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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Esr1tm1.1Mma
targeted mutation 1.1, Manuel Mark
MGI:2386760
Summary 10 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Esr1tm1.1Mma/Esr1tm1.1Mma involves: 129S2/SvPas MGI:5577257
hm2
Esr1tm1.1Mma/Esr1tm1.1Mma involves: 129S2/SvPas * C57BL/6 MGI:3798269
hm3
Esr1tm1.1Mma/Esr1tm1.1Mma involves: 129S2/SvPas * C57BL/6 * SJL MGI:3798303
ht4
Esr1tm1.1Lja/Esr1tm1.1Mma involves: 129P2/OlaHsd * 129S2/SvPas * 129X1/SvJ * C57BL/6 MGI:3798270
cx5
Esr1tm1.1Mma/Esr1tm1.1Mma
Ldlrtm1Her/Ldlrtm1Her
involves: 129S2/SvPas * 129S7/SvEvBrd MGI:3833895
cx6
ApcMin/Apc+
Esr1tm1.1Mma/Esr1tm1.1Mma
involves: 129S2/SvPas * C57BL/6J MGI:5298870
cx7
ApcMin/Apc+
Esr1tm1.1Mma/Esr1+
involves: 129S2/SvPas * C57BL/6J MGI:5298871
cx8
Esr1tm1.1Mma/Esr1+
Esr2tm1Mma/Esr2tm1Mma
involves: 129S2/SvPas * C57BL/6 * SJL MGI:3798306
cx9
Esr1tm1.1Mma/Esr1tm1.1Mma
Esr2tm1Mma/Esr2+
involves: 129S2/SvPas * C57BL/6 * SJL MGI:3798308
cx10
Esr1tm1.1Mma/Esr1tm1.1Mma
Esr2tm1Mma/Esr2tm1Mma
involves: 129S2/SvPas * C57BL/6 * SJL MGI:3798305


Genotype
MGI:5577257
hm1
Allelic
Composition
Esr1tm1.1Mma/Esr1tm1.1Mma
Genetic
Background
involves: 129S2/SvPas
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Esr1tm1.1Mma mutation (0 available); any Esr1 mutation (67 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• no significant vasodilatory response after estradiol or estrogen-macromolecule conjugates treatment unlike in wild-type controls

muscle
• no significant vasodilatory response after estradiol or estrogen-macromolecule conjugates treatment unlike in wild-type controls




Genotype
MGI:3798269
hm2
Allelic
Composition
Esr1tm1.1Mma/Esr1tm1.1Mma
Genetic
Background
involves: 129S2/SvPas * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Esr1tm1.1Mma mutation (0 available); any Esr1 mutation (67 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
skeleton
• total volumetric bone mineral density is decreased compared to in wild-type mice
• however, areal bone mineral density in the femur and lumbar spine is normal
• cortical volumetric bone mineral density in the tibial metaphysis is decreased
• however, cortical volumetric bone mineral densities in the tibial diaphysis and at the lumbar vertebrae are normal
• unlike wild-type mice, cortical bone mineral density is unresponsive to ovariectomization or estrogen replacement
• unlike wild-type mice, high doses of estrogen results in an inhibitory effect on cortical volumetric bone mineral density at the diaphysis
• ovariectomized mice treated with estrogen replacement exhibit no prevention of bone loss in the femur areal volumetric bone mineral density
• trabecular volumetric bone mineral density is increased at the tibial metaphysis and the spine compared to in wild-type mice
• estradiol-treated, ovariectomized mice fail to exhibit an increase in total body areal bone mineral density (aBMD), trabecular bone parameters (trabecular bone volume and trabecular number), and cortical bone parameters unlike similarly treated wild-type mice
• unlike wild-type mice, mineral apposition rates are insensitive to ovariectomization and estrogen treatment

reproductive system
N
• mice exhibit normal numbers of gonocytes
• decreased uterine weight cannot be restored by treatment with estrogen

hematopoietic system
• estradiol-treated, ovariectomized mice fail to exhibit a decrease in thymus weight unlike similarly treated wild-type mice
• estradiol-treated, ovariectomized mice fail to exhibit an increase in IgG, IgM, and IgA secretion unlike in similarly treated wild-type mice
• estradiol-treated, ovariectomized mice fail to exhibit a decrease in bone marrow cellularity and B lymphocytes unlike similarly treated wild-type mice

homeostasis/metabolism
• estradiol-treated, ovariectomized mice fail to exhibit an affect on total body areal bone mineral density (aBMD), trabecular bone parameters (trabecular bone volume and trabecular number), cortical bone parameters, bone marrow parameters, or non-bone parameters (uterus, thymus, and liver weights) unlike similarly treated wild-type mice

