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Former Names B6;129S-Hodtm1Eno/J (Changed: 29-AUG-07 ) Type Mutant Stock; Targeted Mutation; Additional information on Genetically Engineered and Mutant Mice. Visit our online Nomenclature tutorial. Species laboratory mouse Generation ?+N1pN1
Generation DefinitionsDonating Investigator Rhonda Bassel-Duby, University of Texas Southwestern Description
Homozygous mice are viable and fertile on this mixed genetic background. Absence of the targeted protein is confirmed in heart and brain tissues from homozygotes. The lacZ expression pattern is similar to that of the endogenous gene. Homozygous heart tissues show altered serum response factor (SRF)-associated gene expression. Mice homozygous for this null allele segregate into two phenotypic classes characterized by an excess or deficiency of cardiac myocytes. These mutant mice may be useful in studying cardiac growth and development.Development
A targeting vector was designed to replace the entire coding region of the targeted gene with a nuclear lacZ (nLacZ) and neomycin cassette in-frame with the endogenous initiation codon. The construct was electroporated into 129S6/SvEvTac-derived SM1 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6J blastocysts. Chimeric animals were crossed with C57BL/6J. Heterozygotes were intercrossed to homozygosity, and then bred as such for many generations prior to arrival at The Jackson Laboratory. Upon arrival, mice were bred at least one generation to C57BL/6J to establish the colony.
| Control | ||
|---|---|---|
| 101043 B6129SF1/J | (approximate) | |
| 101045 B6129SF2/J | (approximate) | |
| Considerations for Choosing Controls | ||
lacZ Expression Strains
View lacZ Expression Strains (245 strains)
Strains carrying other alleles of lacZ
View Strains carrying other alleles of lacZ (217 strains)
Fluorescent Proteins/lacZ Systems
View Mammalian Phenotype Terms
Mammalian Phenotype Terms provided by MGI
assigned by genotype
The following phenotype information may relate to a genetic background differing from this JAX® Mice strain.
Hopxtm1Eno/Hopxtm1Eno
involves: 129S6/SvEvTac
- mortality/aging
- partial embryonic lethality during organogenesis
- on an isogenic 129/Sv background, ~10% of homozygotes die at E11.5 from cardiac insufficiency; as a result, viable homozygotes represent only 17% of offspring at P10 (MGI Ref ID J:79152)
- on a mixed 129Sv x C57BL/6J genetic background, most homozygotes are viable and represent 23% of heterozygous offspring at P10, closely approximating the expected Mendelian ratio (MGI Ref ID J:79152)
- cardiovascular system phenotype
- abnormal cardiovascular system physiology (MGI Ref ID J:79152)
- abnormal fetal cardiomyocyte proliferation
- at P1, >66% of viable homozygotes exhibit prolonged cardiomyocyte proliferation, as shown by a 19-fold increase in the number of cells staining positive for the mitotic marker phospho-histone H3 (MGI Ref ID J:79152)
- however, delayed withdrawal of mutant cardiomyocytes from the cell cycle is transient, as no phospho-H3-positive cardiomyocytes are detected at 4 weeks of age (MGI Ref ID J:79152)
- decreased cardiac muscle contractility
- at 6 months of age, those homozygotes with hypertrophic hearts display impaired cardiac contractility or cardiac dysfunction (MGI Ref ID J:79152)
- hemopericardium
- on an isogenic 129/Sv background, ~10% of E11.5 homozygotes exhibit pericardial hemorrhaging (MGI Ref ID J:79152)
- cardiac fibrosis
- at 6 months of age, mutant hearts with cardiomyocyte hypertrophy exhibit severe dilation and fibrosis (MGI Ref ID J:79152)
- enlarged heart (MGI Ref ID J:79152)
- cardiac hypertrophy
- at 6 months of age, a subset of viable homozygotes develop late-onset hypertrophy of cardiac myocytes (MGI Ref ID J:79152)
- heart hyperplasia
- at P1 and P28, viable homozygotes of an isogenic or mixed genetic background exhibit a ~30% increase in the number of cardiac myocytes; however, no cardiomyocyte hypertrophy is noted up to 4 weeks of age (MGI Ref ID J:79152)
