DNA antibody level
- in males and females

increased double-positive T cell number
- mice have increased double positive CD4+CD8+ thymocytes compared to in wild-type mice

increased IgG3 level
- in females

increased plasma cell number
- display plasmacytosis of the spleen and kidney
- lymph nodes also display an accumulation of plasma cells

increased spleen germinal center number
- despite being kept in a specific pathogen free environment mice spontaneously develop germinal centers

thymus hypoplasia

limbs/digits/tail phenotype

short femur
- at 118 days of age but not at 31 or 65 days of age
- in post-pubertal mice

short tibia
- at 118 days of age but not at 31 or 65 days of age

short ulna
- ulnae are 4% shorter and straighter than in wild-type mice

Genotype: Esr1^tm1Ksk/Esr1^tm1Ksk
involves: 129P2/OlaHsd

cardiovascular system phenotype

ovary hemorrhage
- atretic hemorrhagic follicular cysts
- hemorrhagic ovarian follicles

skeleton phenotype

abnormal chondrocyte physiology
- chondrocyte proliferation in the femur is increased compared to in Esr1^tm1Ksk Esr2^tm1Unc homozygotes
- Normal - however, chondrocyte proliferation in the tibia and vertebra is normal

abnormal long bone epiphyseal plate morphology
- at 18 months, the growth plates in the femur and tibia are fused unlike in wild-type mice
- column density is decreased compared to in Esr1^tm1Ksk Esr2^tm1Unc homozygotes

abnormal skeleton development
- at 4 months, femur growth velocity is reduced compared to in wild-type mice

abnormal vertebrae morphology
- at 18 months, vertebra height is decreased compared to in Esr1^tm1Ksk Esr2^tm1Unc homozygotes

decreased long bone epiphyseal plate size
- at 18 months, the tibia and femur growth plates exhibit decreased height compared to in wild-type mice
- at 4 months, the femur growth plate exhibit decreased height compared to in wild-type mice

short femur
- at 4, 9, and 18 months, femur length is decreased compared to in Esr1^tm1Ksk Esr2^tm1Unc homozygotes

growth/size/body region phenotype

decreased body length
- at 9 and 18 months, crown to rump length is decreased compared to Esr1^tm1Ksk Esr2^tm1Unc homozygotes

increased body weight
- however, mice do not display diethylstilbestrol (DES) induced increase in body weight
- in female mice
- in untreated females

hematopoietic system phenotype

abnormal bone marrow cell number
- decrease in the percentages of mature and CD45R+, sIgM+ B cells in the bone marrow

decreased immature B cell number
- decrease in the percentage of CD45R+, sIgM+ B cells in the bone marrow

decreased mature B cell number
- decrease in the percentage of mature B cells in the bone marrow

cellular phenotype

oligozoospermia
- cauda epididymides show a reduced concentration of sperm

homeostasis/metabolism phenotype

abnormal physiological response to xenobiotic
- treatment with PPT (propyl(1H) pyrazole-1,3,5-triyl-trisphenol) protects mice from accoustic trauma unlike similarly treated wild-type mice

abnormal response/metabolism to endogenous compounds
- E2 induced accumulation of DN1 and reduction of DN2 thymocytes is completely abrogated compared to in wild-type mice
- following treatment with 17beta-estradiol, female mice does not exhibit an increase in uterine weight unlike similarly treated wild-type mice
- thymic atrophy induced by E2 treatment is attenuated compared to in similarly treated wild type mice

albuminuria
- around 7 to 8 months, female mice exhibit increased albumin excretion compared with wild-type mice
- Normal - however, male mice and ovariectomized female mice exhibit normal albumin excretion

decreased circulating estradiol level
- in ovariectomized female mice

decreased circulating prolactin level
- in adult females
- in ovariectomized females treated with estradiol prolactin levels remain low unlike in wild-type mice

decreased circulating testosterone level
- in ovariectomized female mice

decreased physiological sensitivity to xenobiotic
- do not display diethylstilbestrol (DES) induced reduction in uterine weight, increase in body weight, or pathological changes in reproductive tissues

impaired glucose tolerance
- prior to and after tamoxifen treatment

increased circulating estradiol level

increased circulating glucose level

increased circulating testosterone level
- 8 times higher in female mice compared with wild-type mice