immune system
• estradiol-treated, ovariectomized mice fail to exhibit a decrease in thymus weight unlike similarly treated wild-type mice
• estradiol-treated, ovariectomized mice fail to exhibit an increase in IgG, IgM, and IgA secretion unlike in similarly treated wild-type mice

behavior/neurological
N
• mice exhibit normal anxiety-related behavior
• in female mice in an open field likely due to obesity

growth/size/body
• female mice

endocrine/exocrine glands
• estradiol-treated, ovariectomized mice fail to exhibit a decrease in thymus weight unlike similarly treated wild-type mice




Genotype
MGI:3798303
hm3
Allelic
Composition
Esr1tm1.1Mma/Esr1tm1.1Mma
Genetic
Background
involves: 129S2/SvPas * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Esr1tm1.1Mma mutation (0 available); any Esr1 mutation (67 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• in the seminiferous tubules

reproductive system
• in the seminiferous tubules
• mice exhibit a reduction in the number of glandular interstitial cells compared to wild-type mice and these cells appear loosely arranged as a consequence of edema
• mice exhibit the presence of mast-like cells in the ovaries unlike wild-type mice
• mice exhibit an excess of follicles at advanced stages of atresia
• however, primordial, primary and antral follicles are normal
• unlike in wild-type mice, prepubertal ovaries contain large antral follicles with well-defined antrums
• mice exhibit large, hemorrhagic cysts originating from antral follicles
• mice exhibit a straightening of the rete testis unlike wild-type mice
• mice exhibit a straightening of the seminiferous tubules unlike wild-type mice
• unlike in wild-type mice, cyclic changes to the uterus and vagina are absent

growth/size/body
• mice exhibit large, hemorrhagic cysts originating from antral follicles

homeostasis/metabolism
• superovulation induced by gonadotropin treatment is severely reduced compared to in wild-type mice

endocrine/exocrine glands
• mice exhibit a reduction in the number of glandular interstitial cells compared to wild-type mice and these cells appear loosely arranged as a consequence of edema
• mice exhibit the presence of mast-like cells in the ovaries unlike wild-type mice
• mice exhibit an excess of follicles at advanced stages of atresia
• however, primordial, primary and antral follicles are normal
• unlike in wild-type mice, prepubertal ovaries contain large antral follicles with well-defined antrums
• mice exhibit large, hemorrhagic cysts originating from antral follicles
• mice exhibit a straightening of the rete testis unlike wild-type mice
• mice exhibit a straightening of the seminiferous tubules unlike wild-type mice




Genotype
MGI:3798270
ht4
Allelic
Composition
Esr1tm1.1Lja/Esr1tm1.1Mma
Genetic
Background
involves: 129P2/OlaHsd * 129S2/SvPas * 129X1/SvJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Esr1tm1.1Lja mutation (2 available); any Esr1 mutation (67 available)
Esr1tm1.1Mma mutation (0 available); any Esr1 mutation (67 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
skeleton
• unlike in wild-type mice, bone erosion is decreased following ovariectomization
• at 5 months of age
• the periosteal bone circumference is reduced and the endocortical circumference is increased compared to in wild-type mice
• mice exhibit decreased bone mineral density
• however, volumetric bone mineral densities at the proximal tibial metaphysis and trabeculae are normal
• ovariectomized mice exhibit an increase in cortical volumetric bone mineral density
• ovariectomized mice treated with estrogen replacement exhibit an attenuated response in preventing bone loss in trabecular bone compared to bone loss in cortical bone unlike in similarly treated wild-type mice
• unlike in wild-type mice, ovariectomized mice treated with a low dose of estrogen replacement exhibit no prevention of bone loss in the femur areal volumetric bone mineral density whereas treatment with high doses of estrogen result in further decrease in areal bone mineral density
• cortical volumetric bone mineral density at the tibial metaphysis and diaphysis and in the cortical shell and posterior elements of the lumbar spine are decreased compared to in wild-type mice
• cortical areas and thickness in the tibial metaphysis and diaphysis are reduced compared to in wild-type mice
• cortical areas and thickness in the tibial metaphysis and diaphysis are reduced compared to in wild-type mice
• axial and or appendicular skeletal bone mass is reduced compared to in wild-type mice
• unlike in wild-type mice, endocortical surface mineral apposition is increased after ovariectomization and decreased after treatment with estrogen

homeostasis/metabolism

reproductive system
• estrogen treatment can partially restore decreased uterine weight

immune system
• unlike in wild-type mice, bone erosion is decreased following ovariectomization

limbs/digits/tail
• at 5 months of age

hematopoietic system
• unlike in wild-type mice, bone erosion is decreased following ovariectomization




