All Phenotypes Esr2<tm1Mma> MGI Mouse

Phenotypes associated with this allele

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Esr2^tm1Mma/Esr2^tm1Mma	involves: 129S2/SvPas	MGI:3798307
hm2	Esr2^tm1Mma/Esr2^tm1Mma	involves: 129S2/SvPas * C57BL/6	MGI:5298865
ht3	Esr2^tm1Mma/Esr2⁺	involves: 129S2/SvPas	MGI:5298866
cx4	Esr1^tm1.1Mma/Esr1^tm1.1Mma Esr2^tm1Mma/Esr2^tm1Mma	involves: 129S2/SvPas * C57BL/6 * SJL	MGI:3798305
cx5	Esr1^tm1.1Mma/Esr1⁺ Esr2^tm1Mma/Esr2^tm1Mma	involves: 129S2/SvPas * C57BL/6 * SJL	MGI:3798306
cx6	Esr1^tm1.1Mma/Esr1^tm1.1Mma Esr2^tm1Mma/Esr2⁺	involves: 129S2/SvPas * C57BL/6 * SJL	MGI:3798308
cx7	Apc^Min/Apc⁺ Esr2^tm1Mma/Esr2⁺	involves: 129S2/SvPas * C57BL/6J	MGI:5298868
cx8	Apc^Min/Apc⁺ Esr2^tm1Mma/Esr2^tm1Mma	involves: 129S2/SvPas * C57BL/6J	MGI:5298869

Allelic Composition	Esr2^tm1Mma/Esr2^tm1Mma
Genetic Background	involves: 129S2/SvPas

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Esr2^tm1Mma mutation (0 available); any Esr2 mutation (36 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

cellular

abnormal germ cell morphology ( J:105626 )

• increased gonocytes after birth with decreased gonocyte apoptosis

reproductive system

reproductive system phenotype ( J:64426 , J:105626 )

N	• contrary to previous reports, no hyperplasia of the prostate is observed (J:64426) • mice exhibit normal numbers of Sertoli and Leydig cells and level of testicular testosterone production (J:105626)

abnormal germ cell morphology ( J:105626 )

• increased gonocytes after birth with decreased gonocyte apoptosis

decreased corpora lutea number ( J:64426 )

• despite normal follicle development, the corpus lutea are scarce or absent

reduced female fertility ( J:64426 )

• despite the fertility of male mice, female mice exhibit reduced fertility to infertility

• however, female genital tract morphology is normal

skeleton

skeleton phenotype ( J:123373 )

N	• mice exhibit normal bone mineral content in the lumbar spine and hind leg and normal bone area and bone mineral density in the midfemur

short ulna ( J:123373 )

• slightly

decreased volumetric bone mineral density ( J:123373 )

• mice exhibit lower volumetric bone mineral density in the lumbar spine and distal femur compared with wild-type mice

abnormal bone ossification ( J:123373 )

• unloaded and loaded ulna from female mice exhibit increased bone formation measurements compared with wild-type mice

increased bone strength ( J:123373 )

• female mice exhibit increased bone stiffness and mechanical loading compared with wild-type mice

• however, male mice exhibit normal bone stiffness and mechanical loading

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:123373 )

N	• unlike in previous studies, IGF-I levels are normal

abnormal response/metabolism to endogenous compounds ( J:64426 )

• when treated with gonadotropins to induce superovulation, half of mice failed to ovulate and the other half exhibited reduced yields compared to in similarly treated wild-type mice because follicles reach a preovulatory stage but fail to mature

delayed wound healing ( J:165719 )

• ovariectomized mice treated with 17beta-estradiol exhibit delayed wound healing with increased neutrophil infiltration compared with control mice

renal/urinary system

renal/urinary system phenotype ( J:64426 )

N	• contrary to previous reports, no hyperplasia of the urinary bladder is observed

adipose tissue

increased total body fat amount ( J:123373 )

• in female, but not male, mice

limbs/digits/tail

short ulna ( J:123373 )

• slightly

endocrine/exocrine glands

decreased corpora lutea number ( J:64426 )

• despite normal follicle development, the corpus lutea are scarce or absent

hematopoietic system

increased neutrophil cell number ( J:165719 )

• in the wounds of ovariectomized mice treated with 17beta-estradiol

immune system

increased neutrophil cell number ( J:165719 )

• in the wounds of ovariectomized mice treated with 17beta-estradiol

Allelic Composition	Esr2^tm1Mma/Esr2^tm1Mma
Genetic Background	involves: 129S2/SvPas * C57BL/6

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Esr2^tm1Mma mutation (0 available); any Esr2 mutation (36 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

behavior/neurological

increased anxiety-related response ( J:72240 )