- postnatal cardiac hypercellularity is in stark contrast to the hypocellular cardiac phenotype of embryos that die at E11.5, suggesting a finely tuned mechanism that governs the balance between cardiomyocyte proliferation and differentiation (MGI Ref ID J:79152)
- increased heart weight
- at P1-P28, viable homozygotes exhibit a ~20% increase in heart weight/body weight ratio relative to wild-type mice; increase difference persists through adulthood (MGI Ref ID J:79152)
- thick ventricular wall
- at P1, viable homozygotes display increased ventricular wall thickness relative to wild-type mice (MGI Ref ID J:79152)
- thin myocardium
- on an isogenic 129/Sv background, ~10% of E11.5 homozygotes display a hypocellular, thin-walled ventricular myocardium with numerous ruptures throughout the ventricular walls (MGI Ref ID J:79152)
- embryogenesis phenotype
- embryonic growth arrest
- on an isogenic 129/Sv background, ~10% of homozygotes display a developmental arrest at E11.5 (MGI Ref ID J:79152)
- muscle phenotype
- abnormal muscle physiology (MGI Ref ID J:79152)
- abnormal fetal cardiomyocyte proliferation
- at P1, >66% of viable homozygotes exhibit prolonged cardiomyocyte proliferation, as shown by a 19-fold increase in the number of cells staining positive for the mitotic marker phospho-histone H3 (MGI Ref ID J:79152)
- however, delayed withdrawal of mutant cardiomyocytes from the cell cycle is transient, as no phospho-H3-positive cardiomyocytes are detected at 4 weeks of age (MGI Ref ID J:79152)
- decreased cardiac muscle contractility
- at 6 months of age, those homozygotes with hypertrophic hearts display impaired cardiac contractility or cardiac dysfunction (MGI Ref ID J:79152)
- homeostasis/metabolism phenotype
- hemopericardium
- on an isogenic 129/Sv background, ~10% of E11.5 homozygotes exhibit pericardial hemorrhaging (MGI Ref ID J:79152)
- cellular phenotype
- abnormal fetal cardiomyocyte proliferation
- at P1, >66% of viable homozygotes exhibit prolonged cardiomyocyte proliferation, as shown by a 19-fold increase in the number of cells staining positive for the mitotic marker phospho-histone H3 (MGI Ref ID J:79152)
- however, delayed withdrawal of mutant cardiomyocytes from the cell cycle is transient, as no phospho-H3-positive cardiomyocytes are detected at 4 weeks of age (MGI Ref ID J:79152)
View Research Applications
Research Applications
This mouse can be used to support research in many areas including:
Cardiovascular Research
Heart Abnormalities
cardiomyopathy
Other
Developmental Biology Research
Internal/Organ Defects
heart
Internal/Organ Research
Heart Abnormalities
Research Tools
lacZ Expression
Cardiovascular Research
Developmental Biology Research
Internal/Organ Research
| Allele Symbol | Hopxtm1Eno | ||
|---|---|---|---|
| Allele Name | targeted mutation 1, Eric N Olson | ||
| Allele Type | Targeted (Reporter) | ||
| Common Name(s) | HOP-; | ||
| Mutation Made By | Eric Olson, University of Texas Southwestern Medical | ||
| Strain of Origin | 129S6/SvEvTac | ||
| ES Cell Line Name | SM1 | ||
| ES Cell Line Strain | 129S6/SvEvTac | ||
| Site of Expression | The lacZ expression pattern is similar to that of the endogenous Hopx gene. Highest levels of lacZ staining within cardiomyocyte nuclei in the trabecular zone. lacZ staining was also observed within the neural tube. | ||
| Expressed Gene | lacZ, beta-galactosidase, E. coli | ||
| Molecular Note | The entire coding region was replaced with a cassette containing a nuclear-localized lacZ and neo. Transcript was undetected by Northern blot and RT-PCR analyses of heart and liver tissues from homozygous mutant mice. Western blot analysis confirmed the absence of normal protein in heart and brain tissues. The expression pattern of beta-galactosidase was similar to that of the endogenous gene. [MGI Ref ID J:79152] | ||
