Phenotypes associated with this allele

• Allele Symbol: Nrip1^tm1Mpk
• Allele Name: targeted mutation 1, Malcolm Parker
• Allele ID: MGI:2657149
• Summary: 4 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Nrip1^tm1Mpk/Nrip1^tm1Mpk	involves: 129 * C57BL/6J	MGI:5574445
hm2	Nrip1^tm1Mpk/Nrip1^tm1Mpk	involves: 129/Ola	MGI:2657150
ht3	Nrip1^tm1Mpk/Nrip1^+	involves: 129/Ola	MGI:3041122
cx4	Apc^tm1Cip/Apc^+ Nrip1^tm1Mpk/Nrip1^+	involves: 129P2/OlaHsd * C57BL/6J	MGI:5574446

Genotype
MGI:5574445

hm1

• Allelic Composition: Nrip1^tm1Mpk/Nrip1^tm1Mpk
• Genetic Background: involves: 129 * C57BL/6J

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

cellular

increased enterocyte apoptosis ( J:211324 )

• 3-fold

abnormal enterocyte proliferation ( J:211324 )

• 2.6-fold increase in cells synthesizing DNA compared with wild-type mice

digestive/alimentary system

increased enterocyte apoptosis ( J:211324 )

• 3-fold

abnormal enterocyte proliferation ( J:211324 )

• 2.6-fold increase in cells synthesizing DNA compared with wild-type mice

abnormal small intestine morphology ( J:211324 )

• crypt to villus axis is increased compared to in wild-type mice

• higher increase in villi and crypt length following whole body irradiation

• shorter intestine compared with wild-type mice

• however, total surface area of intestinal epithelium is normal

abnormal Paneth cell morphology ( J:211324 )

• increased differentiation

endocrine/exocrine glands

abnormal Paneth cell morphology ( J:211324 )

• increased differentiation

homeostasis/metabolism

abnormal response to injury ( J:211324 )

• following whole body irradiation, mice exhibit increased number of regenerating villi and a higher increase in villi and crypt length compared with in wild-type mice

Genotype
MGI:2657150

hm2

• Allelic Composition: Nrip1^tm1Mpk/Nrip1^tm1Mpk
• Genetic Background: involves: 129/Ola

cellular

abnormal oocyte morphology ( J:74971 )

♀ • the few oocytes released from homozygous null female mice were devoid of a cumulus cell layer

endocrine/exocrine glands

endocrine/exocrine gland phenotype ( J:74971 )

N • ovarian sections from implanted mutant mice demonstrated the presence of large corpora lutea; pregnancy was maintained and progesterone levels remained increased at 9.5-10.5 dpc, although the proportion of viable embryos was reduced

N • embryo transfer experiments revealed that wild-type and homozygous null mice had similar rates of implantation at 6.5-8.5 dpc

N • measurement of the circulating levels of progesterone indicated no significant differences between wild-type and homozygous null mice

growth/size/body

decreased body size ( J:74971 )

• homozygous null mice were viable and morphologically normal, albeit 15-20% smaller than wild-type and heterozygous littermates throughout postnatal development

reproductive system

abnormal oocyte morphology ( J:74971 )

♀ • the few oocytes released from homozygous null female mice were devoid of a cumulus cell layer

abnormal superovulation ( J:74971 )

♀ • ovarian sections from superovulated immature homozygous null females revealed luteinizing follicles, with occasional hemorrhagic cysts; this phenotype was more pronounced in mature mice

decreased superovulation rate ( J:74971 )

♀ • analysis of the ovarian response to gonadotrophin stimulation using immature female mice indicated that >90% of follicles in mutant females retained an oocyte, although luteinized cells were present

♀ • folliculogenesis proceeded normally and the total numbers of luteinizing follicles were similar between wid-type, heterozygous and homozygous null mice

anovulation ( J:74971 )

♀ • after natural mating, homozygous null females failed to release oocytes at ovulation

abnormal fertility/fecundity ( J:74971 )

• homozygous null male mice had histologically normal testes and normal seminal vesicle weights and were fertile; however, the proportion of null offspring compared with the number of heterozygous mice derived from matings of homozygous null male mice with heterozygous female mice was considerably less than the expected 50%

female infertility ( J:74971 )

♀ • mature homozygous null female mice (7-10 weeks of age) were completely infertile

Genotype
MGI:3041122

ht3

• Allelic Composition: Nrip1^tm1Mpk/Nrip1⁺
• Genetic Background: involves: 129/Ola

endocrine/exocrine glands

endocrine/exocrine gland phenotype ( J:74971 )

♀N • heterozygous null ovaries displayed normal endocrine function

reproductive system

abnormal ovulation ( J:74971 )

♀ • heterozygous null mice showed an ovarian phenotype that was intermediate between wild-type and homozygous null mice

abnormal superovulation ( J:74971 )

♀ • ovarian sections from superovulated immature heterozygotes revealed luteinizing follicles with occasional hemorrhagic cysts; this phenotype was more pronounced in mature mice but to an intermediate extent relative to homozygous null mice

failure of superovulation ( J:74971 )

♀ • superovulation of heterozygous mice resulted in a failure of approximately 50% of the luteinizing follicles to release the oocyte

Genotype
MGI:5574446

cx4

• Allelic Composition: Apc^tm1Cip/Apc⁺; Nrip1^tm1Mpk/Nrip1⁺
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6J

mortality/aging

premature death ( J:211324 )

♀ • compared with Apc^tm1Cip heterozygotes