All Phenotypes Kmt2b<tm1Afst> MGI Mouse

Phenotypes associated with this allele

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Kmt2b^tm1Afst/Kmt2b^tm1Afst	involves: 129P2/OlaHsd * C57BL/6	MGI:3626326
ht2	Kmt2b^tm1Afst/Kmt2b⁺	involves: 129P2/OlaHsd	MGI:5532305
ht3	Kmt2b^Gena263/Kmt2b^tm1Afst	involves: 129P2/OlaHsd * BALB/c * C3H/HeH	MGI:5532306
cn4	Kmt2b^tm1Afst/Kmt2b^tm1.1Afst Tg(Gdf9-icre)5092Coo/0	involves: 129 * 129P2/OlaHsd * C57BL/6	MGI:4867493
cn5	Kmt2b^tm1Afst/Kmt2b^tm1.1Afst Tg(Zp3-cre)3Mrt/0	involves: 129 * 129P2/OlaHsd * C57BL/6 * FVB/N	MGI:4867494
cn6	Kmt2b^tm1Afst/Kmt2b^tm1.1Afst Amhr2^tm3(cre)Bhr/Amhr2⁺	involves: 129P2/OlaHsd * 129S/SvEv * C57BL/6	MGI:4867492
cn7	Kmt2b^tm1Afst/Kmt2b^tm1.1Afst Gt(ROSA)26Sor^{tm9(cre/ESR1)Arte}/Gt(ROSA)26Sor⁺	involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6	MGI:4867495

Allelic Composition	Kmt2b^tm1Afst/Kmt2b^tm1Afst
Genetic Background	involves: 129P2/OlaHsd * C57BL/6

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Kmt2b^tm1Afst mutation (0 available); any Kmt2b mutation (65 available)

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

mortality/aging

embryonic lethality, complete penetrance ( J:107403 )

• before E11.5

• Background Sensitivity: increasing the amount of C57BL/6 in the strain background results in a slight reduction in the severity of the phenotype

nervous system

open neural tube ( J:107403 )

• seen at E9.5 in most homozygotes

• Background Sensitivity: increasing C57BL/6 content decreased this phenotype

kinked neural tube ( J:107403 )

• at E9.5

growth/size/body

embryonic growth retardation ( J:107403 )

• growth is slowed at E6.5 and development is retarded by E7.5

• E9.5 is the 8 somite stage

embryo

embryonic growth retardation ( J:107403 )

• growth is slowed at E6.5 and development is retarded by E7.5

• E9.5 is the 8 somite stage

open neural tube ( J:107403 )

• seen at E9.5 in most homozygotes

• Background Sensitivity: increasing C57BL/6 content decreased this phenotype

kinked neural tube ( J:107403 )

• at E9.5

abnormal somite development ( J:107403 )

• Meox1 expression is initiated normally but then lost from the anterior most somites and somites seem to disappear resulting in kinking of the neural tube

cellular

increased apoptosis ( J:107403 )

• widespread apoptosis is seen at E9.5

Allelic Composition	Kmt2b^tm1Afst/Kmt2b⁺
Genetic Background	involves: 129P2/OlaHsd

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Kmt2b^tm1Afst mutation (0 available); any Kmt2b mutation (65 available)

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

homeostasis/metabolism

decreased insulin secretion ( J:203736 )

• in response to glucose challenge

increased circulating glucose level ( J:203736 )

• in fasted mice and during intraperitoneal glucose tolerance test

increased circulating insulin level ( J:203736 )

• in fasted mice

impaired glucose tolerance ( J:203736 )

insulin resistance ( J:203736 )

adipose tissue

increased epididymal fat pad weight ( J:203736 )

liver/biliary system

liver/biliary system phenotype ( J:203736 )

N	• mice exhibit normal liver weight

endocrine/exocrine glands

decreased insulin secretion ( J:203736 )

• in response to glucose challenge

Allelic Composition	Kmt2b^Gena263/Kmt2b^tm1Afst
Genetic Background	involves: 129P2/OlaHsd * BALB/c * C3H/HeH

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Kmt2b^Gena263 mutation (0 available); any Kmt2b mutation (65 available)
Kmt2b^tm1Afst mutation (0 available); any Kmt2b mutation (65 available)

