Phenotypes associated with this allele

• Allele Symbol: Cebpb^tm1Pfj
• Allele Name: targeted mutation 1, Peter F Johnson
• Allele ID: MGI:2181982
• Summary: 5 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Cebpb^tm1Pfj/Cebpb^tm1Pfj	B6.Cg-Cebpb^tm1Pfj	MGI:3510865
hm2	Cebpb^tm1Pfj/Cebpb^tm1Pfj	either: 129S1/SvImJ-Cebpb^tm1Pfj or (involves: 129S1/SvImJ * C57BL/6)	MGI:3510863
hm3	Cebpb^tm1Pfj/Cebpb^tm1Pfj	involves: 129S1/Sv * C57BL/6	MGI:3510737
ht4	Cebpb^tm1Pfj/Cebpb^+	B6.Cg-Cebpb^tm1Pfj	MGI:3510866
cx5	Cebpb^tm1Pfj/Cebpb^tm1Pfj Tg(Hba-x-v-Ha-ras)TG.ACLed/0	involves: C57BL/6	MGI:3510871

Genotype
MGI:3510865

hm1

• Allelic Composition: Cebpb^tm1Pfj/Cebpb^tm1Pfj
• Genetic Background: B6.Cg-Cebpb^tm1Pfj

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

neoplasm

decreased incidence of induced tumors ( J:73558 )

• homozygotes are completely refractory to skin tumorigenesis induced by a variety of carcinogens, tumor promoters, and carcinogenesis protocols that, in wild-type mice, cause tumors that contain mutant oncogenic Ha-ras or Ki-ras

decreased incidence of tumors by chemical induction ( J:73558 )

• homozygotes are completely resistant to DMBA/TPA-induced papillomas

• also, homozygotes are completely resistant to MNNG/TPA-induced papillomas (involving oncogenic mutations in the 12th codon of either Ha-ras or Ki-ras), and completely resistant to skin tumors in a DMBA/mirex initiation/promotion protocol

integument

increased keratinocyte apoptosis ( J:73558 )

• compared with wild-type, homozygotes show a 17-fold increase in the number of basal apoptotic keratinocytes in response to DMBA treatment

• in contrast, mutant and wild-type mice show a similar increase in the number of apoptotic epidermal keratinocytes in response to ultraviolet-B irradiation

homeostasis/metabolism

decreased incidence of tumors by chemical induction ( J:73558 )

• homozygotes are completely resistant to DMBA/TPA-induced papillomas

• also, homozygotes are completely resistant to MNNG/TPA-induced papillomas (involving oncogenic mutations in the 12th codon of either Ha-ras or Ki-ras), and completely resistant to skin tumors in a DMBA/mirex initiation/promotion protocol

cellular

increased keratinocyte apoptosis ( J:73558 )

• compared with wild-type, homozygotes show a 17-fold increase in the number of basal apoptotic keratinocytes in response to DMBA treatment

• in contrast, mutant and wild-type mice show a similar increase in the number of apoptotic epidermal keratinocytes in response to ultraviolet-B irradiation

Genotype
MGI:3510863

hm2

• Allelic Composition: Cebpb^tm1Pfj/Cebpb^tm1Pfj
• Genetic Background: either: 129S1/SvImJ-Cebpb^tm1Pfj or (involves: 129S1/SvImJ * C57BL/6)

endocrine/exocrine glands

abnormal mammary gland development ( J:48514 )

♀ • virgin, pregnant, and lactating female homozygotes show aberrant mammary gland development

abnormal branching of the mammary ductal tree ( J:48514 )

♀ • virgin homozygotes exhibit abnormal ductal morphogenesis of the mammary gland

♀ • mutant ducts display reduced growth and branching with variable penetrance

♀ • transplants of wild-type ovaries into mutant females partially restore ductal morphogenesis during puberty but fail to support mammopoiesis during pregnancy

abnormal lactation ( J:48514 )

♀ • during pregnancy, homozygotes show no differentiation to secretory cells: no secretory vesicles or fat globules are observed

♀ • at term, pregnant homozygotes harboring wild-type ovary transplants show complete absence of milk protein expression

integument

abnormal mammary gland development ( J:48514 )

♀ • virgin, pregnant, and lactating female homozygotes show aberrant mammary gland development

abnormal branching of the mammary ductal tree ( J:48514 )

♀ • virgin homozygotes exhibit abnormal ductal morphogenesis of the mammary gland

