Tevosian SG; Deconinck AE; Tanaka M; Schinke M; Litovsky SH; Izumo S; Fujiwara Y; Orkin SH. 2000. FOG-2, a cofactor for GATA transcription factors, is essential for heart morphogenesis and development of coronary vessels from epicardium. Cell 101(7):729-39PubMed: 10892744 MGI: J:62879

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Genetics

Zfpm2^tm1Sho

Allele Symbol: Zfpm2^tm1Sho

Allele Name	targeted mutation 1, Stuart Orkin
Allele Type	Targeted (Null/Knockout)
Allele Synonym(s)	Fog2-; FOG-2^-
Gene Symbol and Name	Zfpm2, zinc finger protein, multitype 2
Gene Synonym(s)
Strain of Origin	129S1/Sv-Oca2⁺ Tyr⁺ Kitl⁺
Chromosome	15
Molecular Note	The gene was disrupted by replacement of sequences encoding all of the zinc finger motifs with a floxed neomycin-cytidine deaminase cassette. The floxed cassette was removed by crossing mutant animals to a cre deleter strain. Homozygous mutant embryos were detected by Southern blot analysis up to day E15.5. RNase protection assay showed an absence of Zfpm2 mRNA in hearts of E12.5 homozygous mutant embryos.
Mutations Made By	Stuart Orkin, Harvard University

Disease/Phenotype

Disease Terms

Model with phenotypic similarity to human disease where etiologies involve orthologs. Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).

tetralogy of Fallot

Research Areas By Phenotype

This mouse can be used to support research in many areas including:

Mammalian Phenotype Terms by Genotype

The following phenotype information is associated with a similar, but not exact match to this JAX^® Mice strain

Genotype: Zfpm2^tm1Sho/Zfpm2^tm1Sho
involves: 129S1/Sv

cardiovascular system phenotype

abnormal cardiac epithelial to mesenchymal transition
- an early developmental block prevents epithelial-to-mesenchymal transition of "transforming" epicardial cells and subsequent formation of coronary vascular plexus within the subepicardial space

abnormal heart atrium morphology
- at E13.5, mutant atria are thinner than normal and only a few trabeculae are observed

abnormal heart shape
- by 13.5, mutant hearts are rounder than normal, as sharp ventricular apicies are absent

absent coronary vessels
- coronary vasculature is absent, despite formation of an intact epicardial layer and expression of epicardium-specific genes

atrial septal defect
- atrial septal defects are detected at E13.5-E15.5

common atrioventricular valve
- a common atrioventricular valve is situated between the left and right ventricles

congestive heart failure
- at E13.5, mutant embryos display an overall appearance consistent with heart failure

decreased heart rate
- by E13.5, pulsation is weaker and slower, and blood cells remain within the heart even after contraction

dilated heart atrium
- at E13.5, mutant atria are significantly dilated

heart right ventricle outflow tract stenosis
- subpulmonic stenosis is detected at E13.5-E15.0

hemorrhage
- at E13.5, mutant embryos often display peripheral hemorrhage
- Normal - however, no bleeding is noted around the heart

overriding aortic valve
- an overriding aorta is detected at E13.5-E15.0

supravalvar pulmonary trunk stenosis
- a severely obstructed pulmonary trunk (stenosis) is observed at E12.5

thin myocardium compact layer
- at E13.5-E15.0, mutant embryos display thinning of the compact ventricular myocardium, similar to a "papyraceous phenotype"

thin ventricular wall

ventricular myocardium compact layer hypoplasia
- a striking ventricular compact layer hypoplasia is observed

ventricular septal defect
- a subaortic ventricular septal defect is noted at E13.5-E15.0, as part of a complete common atrioventricular canal

homeostasis/metabolism phenotype

hydrops fetalis
- at E13.5, mutant embryos are edematous

integument phenotype

pallor
- at E13.5, mutant embryos are pale

liver/biliary system phenotype

small liver
- a smaller liver size is observed at E13.5-E15.5, secondary to heart failure

mortality/aging

lethality throughout fetal growth and development, complete penetrance
- at E14.5, approximately 50% of mutant embryos are necrotic and undergoing resorption
- mutant embryos die at midgestation between E12.5 and E15.5; some are found dead by E13.5

muscle phenotype

thin myocardium compact layer
- at E13.5-E15.0, mutant embryos display thinning of the compact ventricular myocardium, similar to a "papyraceous phenotype"

ventricular myocardium compact layer hypoplasia
- a striking ventricular compact layer hypoplasia is observed

respiratory system phenotype

abnormal lung development
- branching in unaffected lobes appears delayed by 6 - 12 hours in homozygous lung culture explants; however, all mutant lungs do develop the normal branching pattern after 5 days in culture
- underdevelopment of lungs is observed at E13.5-E15, secondary to heart failure

absent right lung accessory lobe
- the right lung accessory lobe fails to develop

pulmonary hypoplasia
- at E12, prior to onset of diaphragm function, mutant lungs are smaller and lack development of an accessory lobe

References

Tevosian SG; Deconinck AE; Tanaka M; Schinke M; Litovsky SH; Izumo S; Fujiwara Y; Orkin SH. 2000. FOG-2, a cofactor for GATA transcription factors, is essential for heart morphogenesis and development of coronary vessels from epicardium. Cell 101(7):729-39PubMed: 10892744 MGI: J:62879

Additional - Zfpm2^tm1Sho related

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When using the Fog2- mouse strain in a publication, please cite the originating article(s) and include JAX stock #005646 in your Materials and Methods section.

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Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200

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Cryo Recovery

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Live Mouse

Age

Genotype

Price

weeks

Cryorecovery - Pricing

Service/Product	Description	Price
	Heterozygous or Wild-type for Zfpm2<tm1Sho>

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Also Known As:Fog2-

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Selected References

Zfpm2tm1Sho

Allele Symbol: Zfpm2tm1Sho