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 (32 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 (32 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 (32 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 (67 available)
Esr2^tm1Mma mutation (0 available); any Esr2 mutation (32 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 (154 available)
Esr2^tm1Mma mutation (0 available); any Esr2 mutation (32 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 )

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

• 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

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

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