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

mortality/aging

embryonic lethality during organogenesis, complete penetrance ( J:203736 )

• mice die between E8.5 and E12.5

embryonic lethality between somite formation and embryo turning, incomplete penetrance ( J:203736 )

• mice die between E8.5 and E12.5

nervous system

exencephaly ( J:203736 )

cardiovascular system

pericardial effusion ( J:203736 )

homeostasis/metabolism

pericardial effusion ( J:203736 )

edema ( J:203736 )

• generalized

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

reproductive system

abnormal female meiosis I arrest ( J:166778 )

• a small but significant fraction remains arrested in meiosis I in cultured peri-ovulatory oocytes for in vitro oocyte maturation studies

abnormal ovarian follicle number ( J:166778 )

• very few follicles at 36 weeks old

increased primary ovarian follicle number ( J:166778 )

• a higher number of primary growing follicles at 2 weeks old

decreased primordial ovarian follicle number ( J:166778 )

• a 50% decrease in primordial follicles at 3 weeks old

• an 80% reduction in primordial follicles at 8 weeks old

increased secondary ovarian follicle number ( J:166778 )

• increase in growing preantral follicles at 3 weeks old

increased atretic ovarian follicle number ( J:166778 )

• increased number of atretic follicles from 3 week of age onwards

increased follicle recruitment ( J:166778 )

• a higher number of primary growing follicles at 2 weeks old

• a 50% decrease in primordial follicles and an increase in growing preantral follicles at 3 weeks old

• an 80% reduction in primordial follicles at 8 weeks old

• increased number of atretic follicles from 3 week of age onwards

• very few follicles at 36 weeks old

decreased superovulation rate ( J:166778 )

• reduced ovulation rates in 3-week-old superovulated females

• trapped oocytes in luteinizing structures in hormonally stimulated females

female infertility ( J:166778 )

homeostasis/metabolism

decreased circulating estradiol level ( J:166778 )

• decreased serum estradiol levels at 8 weeks old

increased circulating follicle stimulating hormone level ( J:166778 )

• increased serum FSH levels at 8 weeks old

increased circulating luteinizing hormone level ( J:166778 )

• increased serum LH levels at 8 weeks old

cellular

abnormal cell physiology ( J:166778 )

• increased H4K12 acetylation

abnormal female meiosis I arrest ( J:166778 )

• a small but significant fraction remains arrested in meiosis I in cultured peri-ovulatory oocytes for in vitro oocyte maturation studies

abnormal DNA methylation ( J:166778 )

• increased mono-methylated H3K4 in oocytes

• decreased bi- and tri-methylated H3K4 in oocytes

abnormal imprinting ( J:166778 )

• fail to establish transcriptional repression

• 80% of the oocytes are still transcriptionally active at the peri-ovulatory stage

• normal nucleolus configuration

endocrine/exocrine glands

abnormal ovarian follicle number ( J:166778 )

• very few follicles at 36 weeks old

increased primary ovarian follicle number ( J:166778 )

• a higher number of primary growing follicles at 2 weeks old

decreased primordial ovarian follicle number ( J:166778 )

• a 50% decrease in primordial follicles at 3 weeks old

• an 80% reduction in primordial follicles at 8 weeks old

increased secondary ovarian follicle number ( J:166778 )

• increase in growing preantral follicles at 3 weeks old

increased atretic ovarian follicle number ( J:166778 )

• increased number of atretic follicles from 3 week of age onwards

increased follicle recruitment ( J:166778 )

• a higher number of primary growing follicles at 2 weeks old

• a 50% decrease in primordial follicles and an increase in growing preantral follicles at 3 weeks old

• an 80% reduction in primordial follicles at 8 weeks old

• increased number of atretic follicles from 3 week of age onwards

• very few follicles at 36 weeks old

Allelic Composition	Kmt2b^tm1Afst/Kmt2b^tm1.1Afst Tg(Zp3-cre)3Mrt/0
Genetic Background	involves: 129 * 129P2/OlaHsd * C57BL/6 * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Kmt2b^tm1.1Afst mutation (0 available); any Kmt2b mutation (65 available)
Kmt2b^tm1Afst mutation (0 available); any Kmt2b mutation (65 available)
Tg(Zp3-cre)3Mrt mutation (2 available)