| Gene Symbol and Name | Hopx, HOP homeobox | ||
| Chromosome | 5 | ||
| Gene Common Name(s) | 1110018K11Rik; 1200015P04Rik; 2300002F06Rik; AI848177; AW490897; CAMEO; GIIg15b; HOD; HOP; Hod; LAGY; NECC1; OB1; Obl; RIKEN cDNA 1110018K11 gene; RIKEN cDNA 1200015P04 gene; RIKEN cDNA 2300002F06 gene; SMAP31; TOTO; expressed sequence AI848177; expressed sequence AW490897; homeobox only domain; | ||
Genotyping Protocols
Generic LacZ, Standard PCR
Hopxtm1Eno, Separated PCR
Helpful Links
Genotyping resources and troubleshooting
Shin CH; Liu ZP; Passier R; Zhang CL; Wang DZ; Harris TM; Yamagishi H; Richardson JA; Childs G; Olson EN. 2002. Modulation of cardiac growth and development by HOP, an unusual homeodomain protein. Cell 110(6):725-35. [PubMed: 12297046] [MGI Ref ID J:79152]
Hopxtm1Eno relatedAsanoma K; Kato H; Yamaguchi S; Shin CH; Liu ZP; Kato K; Inoue T; Miyanari Y; Yoshikawa K; Sonoda K; Fukushima K; Wake N. 2007. HOP/NECC1, a novel regulator of mouse trophoblast differentiation. J Biol Chem 282(33):24065-74. [PubMed: 17576768] [MGI Ref ID J:124707]
Hawiger D; Wan YY; Eynon EE; Flavell RA. 2010. The transcription cofactor Hopx is required for regulatory T cell function in dendritic cell-mediated peripheral T cell unresponsiveness. Nat Immunol 11(10):962-8. [PubMed: 20802482] [MGI Ref ID J:164689]
Vasiliev O; Rhodes SJ; Beebe DC. 2007. Identification and expression of Hop, an atypical homeobox gene expressed late in lens fiber cell terminal differentiation. Mol Vis 13:114-24. [PubMed: 17277742] [MGI Ref ID J:141592]
Animal Health Reports
Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, RG10/RG30.Colony Maintenance
Breeding & Husbandry When maintaining a live colony on this mixed B6;129S genetic background, homozygous mice are bred.
| Pricing for USA, Canada and Mexico shipping destinations |
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Cryopreserved Mice - Ready for Recovery
Animals Provided
Price (US dollars $) Cryorecovery* $1980.00 At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.
Standard Supply
Cryopreserved. Ready for recovery. Please refer to pricing and supply notes for further information.
Supply Notes
- Cryorecovery - Standard.
We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. The total number of animals provided, their gender and genotype will vary. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 13 and 16 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.Cryorecovery to establish a Dedicated Supply for greater quantities of mice.
Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).
| Pricing for International shipping destinations |
|
![]() |
Cryopreserved Mice - Ready for Recovery
Animals Provided
Price (US dollars $) Cryorecovery* $2574.00 At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.
Standard Supply
Cryopreserved. Ready for recovery. Please refer to pricing and supply notes for further information.
Supply Notes
- Cryorecovery - Standard.
We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. The total number of animals provided, their gender and genotype will vary. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 13 and 16 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.Cryorecovery to establish a Dedicated Supply for greater quantities of mice.
Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).
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Cryopreserved. Ready for recovery. Please refer to pricing and supply notes for further information.
| Control | ||
|---|---|---|
| 101043 B6129SF1/J | (approximate) | |
| 101045 B6129SF2/J | (approximate) | |
| Considerations for Choosing Controls | ||
| Control Pricing Information for Genetically Engineered Mutant Strains. | ||
For Licensing and Use Restrictions view the link(s) below:
- Use of MICE by companies or for-profit entities requires a license prior to shipping.
| phone: | 207-288-6470 |
| fax: | 207-288-6655 |
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