insulin resistance
- Normal - however, tamoxifen-treatment eventually restores normal insulin sensitivity
- mice exhibit insulin resistance compared with wild-type mice
- treatment with tamoxifen increases insulin sensitivity but mice remain insulin resistant compared with wild-type mice 15 and 30 minutes after treatment

endocrine/exocrine gland phenotype

abnormal mammary gland development
- hormone treatment with estradiol and progesterone stimulates ductal branching and lobuloalveolar development and terminal end bud formation
- in ovariectomized females treated with estradiol mammary glands do not exhibit any growth
- only a rudimentary ductal structure is present
- restoring prolactin levels by grafting half a heterozygous pituitary gland induces dramatic mammary gland growth in ovary intact females

abnormal ovary morphology

abnormal pituitary gland physiology
- patterns of staining for a gonadotropin subunit proteins are altered

abnormal testis morphology
- at 21 to 25 weeks of age in 4 males 6 of 8 testis were retracted up to near the bladder neck
- Normal - however, external examination did not reveal any defect in testicular descent
- mutants exhibit glycogen-containing cells at the rete testis-efferent ductile junction

abnormal testis weight
- after ductal occlusion testes of mutants weigh 30% more than wild-type, due to luminal fluid accumulation
- transient increase in testis weight between 32 and 81 days of age and a decrease by 185 days

absent corpus luteum
- however, females grafted with a heterozygous pituitary gland display hypertrophied luteal cells that are highly vacuolated with lipid droplets indicating steroidogenesis
- in untreated females

decreased lactotroph cell number
- modest decrease in lactotroph cell density

dilated rete testis
- dilated rete testis compared to wild-type

impaired ovarian folliculogenesis
- antral stage follicles contain apoptotic granulosa cells and degenerating oocytes
- follicles develop to the large antral stage but fail to progress further

ovarian follicular cyst
- atretic hemorrhagic follicular cysts

ovary hemorrhage
- atretic hemorrhagic follicular cysts
- hemorrhagic ovarian follicles

seminiferous tubule degeneration
- degenerate, empty tubules

immune system phenotype

decreased immature B cell number
- decrease in the percentage of CD45R+, sIgM+ B cells in the bone marrow

decreased mature B cell number
- decrease in the percentage of mature B cells in the bone marrow

spermatic granuloma
- sperm granulomas are seen in the corpus and cauda regions of 1/3 of mutant males

integument phenotype

abnormal mammary gland development
- hormone treatment with estradiol and progesterone stimulates ductal branching and lobuloalveolar development and terminal end bud formation
- in ovariectomized females treated with estradiol mammary glands do not exhibit any growth
- only a rudimentary ductal structure is present
- restoring prolactin levels by grafting half a heterozygous pituitary gland induces dramatic mammary gland growth in ovary intact females

limbs/digits/tail phenotype

short femur
- at 4, 9, and 18 months, femur length is decreased compared to in Esr1^tm1Ksk Esr2^tm1Unc homozygotes

mammalian phenotype

cardiovascular system phenotype
- Normal - mice exhibit normal estrogen- and estrogen-dendrimer conjugate (EDC)-induced reendothelialization following arterial denudation

hematopoietic system phenotype
- Normal - despite absence of Esr1, cultured bone marrow stromal cells respond to estrogen to depress B cell precursor expansion

muscle phenotype

abnormal cremaster muscle morphology
- cross sectional width of the cremaster muscle at its abdominal wall attachment and at its tip is about twice that of wild-type controls
- the cremaster sac is smaller in length and width and has a much thicker layer of cremaster muscle

nervous system phenotype

abnormal pituitary gland physiology
- patterns of staining for a gonadotropin subunit proteins are altered

decreased lactotroph cell number
- modest decrease in lactotroph cell density

renal/urinary system phenotype

albuminuria
- around 7 to 8 months, female mice exhibit increased albumin excretion compared with wild-type mice
- Normal - however, male mice and ovariectomized female mice exhibit normal albumin excretion

expanded mesangial matrix
- female mice exhibit diffuse mesangial matrix expansion compared with wild-type mice

renal glomerulus hypertrophy
- at 9 months, female mice exhibit an increase in glomerular size compared with wild-type mice
- Normal - however, ovariectomized female mice exhibit normal glomerular size

