About   Help   FAQ
Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
CrebbpGt(U-San)112Imeg
gene trap 112, Institute of Molecular Embryology and Genetics
MGI:1928775
Summary 2 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
CrebbpGt(U-San)112Imeg/CrebbpGt(U-San)112Imeg involves: C57BL/6 * CBA MGI:2175791
ht2
CrebbpGt(U-San)112Imeg/Crebbp+ involves: C57BL/6 * CBA MGI:2175792


Genotype
MGI:2175791
hm1
Allelic
Composition
CrebbpGt(U-San)112Imeg/CrebbpGt(U-San)112Imeg
Genetic
Background
involves: C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
CrebbpGt(U-San)112Imeg mutation (0 available); any Crebbp mutation (99 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• embryos obtained from F3 or F4 intercrosses die between E9.5 and E10.5

cardiovascular system
• in the trunk, E9.5 mutants lack sprouting vessels from the dorsal aorta or umbilical vein in parietal mesoderm
• in the head region, E9.5 mutants display a disoriented posterior branch of primary head vein and reduced numbers of blood cells in the dorsal aorta
• ectopic blood cells are detected in the hindgut diverticulum and coelomic cavity
• in the trunk, E9.5 mutant embryos show reduced endothelial cells in the omphalomesenteric artery and dorsal aorta
• organ culture of para-aortic splanchnopleural mesoderm (P-Sp) with stromal cells indicates defects in both vasculogenesis and angiogenesis (J:53370)
• addition of VEGF to mutant cultures partially rescues these defects (J:53370)
• at E9.5, homozygotes show gross vascular branching defects in the head and trunk, including the para-aortic splanchnopleural region: both large vessels and smaller vascular branches are absent
• at E9.5, homozygotes lack an organized vascular network
• at E9.5, mutant yolk sacs exhibit a significant reduction in vitelline vessels

embryo
• homozygotes become growth arrested at E8.75-E9.0
• at E9.5, homozygous embryos are smaller than wild-type embryos
• at E9.5, homozygous embryos display an open neural tube
• at E9.5, mutant yolk sacs exhibit a significant reduction in vitelline vessels
• at E9.5, homozygotes display a pale yolk sac

hematopoietic system
• at E9.5, homozygotes exhibit marked anemia and fail to survive beyond the stage of primitive hematopoiesis
• at E9.5, mutant yolk sacs exhibit 22% and 69%, respectively, of erythroid and granulocyte-macrophage colony-forming capacity relative to wild-type counterparts
• at E9.5, the total number of nucleated erythroid cells present in mutant yolk sacs is reduced to 20% of wild-type

nervous system
• at E9.5, homozygous embryos display an open neural tube

growth/size/body
• at E9.5, homozygous embryos are smaller than wild-type embryos

integument
• at E9.5, homozygous mutant embryos are much paler than wild-type embryos




Genotype
MGI:2175792
ht2
Allelic
Composition
CrebbpGt(U-San)112Imeg/Crebbp+
Genetic
Background
involves: C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
CrebbpGt(U-San)112Imeg mutation (0 available); any Crebbp mutation (99 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• a subset of F2 heterozygous pups die within several days after birth

growth/size/body
• at 2-14 weeks, heterozygotes show a 30% reduction in body weight relative to wild-type mice
• however, heterozygotes gain weight at a rate that is comparable to that observed in wild-type mice
• in contrast to wild-type mice, heterozygotes fail to show a time-dependent increase in weight on a high-fat (HF) diet
• heterozygotes appear to be protected against HF diet-induced triglyceride accumulation in WAT
• heterozygotes exhibit significant intrauterine growth retardation in both weight and height relative to wild-type embryos

craniofacial
• at 19 dpc, heterozygotes exhibit a large anterior fontanel
• heterozygotes display widening of the frontal bone

skeleton
• at 19 dpc, heterozygotes exhibit a large anterior fontanel
• heterozygotes display widening of the frontal bone
• 1 of 30 heterozygotes display severe scoliosis
• heterozygotes exhibit delayed osseous maturation; notably, neither broad thumbs nor broad halluces are observed