Genotype
MGI:3833895
cx5
Allelic
Composition
Esr1tm1.1Mma/Esr1tm1.1Mma
Ldlrtm1Her/Ldlrtm1Her
Genetic
Background
involves: 129S2/SvPas * 129S7/SvEvBrd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Esr1tm1.1Mma mutation (0 available); any Esr1 mutation (67 available)
Ldlrtm1Her mutation (19 available); any Ldlr mutation (76 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• estrogen fails to prevent fatty streak deposits in the aorta of these mice as it does in Ldlr null homozygote controls

cardiovascular system
• lacking functional Ldlr receptors makes this mice prone to developing atherosclerosis




Genotype
MGI:5298870
cx6
Allelic
Composition
ApcMin/Apc+
Esr1tm1.1Mma/Esr1tm1.1Mma
Genetic
Background
involves: 129S2/SvPas * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (12 available); any Apc mutation (154 available)
Esr1tm1.1Mma mutation (0 available); any Esr1 mutation (67 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging




Genotype
MGI:5298871
cx7
Allelic
Composition
ApcMin/Apc+
Esr1tm1.1Mma/Esr1+
Genetic
Background
involves: 129S2/SvPas * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (12 available); any Apc mutation (154 available)
Esr1tm1.1Mma mutation (0 available); any Esr1 mutation (67 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mice develop increased tumors in the small and large intestines, including the cecum and one third of the colons, compared with Apcmin heterozygotes
• mice develop sessile and pedunculated forms of colonic adenomas unlike Apcmin heterozygotes
• while tumor progression is stimulated to a greater extent than in Apcmin heterozygotes, tumor initiation is the same
• all mice develop invasive carcinomas in the intestine and colon unlike Apcmin heterozygotes

digestive/alimentary system
• increased proliferation of cells in the colon
• some mice exhibit abnormal submucosal with thickening of the muscularis mucosae and enrichment of stromal components compared with Apcmin heterozygotes
• some mice exhibit reduced crypt length and distortion of surface epithelial cells in the colon compared with control mice
• fewer mature goblet cells in the colon with prevalent pregoblet cells
• mice develop increased tumors in the small and large intestines, including the cecum and one third of the colons, compared with Apcmin heterozygotes
• mice develop sessile and pedunculated forms of colonic adenomas unlike Apcmin heterozygotes
• while tumor progression is stimulated to a greater extent than in Apcmin heterozygotes, tumor initiation is the same

endocrine/exocrine glands
• some mice exhibit reduced crypt length and distortion of surface epithelial cells in the colon compared with control mice
• fewer mature goblet cells in the colon with prevalent pregoblet cells

cellular
• fewer mature goblet cells in the colon with prevalent pregoblet cells
• increased proliferation of cells in the colon




Genotype
MGI:3798306
cx8
Allelic
Composition
Esr1tm1.1Mma/Esr1+
Esr2tm1Mma/Esr2tm1Mma
Genetic
Background
involves: 129S2/SvPas * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Esr1tm1.1Mma mutation (0 available); any Esr1 mutation (67 available)
Esr2tm1Mma mutation (0 available); any Esr2 mutation (32 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
reproductive system
• unlike in wild-type mice, follicles exhibit a marked deficiency in granulose cells
• mice exhibit increased antral follicle numbers compared to in wild-type mice
• however, no cysts form and interstitial glandular cell organization is normal
• despite the fertility of male mice, female mice exhibit reduced fertility to infertility

homeostasis/metabolism
• mice fail to superovulate when treated with gonadotropins because follicles reach a preovulatory stage but fail to mature unlike in similarly treated wild-type mice

endocrine/exocrine glands
• unlike in wild-type mice, follicles exhibit a marked deficiency in granulose cells
• mice exhibit increased antral follicle numbers compared to in wild-type mice
• however, no cysts form and interstitial glandular cell organization is normal

cellular
• unlike in wild-type mice, follicles exhibit a marked deficiency in granulose cells




Genotype
MGI:3798308
cx9
Allelic
Composition
Esr1tm1.1Mma/Esr1tm1.1Mma
Esr2tm1Mma/Esr2+
Genetic
Background
involves: 129S2/SvPas * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Esr1tm1.1Mma mutation (0 available); any Esr1 mutation (67 available)
Esr2tm1Mma mutation (0 available); any Esr2 mutation (32 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• superovulation induced by gonadotropin treatment is severely reduced compared to in wild-type mice