reproductive system phenotype

abnormal efferent ductules of testis morphology
- efferent ductule epithelial height is reduced by 48%
- increase in the prevalence of blind-ending efferent tubules; these blind-ending tubules have an empty and collapsaed lumen, and epithelial cells contain fewer cytoplasmic organelles, particularly lysosomes and endocytotic vesicles
- microvilli of nonciliated cells of efferent ductules along the apical border are often missing and when present, are 64% shorter in length
- nonciliated cells have missing or greatly reduced endocytotic apparatus
- number of cilia per epithelial cell is reduced and the cilia do not show the typical parallel arrangement
- the blind-ending tubules often contain enlarged bulbous endings that are never seen in wild-type

abnormal epididymis epithelium morphology
- endocytotic vesicles and large PAS+ lysosomal granules are reduced or missing in the epithelium of the epididymis
- epididymal epithelium is decreased in height by 45%
- initial segment epithelium is displaced into regions adjacent to the rete tesis and in short segments of the common region of efferent ductule

abnormal epididymis morphology
- apical, narrow, and clear cells of the epididymis are abnormal in some regions
- increase in the prevalence of blind-ending efferent tubules
- tubular diameters of the initial segment epididymides are dilated

abnormal internal male genitalia morphology
- descended testes are higher in the cremaster sac compared to wild-type littermates
- the cremaster sac is smaller in length and width and has a much thicker layer of cremaster muscle

abnormal male reproductive system physiology
- after unilateral occlusion, rete testes secretes significantly less fluid in 24 hours than wild-type
- efferent ductules from mutants treated with an anti-estorgen compound are incapable of reabsorbing luminal fluid while wild-type ductules remove most of the fluid within 3 hours

abnormal ovary morphology

abnormal superovulation
- treatment with exogenous pregnant mare serum gonadotropin followed by human chorionic gonadotropin fails to induce ovulation

abnormal testis morphology
- at 21 to 25 weeks of age in 4 males 6 of 8 testis were retracted up to near the bladder neck
- Normal - however, external examination did not reveal any defect in testicular descent
- mutants exhibit glycogen-containing cells at the rete testis-efferent ductile junction

abnormal testis weight
- after ductal occlusion testes of mutants weigh 30% more than wild-type, due to luminal fluid accumulation
- transient increase in testis weight between 32 and 81 days of age and a decrease by 185 days

abnormal vagina epithelium morphology
- epithelium is not cornified

absent corpus luteum
- however, females grafted with a heterozygous pituitary gland display hypertrophied luteal cells that are highly vacuolated with lipid droplets indicating steroidogenesis
- in untreated females

anovulation

decreased uterus weight
- however, mice do not display diethylstilbestrol (DES) induced reduction in uterine weight
- in untreated mice

dilated efferent ductules of testis
- efferent ductules are swollen, with luminal areas more than twice the size of wild-type males
- efferent tubules are dilated between 130 to 300% over wild-type ductules

dilated rete testis
- dilated rete testis compared to wild-type

failure of embryo implantation
- nodules that do form contain only decidualized uterine tissue
- transplanted wild-type embryos fail to implant in ovariectomized hormone treated females

impaired ovarian folliculogenesis
- antral stage follicles contain apoptotic granulosa cells and degenerating oocytes
- follicles develop to the large antral stage but fail to progress further

male infertility
- males are sterile

oligozoospermia
- cauda epididymides show a reduced concentration of sperm

ovarian follicular cyst
- atretic hemorrhagic follicular cysts

ovary hemorrhage
- atretic hemorrhagic follicular cysts
- hemorrhagic ovarian follicles

seminiferous tubule degeneration
- degenerate, empty tubules

spermatic granuloma
- sperm granulomas are seen in the corpus and cauda regions of 1/3 of mutant males

uterus hypoplasia

Genotype: Esr1^tm1Ksk/Esr1⁺
involves: 129P2/OlaHsd

endocrine/exocrine gland phenotype

abnormal testis morphology
- at 21 to 25 weeks of age in 4 males 5 of 8 testis were retracted up to near the bladder neck
- Normal - however, external examination did not reveal any defect in testicular descent

muscle phenotype

abnormal cremaster muscle morphology
- cross sectional width of the cremaster muscle at its abdominal wall attachment and at its tip is about twice that of wild-type controls
- the cremaster sac is smaller in length and width and has a much thicker layer of cremaster muscle

reproductive system phenotype

abnormal testis morphology
- at 21 to 25 weeks of age in 4 males 5 of 8 testis were retracted up to near the bladder neck
- Normal - however, external examination did not reveal any defect in testicular descent

