Phenotypes associated with this allele

• Allele Symbol: Cebpd^tm1Aki
• Allele Name: targeted mutation 1, Shizuo Akira
• Allele ID: MGI:2180837
• Summary: 2 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Cebpd^tm1Aki/Cebpd^tm1Aki	involves: 129P2/OlaHsd	MGI:2656638
cx2	Cebpb^tm1Kish/Cebpb^tm1Kish Cebpd^tm1Aki/Cebpd^tm1Aki	involves: 129P2/OlaHsd	MGI:2656639

Genotype
MGI:2656638

hm1

• Allelic Composition: Cebpd^tm1Aki/Cebpd^tm1Aki
• Genetic Background: involves: 129P2/OlaHsd

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

mortality/aging

mortality/aging ( J:45062 )

N • at 4 weeks, homozygotes are present at the expected Mendelian ratio, with no incidence of mortality observed thereafter; both sexes are fertile

adipose tissue

abnormal brown adipose tissue morphology ( J:45062 )

• at 20 hrs after birth, newborn homozygotes exhibit a nearly normal or slightly reduced intracytoplasmic lipid content in intercapsular brown adipocytes, suggesting a relatively normal adipocyte differentiation

abnormal epididymal fat pad morphology ( J:45062 )

• homozygotes tend to exhibit lower epididymal WAT weights relative to wild-type mice; however, this difference does not reach statistical significance

cellular

abnormal cell differentiation ( J:45062 )

• in response to hormonal stimulants, mutant embryonic fibroblasts show only a slight reduction in adipogenic differentiation and accumulation of lipid droplets relative to wild-type fibroblasts

Genotype
MGI:2656639

cx2

• Allelic Composition: Cebpb^tm1Kish/Cebpb^tm1Kish; Cebpd^tm1Aki/Cebpd^tm1Aki
• Genetic Background: involves: 129P2/OlaHsd

mortality/aging

neonatal lethality, complete penetrance ( J:45062 )

• only 13% of double homozygotes are obtained at 10 hrs after birth; others die within 24 hrs after birth

• as a result, only 3.8% of double homozygotes are obtained at 4 weeks

perinatal lethality, incomplete penetrance ( J:45062 )

• 85% of double homozygotes die during the perinatal or early postnatal stage in the absence of a sucking defect or other overt abnormalities

• surviving homozygotes appear normal and display a normal rate of mortality in adulthood

adipose tissue

decreased white adipose tissue amount ( J:45062 )

• double homozygotes display a decreased weight of epididymal WAT, probably as a result of a reduced adipocyte number

abnormal brown fat cell morphology ( J:45062 )

• at 20 hrs after birth, newborn homozygotes fail to exhibit lipid accumulation in intercapsular brown adipocytes

abnormal brown fat lipid droplet number ( J:45062 )

• the near absence of fat droplets in intercapsular BAT suggests that adipocyte differentiation is arrested at the pre-adipocyte stage in most cells

decreased epididymal fat pad weight ( J:45062 )

• surviving adults exhibit a significant reduction in epididymal WAT weight (~30% of wild-type), despite a normal body weight

• however, epididymal WAT from double mutants appears histologically unremarkable, with mature adipocytes of a typical unilocular or signet-ring morphology

abnormal brown adipose tissue thermogenesis ( J:45062 )

• homozygotes exhibit reduced levels of UCP1 in intercapsular BAT, suggesting reduced thermogenic activity

cellular

abnormal cell differentiation ( J:45062 )

• in culture, embryonic fibroblasts obtained from double homozygotes fail to differentiate into adipogenic cells and accumulate very few lipid droplets relative to wild-type fibroblasts in response to hormonal stimulants