♀ • mutant ducts display reduced growth and branching with variable penetrance

♀ • transplants of wild-type ovaries into mutant females partially restore ductal morphogenesis during puberty but fail to support mammopoiesis during pregnancy

abnormal lactation ( J:48514 )

♀ • during pregnancy, homozygotes show no differentiation to secretory cells: no secretory vesicles or fat globules are observed

♀ • at term, pregnant homozygotes harboring wild-type ovary transplants show complete absence of milk protein expression

Genotype
MGI:3510737

hm3

• Allelic Composition: Cebpb^tm1Pfj/Cebpb^tm1Pfj
• Genetic Background: involves: 129S1/Sv * C57BL/6

mortality/aging

prenatal lethality, incomplete penetrance ( J:43075 , J:150006 )

• homozygotes are viable but are born at approximately half the expected frequency (J:43075)

• fewer than expected mice are born (J:150006)

reproductive system

reproductive system phenotype ( J:43075 )

N • mutant females display normal uterine tissue histology

N • in addition, the wet weights of uteri from superovulated mutant and wild-type females appear to be indistinguishable

impaired granulosa cell differentiation ( J:43075 )

♀ • females exhibit defective ovarian granulosa cell function at postovulatory stages of follicular development

♀ • following LH/hCG-receptor activation, mutant granulosa cells fail to transgress to the luteal stage

absent corpus luteum ( J:43075 )

♀ • ovaries of virgin mutant females ages 5 weeks to 3 months show a complete absence of mature corpora lutea; ovarian development is otherwise normal

♀ • notably, all stages of primary and antral follicles are present and histologically normal

impaired ovarian folliculogenesis ( J:43075 )

♀ • mutant superovulated ovaries contain large, often hemorrhagic antral follicles after 14 hr of hCG treatment

decreased superovulation rate ( J:43075 )

♀ • homozygous mutant females produce a low yield of ovulated oocytes following injections of ovulatory doses of gonadotropins

♀ • in superovulation experiments, ovulation occurs at ~10% the efficiency of wild-type mice

absent estrous cycle ( J:43075 )

♀ • female homozygotes do NOT display asexual behavior; however, mating frequency is mostly acyclic, with periods of 2 days to >13 days between matings

impaired luteinization ( J:43075 )

♀ • follicles begin luteinization but contain oocytes that fail to be expelled, indicating impaired luteinization

female infertility ( J:43075 )

♀ • male homozygotes and female heterozygotes are fertile

♀ • in contrast, adult female homozygotes are completely infertile

♀ • when superovulated female homozygotes are mated to C57BL/6 males, they fail to become pregnant and no pups are delivered

♀ • fertility can be restored by implanting wild-type ovaries; however, resulting offspring die shortly after birth and, despite apparently normal suckling behavior, pups do not contain milk in their stomachs

skeleton

abnormal osteoblast physiology ( J:150006 )

• the osteoblast surface to bone surface is decreased compared to in wild-type mice

abnormal osteoclast physiology ( J:150006 )

• enhanced osteoclast formation is accompanied by enhanced osteoclast activity

• autocrine stimulation by TNFalpha enhances osteoclastogenesis compared to in wild-type mice

• the number of osteoclasts to bone perimeter is decreased compared to in wild-type mice

abnormal skeleton morphology ( J:150006 )

• bone length is reduced

abnormal osteoclast morphology ( J:150006 )

• mice exhibit enlarged osteoclasts and an increase in the number of multinucleated osteoclasts compared to in wild-type mice

abnormal osteoclast differentiation ( J:150006 )

• bone marrow cells exhibit enhanced osteoclast differentiation with increased number of mononuclear and multinucleated osteoclasts compared to in wild-type mice

decreased bone volume ( J:150006 )

• bone volume is diminished 1.6-fold compared to in wild-type mice

decreased bone trabecula number ( J:150006 )

• the number of bone trabeculae is reduced compared to in wild-type mice

decreased trabecular bone thickness ( J:150006 )

• the thickness of bone trabeculae is reduced compared to in wild-type mice

decreased bone mineralization ( J:150006 )

• mineral apposition is decreased compared to in wild-type mice

decreased bone ossification ( J:150006 )

• bone formation is decreased compared to in wild-type mice

increased bone resorption ( J:150006 )

hematopoietic system

abnormal osteoclast morphology ( J:150006 )

• mice exhibit enlarged osteoclasts and an increase in the number of multinucleated osteoclasts compared to in wild-type mice

abnormal osteoclast differentiation ( J:150006 )