Genotype: Esr1^tm1Ksk/Esr1^tm1Ksk
involves: 129P2/OlaHsd * C57BL/6N

endocrine/exocrine gland phenotype

abnormal thymus physiology
- estradiol induced thymic atrophy is reduced compared to wild-type controls and the subpopulation profile is not altered unlike in wild-type controls

decreased thymocyte number

decreased thymus weight
- about a 50% reduction in thymus weight

immune system phenotype

abnormal B cell differentiation
- unlike in wild-type mice, estradiol treatment does not change the numbers of immature or mature B cells

abnormal thymus physiology
- estradiol induced thymic atrophy is reduced compared to wild-type controls and the subpopulation profile is not altered unlike in wild-type controls

decreased B cell number

decreased immature B cell number
- decrease in the number of pre/pro and immature B cells

decreased mature B cell number

decreased thymocyte number

decreased thymus weight
- about a 50% reduction in thymus weight

hematopoietic system phenotype

abnormal B cell differentiation
- unlike in wild-type mice, estradiol treatment does not change the numbers of immature or mature B cells

abnormal definitive hematopoiesis
- following estradiol treatment hematopoietic progenitor subsets that are decreased in number in wild-type mice are not decreased in mutants

abnormal thymus physiology
- estradiol induced thymic atrophy is reduced compared to wild-type controls and the subpopulation profile is not altered unlike in wild-type controls

decreased B cell number

decreased immature B cell number
- decrease in the number of pre/pro and immature B cells

decreased mature B cell number

decreased thymocyte number

decreased thymus weight
- about a 50% reduction in thymus weight

Genotype: Esr1^tm1Ksk/Esr1^tm1Ksk
involves: 129P2/OlaHsd * C57BL/6

cardiovascular system phenotype

altered response of heart to induced stress
- damage
- following induced ischemia hearts take longer to resume regular beating, produce more nitrite, accumulate more calcium, reduce less MTT indicting a more severe impairment of mitochondrial respiratory function, and show more extensive and intense cellular damage

homeostasis/metabolism phenotype

altered response of heart to induced stress
- damage
- following induced ischemia hearts take longer to resume regular beating, produce more nitrite, accumulate more calcium, reduce less MTT indicting a more severe impairment of mitochondrial respiratory function, and show more extensive and intense cellular damage

Genotype: Esr1^tm1Ksk/Esr1^tm1Ksk
involves: 129P2/OlaHsd * 129S6/SvEvTac

endocrine/exocrine gland phenotype

dilated seminiferous tubules

homeostasis/metabolism phenotype

increased circulating estradiol level

reproductive system phenotype

dilated seminiferous tubules

Genotype: Esr1^tm1Ksk/Esr1^tm1Ksk
involves: 129P2/OlaHsd * C57BL/6 * SJL

endocrine/exocrine gland phenotype

abnormal mammary gland development
- underdeveloped at 10 weeks of age with a rudimentary ductal network confined to the nipple region

integument phenotype

abnormal mammary gland development
- underdeveloped at 10 weeks of age with a rudimentary ductal network confined to the nipple region

The following phenotype relates to a compound genotype created using this strain

Genotype: Esr1^tm1Ksk/Esr1^tm1Ksk
B6.129P2-Esr1/J

cellular phenotype

oligozoospermia
- in some mice

endocrine/exocrine gland phenotype

seminiferous tubule degeneration
- in some mice

reproductive system phenotype

oligozoospermia
- in some mice

seminiferous tubule degeneration
- in some mice

Genotype: Esr1^tm1Ksk/Esr1^tm1Ksk
B6.129P2-Esr1

adipose tissue phenotype

increased epididymal fat pad weight
- in males at 30 and 90 days of age

increased inguinal fat pad weight
- in males and females at 90 days of age

increased parametrial fat pad weight
- at 90 days of age

increased renal fat pad weight
- in females at 90 days of age
- in males at between 270 and 360 days of age