cardiovascular system
• at 19.5 dpc, 9 of 54 heterozygous fetuses (16.6%) display non-overlapping cardiac abnormalities
• at 19.5 dpc, 1 of 54 heterozygous fetuses exhibit an atrial septal defect
• at 19.5 dpc, 7 of 54 heterozygous fetuses exhibit a ventricular septal defect of the membranous type

behavior/neurological
• heterozygotes display impaired long-term memory (LTM) in a step-through-type passive avoidance test and a cued fear-conditioning test
• in contrast, heterozygotes exhibit normal short-term memory in a Y-maze test as well as normal spatial learning in a water maze test
• hypolocomotion in a dark environment is noted throughout the entire 60 min observation period in the vertical activity, but only in the first 5 min in the horizontal activity
• heterozygotes display hypolocomotion in a dark environment but not in a light environment
• at least 2 of 54 heterozygotes display seizures

nervous system
N
• heterozygotes exhibit a normal brain morphology: despite the LTM deficit, neither sensorimotor nor gross neuroanatomical anomalies are observed
• at least 2 of 54 heterozygotes display seizures

limbs/digits/tail
• 1 of 30 heterozygotes exhibit oligodactyly

adipose tissue
• at 8 months, heterozygotes show a significant reduction in WAT weight per body weight; the weight of other tissues, including brown adipose tissue, remains unchanged
• reduced WAT mass is attributed to the inhibition of triglyceride accumulation in WAT
• at 8 months, heterozygotes fed a HC diet show a marked reduction in adipocyte size relative to similarly fed wild-type mice
• at death, heterozygotes fed a high-carbohydrate (HC) diet display a significantly reduced fat mass relative to similarly fed wild-type mice
• however, at P3, heterozygotes contain the same amount of BAT and WAT as wild-type mice

cellular
in vitro, embryonic fibroblasts from heterozygous mice exhibit a reduced ability to differentiate into adipocytes upon induction with conventional hormonal stimuli

homeostasis/metabolism
• in contrast to wild-type mice, heterozygotes fail to show a time-dependent increase in weight on a high-fat (HF) diet
• heterozygotes appear to be protected against HF diet-induced triglyceride accumulation in WAT
• heterozygotes show higher plasma insulin levels during glucose tolerance tests suggesting increased insulin secretion; however, this rise in insulin levels does not reach statistical significance
• heterozygotes fed a HF diet display increased serum leptin levels relative to the severely reduced WAT mass
• in addition, heterozygotes fed a HF diet exhibit increased leptin sensitivity in response to exogenous leptin
• heterozygotes fed a HF diet display reduced serum levels of free fatty acids relative to wild-type mice
• heterozygotes exhibit a marked increase in resting oxygen consumption relative to wild-type mice
• in contrast, food intake remains relatively unchanged on either the HC or HF diet
• heterozygotes display increased glucose tolerance relative to wild-type mice on both a HC and a HF diet
• despite lipodystrophy, heterozygotes exhibit an enhanced glucose-lowering insulin effect relative to wild-type mice
• heterozygotes fed a HF diet show a significant increase in serum adiponectin levels, despite their markedly reduced WAT mass
• heterozygotes display changes in gene expression associated with decreased tissue triglyceride content in skeletal muscle and liver
• heterozygotes fed a HF diet display reduced Tnfa mRNA levels in WAT relative to wild-type mice

immune system
• heterozygotes fed a HF diet display reduced Tnfa mRNA levels in WAT relative to wild-type mice

respiratory system

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
Rubinstein-Taybi syndrome DOID:1933 OMIM:180849
OMIM:610543
OMIM:613684
J:53370





Contributing Projects:
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO)
Citing These Resources
Funding Information
Warranty Disclaimer, Privacy Notice, Licensing, & Copyright
Send questions and comments to User Support.
last database update
04/23/2024
MGI 6.23
The Jackson Laboratory