• in an elevated plus maze, female mice exhibit fewer time in open arms and head dips compared with wild-type mice

• however, male mice exhibit normal anxiety-related behavior

increased thigmotaxis ( J:72240 )

• in female mice in an open field

decreased vertical activity ( J:72240 )

• in female mice in an open field

decreased locomotor activity ( J:72240 )

• in female mice in an open field

decreased chemical nociceptive threshold ( J:130786 )

• in ovariectomized female mice during the interphase and early tonic phase II of the formalin test but not during acute and late tonic phases

nervous system

abnormal synaptic plasticity ( J:72240 )

• female mice exhibit reduced threshold for the induction of synaptic plasticity in the basolateral amygdala compared with wild-type mice

Allelic Composition	Esr2^tm1Mma/Esr2⁺
Genetic Background	involves: 129S2/SvPas

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Esr2^tm1Mma mutation (0 available); any Esr2 mutation (36 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

reproductive system

reproductive system phenotype ( J:105626 )

N	• mice exhibit normal numbers of Sertoli and Leydig cells and level of testicular testosterone production

abnormal germ cell morphology ( J:105626 )

• increased gonocytes after birth with decreased gonocyte apoptosis

cellular

abnormal germ cell morphology ( J:105626 )

• increased gonocytes after birth with decreased gonocyte apoptosis

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

growth/size/body

ovarian follicular cyst ( J:64426 )

• mice exhibit large, hemorrhagic cysts originating from antral follicles

reproductive system

decreased male germ cell number ( J:64426 )

• in the seminiferous tubules

impaired granulosa cell differentiation ( J:64426 )

• 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

abnormal ovary morphology ( J:64426 )

• 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

abnormal ovarian follicle morphology ( J:64426 )

• 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

increased atretic ovarian follicle number ( J:64426 )

• mice exhibit an excess of follicles at advanced stages of atresia

abnormal tertiary ovarian follicle morphology ( J:64426 )

• 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

decreased theca cell number ( J:64426 )

• theca cell proliferation is decreased compared to in wild-type mice

ovarian follicular cyst ( J:64426 )

• mice exhibit large, hemorrhagic cysts originating from antral follicles

abnormal rete testis morphology ( J:64426 )

• mice exhibit a straightening of the rete testis unlike wild-type mice

abnormal seminiferous tubule morphology ( J:64426 )

• mice exhibit a straightening of the seminiferous tubules unlike wild-type mice

abnormal Sertoli cell morphology ( J:64426 )

• 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

thin uterus ( J:64426 )

• despite normal genital tract anterior-posterior development, mice exhibit a 2-fold reduction in uterus diameter and wall thickness

uterus hypoplasia ( J:64426 )

• mice exhibit a reduction in cell number and size that affects all tissue types

small vagina ( J:64426 )

• despite normal genital tract anterior-posterior development, mice exhibit a 2-fold reduction in vagina diameter and wall thickness

vagina hypoplasia ( J:64426 )

• mice exhibit hypoplastic vaginas with a reduction in both cell number and size that affects all tissue types

male infertility ( J:64426 )

homeostasis/metabolism

abnormal response/metabolism to endogenous compounds ( J:64426 )

• 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

impaired granulosa cell differentiation ( J:64426 )

• 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

abnormal ovary morphology ( J:64426 )

• 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

abnormal ovarian follicle morphology ( J:64426 )

• 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

increased atretic ovarian follicle number ( J:64426 )

• mice exhibit an excess of follicles at advanced stages of atresia

abnormal tertiary ovarian follicle morphology ( J:64426 )

• the largest antral follicles exhibit very thin walls due to the absence of granulosa cells

decreased theca cell number ( J:64426 )

• theca cell proliferation is decreased compared to in wild-type mice

ovarian follicular cyst ( J:64426 )

• mice exhibit large, hemorrhagic cysts originating from antral follicles

abnormal rete testis morphology ( J:64426 )

• mice exhibit a straightening of the rete testis unlike wild-type mice

abnormal seminiferous tubule morphology ( J:64426 )

• mice exhibit a straightening of the seminiferous tubules unlike wild-type mice

abnormal Sertoli cell morphology ( J:64426 )

• 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

decreased male germ cell number ( J:64426 )

• in the seminiferous tubules

impaired granulosa cell differentiation ( J:64426 )

• 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

Allelic Composition	Esr1^tm1.1Mma/Esr1⁺ Esr2^tm1Mma/Esr2^tm1Mma
Genetic Background	involves: 129S2/SvPas * C57BL/6 * SJL

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Esr1^tm1.1Mma mutation (0 available); any Esr1 mutation (68 available)
Esr2^tm1Mma mutation (0 available); any Esr2 mutation (36 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

reproductive system

impaired granulosa cell differentiation ( J:64426 )