increased white adipose tissue amount
- progressive increase in the amount of white adipose tissue with age in males

increased white fat cell number
- at 180 days of age the numbers of adipocytes in the perirenal and epididymal fat pads are significantly increased
- at 90 days of age the number of adipocytes is increased in females

increased white fat cell size
- at 180 days of age the areas of adipocytes from the perirenal and epididymal fat pads are significantly increased
- at 90 days of age the size of adipocytes is increased in females

behavior/neurological phenotype

abnormal nociception after inflammation
- female mice exhibit an increased threshold to mechanical nociception following inflammation compared with similarly treated wild-type female mice
- Normal - however, male mice exhibit normal mechanical nociception after inflammation

hyporesponsive to tactile stimuli
- female mice exhibit an increased threshold to mechanical nociception compared with similarly treated wild-type female mice
- Normal - however, male mice exhibit normal mechanical nociception

impaired passive avoidance behavior
- retention is impaired in an inhibitory avoidance assay
- treatment with estradiol improves retention to a level similar to that in estradiol treated wild-type controls

growth/size/body region phenotype

decreased birth weight
- in males

increased body weight
- by 11 months of age males weigh 16% more than wild-type males

homeostasis/metabolism phenotype

decreased energy expenditure
- in males compared to wild-type littermate controls

impaired glucose tolerance
- glucose levels are higher at 30, 60 and 120 min after a glucose challenge in males compared to similarly treated wild-type males
- glucose tolerance is also impaired in females

insulin resistance
- following a glucose challenge insulin levels are significantly increased in males and females compared to wild-type controls

integument phenotype

abnormal nociception after inflammation
- female mice exhibit an increased threshold to mechanical nociception following inflammation compared with similarly treated wild-type female mice
- Normal - however, male mice exhibit normal mechanical nociception after inflammation

hyporesponsive to tactile stimuli
- female mice exhibit an increased threshold to mechanical nociception compared with similarly treated wild-type female mice
- Normal - however, male mice exhibit normal mechanical nociception

mammalian phenotype

adipose tissue phenotype
- Normal - no significant difference in the amount of brown adipose tissue is detected in male or females at any age

behavior/neurological phenotype
- Normal - no increase in food intake is seen despite the increase in the amount of white adipose tissue

References

Lubahn DB; Moyer JS; Golding TS; Couse JF; Korach KS; Smithies O. 1993. Alteration of reproductive function but not prenatal sexual development after insertional disruption of the mouse estrogen receptor gene. Proc Natl Acad Sci U S A 90(23):11162-6PubMed: 8248223 MGI: J:16338

Additional - Esr1^tm1Ksk related

Technical Support

CONTACT TECHNICAL SUPPORT

Genotyping Protocols
- Standard PCR:Esr1-Alterante 2
- Genotyping resources and troubleshooting
Breeding Considerations

When maintaining a live colony, heterozygous mice may be bred to wildtype siblings, or to C57BL/6J inbred mice (Stock No. 000664). Homozygous females are infertile. The fertility of homozygous males is greatly reduced, but not abolished. The expected coat color is black.
- Additional Breeding and Husbandry Support
Citation
When using the ERα KO mouse strain in a publication, please cite the originating article(s) and include JAX stock #004744 in your Materials and Methods section.

Animal Health Reports

Facility Barrier Level Descriptions

Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200

Pricing & Availability

Cryo Recovery

Domestic
International

Live Mouse

Age

Genotype

Price

weeks

Cryorecovery - Pricing

Service/Product	Description	Price
	Heterozygous or Wild-type for Esr1<tm1Ksk>

Related Products and Services

Frozen Mouse Embryo	B6.129P2-Esr1<tm1Ksk>/J Frozen Embryos	$2595.00
Frozen Mouse Embryo	B6.129P2-Esr1<tm1Ksk>/J Frozen Embryos	$2595.00
Frozen Mouse Embryo	B6.129P2-Esr1<tm1Ksk>/J Frozen Embryos	$3373.50
Frozen Mouse Embryo	B6.129P2-Esr1<tm1Ksk>/J Frozen Embryos	$3373.50

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The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project. We do not guarantee breeding performance and therefore suggest that investigators order more than one breeding pair to avoid delays in their research.