Genotype
MGI:3798305
cx10
Allelic
Composition
Esr1tm1.1Mma/Esr1tm1.1Mma
Esr2tm1Mma/Esr2tm1Mma
Genetic
Background
involves: 129S2/SvPas * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Esr1tm1.1Mma mutation (0 available); any Esr1 mutation (67 available)
Esr2tm1Mma mutation (0 available); any Esr2 mutation (32 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
• mice exhibit large, hemorrhagic cysts originating from antral follicles

reproductive system
• in the seminiferous tubules
• unlike in wild-type mice, follicles exhibit a marked deficiency in granulosa cells
• the largest antral follicles exhibit very thin walls due to the absence of granulosa cells
• mice exhibit a reduction in the number of glandular interstitial cells compared to wild-type mice and these cells appear loosely arranged as a consequence of edema
• mice exhibit the presence of mast-like cells in the ovaries unlike wild-type mice
• ovaries contain fully differentiated Sertoli cells
• however, female mice do not exhibit an increase in anti-Mullerian hormone
• however, primordial, and primary follicles are normal
• Sertoli cells develop between ovarian follicles after the onset of puberty and appear to arise within the epithelium of atretic follicles
• mice exhibit an excess of follicles at advanced stages of atresia
• the largest antral follicles exhibit very thin walls due to the absence of granulosa cells
• unlike in wild-type mice, prepubertal antral follicles are surrounded by a single layer or loosely packed organization of granulosa cells and a single layer of theca cells, and contain a suspended oocyte completely detached from the follicular wall
• theca cell proliferation is decreased compared to in wild-type mice
• mice exhibit large, hemorrhagic cysts originating from antral follicles
• mice exhibit a straightening of the rete testis unlike wild-type mice
• mice exhibit a straightening of the seminiferous tubules unlike wild-type mice
• ovaries contain fully differentiated Sertoli cells
• Sertoli cells in the ovaries develop between ovarian follicles after the onset of puberty and appear to arise within the epithelium of atretic follicles
• despite normal genital tract anterior-posterior development, mice exhibit a 2-fold reduction in uterus diameter and wall thickness
• mice exhibit a reduction in cell number and size that affects all tissue types
• despite normal genital tract anterior-posterior development, mice exhibit a 2-fold reduction in vagina diameter and wall thickness
• mice exhibit hypoplastic vaginas with a reduction in both cell number and size that affects all tissue types

homeostasis/metabolism
• mice fail to superovulate when treated with gonadotropins and follicles fail to even reach the preovulatory stage unlike in similarly treated wild-type mice

endocrine/exocrine glands
• unlike in wild-type mice, follicles exhibit a marked deficiency in granulosa cells
• the largest antral follicles exhibit very thin walls due to the absence of granulosa cells
• mice exhibit a reduction in the number of glandular interstitial cells compared to wild-type mice and these cells appear loosely arranged as a consequence of edema
• mice exhibit the presence of mast-like cells in the ovaries unlike wild-type mice
• ovaries contain fully differentiated Sertoli cells
• however, female mice do not exhibit an increase in anti-Mullerian hormone
• however, primordial, and primary follicles are normal
• Sertoli cells develop between ovarian follicles after the onset of puberty and appear to arise within the epithelium of atretic follicles
• mice exhibit an excess of follicles at advanced stages of atresia
• the largest antral follicles exhibit very thin walls due to the absence of granulosa cells
• unlike in wild-type mice, prepubertal antral follicles are surrounded by a single layer or loosely packed organization of granulosa cells and a single layer of theca cells, and contain a suspended oocyte completely detached from the follicular wall
• theca cell proliferation is decreased compared to in wild-type mice
• mice exhibit large, hemorrhagic cysts originating from antral follicles
• mice exhibit a straightening of the rete testis unlike wild-type mice
• mice exhibit a straightening of the seminiferous tubules unlike wild-type mice
• ovaries contain fully differentiated Sertoli cells
• Sertoli cells in the ovaries develop between ovarian follicles after the onset of puberty and appear to arise within the epithelium of atretic follicles

cellular
• in the seminiferous tubules
• unlike in wild-type mice, follicles exhibit a marked deficiency in granulosa cells
• the largest antral follicles exhibit very thin walls due to the absence of granulosa cells





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last database update
04/16/2024
MGI 6.23
The Jackson Laboratory