• bone marrow cells exhibit enhanced osteoclast differentiation with increased number of mononuclear and multinucleated osteoclasts compared to in wild-type mice

abnormal osteoclast physiology ( J:150006 )

• enhanced osteoclast formation is accompanied by enhanced osteoclast activity

• autocrine stimulation by TNFalpha enhances osteoclastogenesis compared to in wild-type mice

• the number of osteoclasts to bone perimeter is decreased compared to in wild-type mice

immune system

abnormal osteoclast morphology ( J:150006 )

• mice exhibit enlarged osteoclasts and an increase in the number of multinucleated osteoclasts compared to in wild-type mice

abnormal osteoclast differentiation ( J:150006 )

• bone marrow cells exhibit enhanced osteoclast differentiation with increased number of mononuclear and multinucleated osteoclasts compared to in wild-type mice

abnormal osteoclast physiology ( J:150006 )

• enhanced osteoclast formation is accompanied by enhanced osteoclast activity

• autocrine stimulation by TNFalpha enhances osteoclastogenesis compared to in wild-type mice

• the number of osteoclasts to bone perimeter is decreased compared to in wild-type mice

abnormal tumor necrosis factor level ( J:192313 )

• mice exhibit a normal response to LPS-induced lung injury, except for an increase in TNF-alpha production in bronchial alveolar lavage (BAL) fluids compared to wild-type mice

endocrine/exocrine glands

impaired granulosa cell differentiation ( J:43075 )

♀ • females exhibit defective ovarian granulosa cell function at postovulatory stages of follicular development

♀ • following LH/hCG-receptor activation, mutant granulosa cells fail to transgress to the luteal stage

absent corpus luteum ( J:43075 )

♀ • ovaries of virgin mutant females ages 5 weeks to 3 months show a complete absence of mature corpora lutea; ovarian development is otherwise normal

♀ • notably, all stages of primary and antral follicles are present and histologically normal

impaired ovarian folliculogenesis ( J:43075 )

♀ • mutant superovulated ovaries contain large, often hemorrhagic antral follicles after 14 hr of hCG treatment

cellular

abnormal osteoclast differentiation ( J:150006 )

• bone marrow cells exhibit enhanced osteoclast differentiation with increased number of mononuclear and multinucleated osteoclasts compared to in wild-type mice

impaired granulosa cell differentiation ( J:43075 )

♀ • females exhibit defective ovarian granulosa cell function at postovulatory stages of follicular development

♀ • following LH/hCG-receptor activation, mutant granulosa cells fail to transgress to the luteal stage

abnormal osteoblast physiology ( J:150006 )

• the osteoblast surface to bone surface is decreased compared to in wild-type mice

homeostasis/metabolism

abnormal tumor necrosis factor level ( J:192313 )

• mice exhibit a normal response to LPS-induced lung injury, except for an increase in TNF-alpha production in bronchial alveolar lavage (BAL) fluids compared to wild-type mice

Genotype
MGI:3510866

ht4

• Allelic Composition: Cebpb^tm1Pfj/Cebpb⁺
• Genetic Background: B6.Cg-Cebpb^tm1Pfj

neoplasm

decreased incidence of tumors by chemical induction ( J:73558 )

• heterozygous mutant mice are partially resistant to DMBA/TPA-induced papillomas

homeostasis/metabolism

decreased incidence of tumors by chemical induction ( J:73558 )

• heterozygous mutant mice are partially resistant to DMBA/TPA-induced papillomas

Genotype
MGI:3510871

cx5

• Allelic Composition: Cebpb^tm1Pfj/Cebpb^tm1Pfj; Tg(Hba-x-v-Ha-ras)TG.ACLed/0
• Genetic Background: involves: C57BL/6

neoplasm

decreased incidence of tumors by chemical induction ( J:73558 )

• TPA-treated Cebpb^tm1Pfj homozygotes carrying the v-Ha-ras transgene develop 65% fewer Ras-induced papillomas than wild-type, transgene-positive mice

decreased tumor growth/size ( J:73558 )

• notably, the tumor size is reduced by 60% in the Cebpb^tm1Pfj homozygous null background

homeostasis/metabolism

decreased incidence of tumors by chemical induction ( J:73558 )

• TPA-treated Cebpb^tm1Pfj homozygotes carrying the v-Ha-ras transgene develop 65% fewer Ras-induced papillomas than wild-type, transgene-positive mice