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Also Known As:ERα KO

Donating Investigator

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Control Suggestions

Additional Information

Selected References

Esr1tm1Ksk

Allele Symbol: Esr1tm1Ksk

Disease Terms

Research Areas By Phenotype

This mouse can be used to support research in many areas including:

Genotype: Esr1tm1Ksk related

Mammalian Phenotype Terms by Genotype

Genotype: Esr1tm1Ksk/Esr1tm1Kskinvolves: 129P2/OlaHsd * C57BL/6J

adipose tissue phenotype

mammalian phenotype

nervous system phenotype

renal/urinary system phenotype

reproductive system phenotype

respiratory system phenotype

skeleton phenotype

cardiovascular system phenotype

cellular phenotype

embryo phenotype

endocrine/exocrine gland phenotype

behavior/neurological phenotype

growth/size/body region phenotype

hematopoietic system phenotype

homeostasis/metabolism phenotype

immune system phenotype

limbs/digits/tail phenotype

Genotype: Esr1tm1Ksk/Esr1tm1Kskinvolves: 129P2/OlaHsd

cardiovascular system phenotype

skeleton phenotype

growth/size/body region phenotype

hematopoietic system phenotype

cellular phenotype

homeostasis/metabolism phenotype

endocrine/exocrine gland phenotype

immune system phenotype

integument phenotype

limbs/digits/tail phenotype

mammalian phenotype

muscle phenotype

nervous system phenotype

renal/urinary system phenotype

reproductive system phenotype

Genotype: Esr1tm1Ksk/Esr1+involves: 129P2/OlaHsd

endocrine/exocrine gland phenotype

muscle phenotype

reproductive system phenotype

Genotype: Esr1tm1Ksk/Esr1tm1Kskinvolves: 129P2/OlaHsd * C57BL/6N

endocrine/exocrine gland phenotype

immune system phenotype

hematopoietic system phenotype

Genotype: Esr1tm1Ksk/Esr1tm1Kskinvolves: 129P2/OlaHsd * C57BL/6

cardiovascular system phenotype

homeostasis/metabolism phenotype

Genotype: Esr1tm1Ksk/Esr1tm1Kskinvolves: 129P2/OlaHsd * 129S6/SvEvTac

endocrine/exocrine gland phenotype

homeostasis/metabolism phenotype

reproductive system phenotype

Genotype: Esr1tm1Ksk/Esr1tm1Kskinvolves: 129P2/OlaHsd * C57BL/6 * SJL

endocrine/exocrine gland phenotype

integument phenotype

Genotype: Esr1tm1Ksk/Esr1tm1KskB6.129P2-Esr1/J

cellular phenotype

endocrine/exocrine gland phenotype

reproductive system phenotype

Genotype: Esr1tm1Ksk/Esr1tm1KskB6.129P2-Esr1

adipose tissue phenotype

behavior/neurological phenotype

growth/size/body region phenotype

homeostasis/metabolism phenotype

integument phenotype

mammalian phenotype

Esr1^tm1Ksk

Allele Symbol: Esr1^tm1Ksk

Genotype: Esr1^tm1Ksk related

Genotype: Esr1^tm1Ksk/Esr1^tm1Ksk
involves: 129P2/OlaHsd * C57BL/6J

Genotype: Esr1^tm1Ksk/Esr1^tm1Ksk
involves: 129P2/OlaHsd

Genotype: Esr1^tm1Ksk/Esr1⁺
involves: 129P2/OlaHsd

Genotype: Esr1^tm1Ksk/Esr1^tm1Ksk
involves: 129P2/OlaHsd * C57BL/6N

Genotype: Esr1^tm1Ksk/Esr1^tm1Ksk
involves: 129P2/OlaHsd * C57BL/6

Genotype: Esr1^tm1Ksk/Esr1^tm1Ksk
involves: 129P2/OlaHsd * 129S6/SvEvTac

Genotype: Esr1^tm1Ksk/Esr1^tm1Ksk
involves: 129P2/OlaHsd * C57BL/6 * SJL

Genotype: Esr1^tm1Ksk/Esr1^tm1Ksk
B6.129P2-Esr1/J

Genotype: Esr1^tm1Ksk/Esr1^tm1Ksk
B6.129P2-Esr1

Additional - Esr1^tm1Ksk related