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

reproductive system

abnormal ovarian follicle number ( J:166778 )

• increased number of secondary and preantral follicles at 3 weeks old

• decreased number of preantral follicles at 8 weeks old

decreased primordial ovarian follicle number ( J:166778 )

• decreased number of primordial follicles at 3 and 8 weeks old

increased atretic ovarian follicle number ( J:166778 )

• increased number of atretic follicles at 8 weeks old

decreased superovulation rate ( J:166778 )

• reduced ovulation rates (20%-25% of control rates) in 3-week-old superovulated females

• trapped oocytes in luteinizing structures in hormonally stimulated females

female infertility ( J:166778 )

embryo

embryonic growth arrest ( J:166778 )

• embryos generated from matings of mutant females and wild-type males become developmentally arrested between the 1-cell and 4-cell stages

cellular

abnormal DNA methylation ( J:166778 )

• increased mono-methylated H3K4 in oocytes

• decreased tri-methylated H3K4 in oocytes

homeostasis/metabolism

increased circulating follicle stimulating hormone level ( J:166778 )

• increased serum FSH levels at 8 weeks old

endocrine/exocrine glands

abnormal ovarian follicle number ( J:166778 )

• increased number of secondary and preantral follicles at 3 weeks old

• decreased number of preantral follicles at 8 weeks old

decreased primordial ovarian follicle number ( J:166778 )

• decreased number of primordial follicles at 3 and 8 weeks old

increased atretic ovarian follicle number ( J:166778 )

• increased number of atretic follicles at 8 weeks old

Allelic Composition	Kmt2b^tm1Afst/Kmt2b^tm1.1Afst Amhr2^tm3(cre)Bhr/Amhr2⁺
Genetic Background	involves: 129P2/OlaHsd * 129S/SvEv * C57BL/6

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Amhr2^tm3(cre)Bhr mutation (1 available); any Amhr2 mutation (29 available)
Kmt2b^tm1.1Afst mutation (0 available); any Kmt2b mutation (65 available)
Kmt2b^tm1Afst mutation (0 available); any Kmt2b mutation (65 available)

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

reproductive system

abnormal ovarian follicle number ( J:166778 )

• decreased number of primordial, primary, secondary and preantral follicles at 36 weeks old

decreased primary ovarian follicle number ( J:166778 )

decreased primordial ovarian follicle number ( J:166778 )

decreased secondary ovarian follicle number ( J:166778 )

increased atretic ovarian follicle number ( J:166778 )

• increased number of atretic follicles at 36 weeks of age

reduced female fertility ( J:166778 )

• a small reduction in fertility

cellular

abnormal DNA methylation ( J:166778 )

• 50% decrease in global tri-methylated H3K4 levels in granulosa cells

homeostasis/metabolism

increased circulating follicle stimulating hormone level ( J:166778 )

• increased serum FSH levels at 8 weeks old

endocrine/exocrine glands

abnormal ovarian follicle number ( J:166778 )

• decreased number of primordial, primary, secondary and preantral follicles at 36 weeks old

decreased primary ovarian follicle number ( J:166778 )

decreased primordial ovarian follicle number ( J:166778 )

decreased secondary ovarian follicle number ( J:166778 )

increased atretic ovarian follicle number ( J:166778 )

• increased number of atretic follicles at 36 weeks of age

Allelic Composition	Kmt2b^tm1Afst/Kmt2b^tm1.1Afst Gt(ROSA)26Sor^{tm9(cre/ESR1)Arte}/Gt(ROSA)26Sor⁺
Genetic Background	involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sor^{tm9(cre/ESR1)Arte} mutation (2 available); any Gt(ROSA)26Sor mutation (993 available)
Kmt2b^tm1.1Afst mutation (0 available); any Kmt2b mutation (65 available)
Kmt2b^tm1Afst mutation (0 available); any Kmt2b mutation (65 available)

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

reproductive system

female infertility ( J:166778 )

• tamoxifen treatment provokes infertility in females regardless of genotype

• after treatment is discontinued, control animals fully recover fertility, whereas mutant females remain infertile

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