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

absent corpus luteum ( J:64426 )

increased tertiary ovarian follicle number ( J:64426 )

• mice exhibit increased antral follicle numbers compared to in wild-type mice

• however, no cysts form and interstitial glandular cell organization is normal

reduced female fertility ( J:64426 )

• despite the fertility of male mice, female mice exhibit reduced fertility to infertility

homeostasis/metabolism

abnormal response/metabolism to endogenous compounds ( J:64426 )

• 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

impaired granulosa cell differentiation ( J:64426 )

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

absent corpus luteum ( J:64426 )

increased tertiary ovarian follicle number ( J:64426 )

• mice exhibit increased antral follicle numbers compared to in wild-type mice

• however, no cysts form and interstitial glandular cell organization is normal

cellular

impaired granulosa cell differentiation ( J:64426 )

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

Allelic Composition	Esr1^tm1.1Mma/Esr1^tm1.1Mma Esr2^tm1Mma/Esr2⁺
Genetic Background	involves: 129S2/SvPas * C57BL/6 * SJL

Find Mice

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

homeostasis/metabolism

abnormal response/metabolism to endogenous compounds ( J:64426 )

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

Allelic Composition	Apc^Min/Apc⁺ Esr2^tm1Mma/Esr2⁺
Genetic Background	involves: 129S2/SvPas * C57BL/6J

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apc^Min mutation (12 available); any Apc mutation (158 available)
Esr2^tm1Mma mutation (0 available); any Esr2 mutation (36 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

neoplasm

increased gastrointestinal tumor incidence ( J:118600 )

• mice develop increased tumors in the small and large intestines, including the cecum and one third of the colons, compared with Apc^min heterozygotes

• mice develop sessile and pedunculated forms of colonic adenomas unlike Apc^min heterozygotes

• while tumor progression is stimulated to a greater extent than in Apc^min heterozygotes, tumor initiation is the same

digestive/alimentary system

abnormal enterocyte proliferation ( J:118600 )

• increased proliferation of cells in the colon in ovariectomized

increased gastrointestinal tumor incidence ( J:118600 )

• mice develop increased tumors in the small and large intestines, including the cecum and one third of the colons, compared with Apc^min heterozygotes

• mice develop sessile and pedunculated forms of colonic adenomas unlike Apc^min heterozygotes

• while tumor progression is stimulated to a greater extent than in Apc^min heterozygotes, tumor initiation is the same

cellular

abnormal enterocyte proliferation ( J:118600 )

• increased proliferation of cells in the colon in ovariectomized

Allelic Composition	Apc^Min/Apc⁺ Esr2^tm1Mma/Esr2^tm1Mma
Genetic Background	involves: 129S2/SvPas * C57BL/6J

Find Mice

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

digestive/alimentary system

abnormal colon goblet cell morphology ( J:118600 )

• fewer mature goblet cells in the colon with prevalent pregoblet cells

abnormal enterocyte proliferation ( J:118600 )

• increased proliferation of cells in the colon

increased gastrointestinal tumor incidence ( J:118600 )

• mice develop increased tumors in the large intestine, including the cecum and one third of the colons, compared with Apc^min heterozygotes

• mice develop sessile and pedunculated forms of colonic adenomas unlike Apc^min heterozygotes

• while tumor progression is stimulated to a greater extent than in Apc^min heterozygotes, tumor initiation is the same

increased colon adenoma incidence ( J:118600 )

• noninvasive

colitis ( J:118600 )

• mononuclear cell infiltrates in the colon

neoplasm

increased gastrointestinal tumor incidence ( J:118600 )

• mice develop increased tumors in the large intestine, including the cecum and one third of the colons, compared with Apc^min heterozygotes

• mice develop sessile and pedunculated forms of colonic adenomas unlike Apc^min heterozygotes

• while tumor progression is stimulated to a greater extent than in Apc^min heterozygotes, tumor initiation is the same

increased colon adenoma incidence ( J:118600 )

• noninvasive

immune system

colitis ( J:118600 )

• mononuclear cell infiltrates in the colon

cellular

abnormal colon goblet cell morphology ( J:118600 )

• fewer mature goblet cells in the colon with prevalent pregoblet cells

abnormal enterocyte proliferation ( J:118600 )

• increased proliferation of cells in the colon

endocrine/exocrine glands

abnormal colon goblet cell morphology ( J:118600 )

• fewer mature goblet cells in the colon with prevalent pregoblet cells

Contributing Projects: Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO)
Citing These Resources Funding Information Warranty Disclaimer, Privacy Notice, Licensing, & Copyright Send questions and comments to User Support.	last database update 10/22/2024 MGI 6.24