Overview

Also Known As: loxTB Mc4r

loxTB Mc4r has a loxP-flanked transcriptional blocker upstream of the Mrc4 ATG site - resulting in disrupted Mrc4 expression. Exposure to Cre recombinase restores endogenous Mrc4 expression. These mutant mice may be useful in studies of neurobiology, obesity, diabetes, hunger/appetite, and fat and energy metabolism.
Of note, loxTB Mc4r mice are available on a B6;129 mixed genetic background (Stock No. 006414) and C57BL/6J-congenic background (Stock No. 032518).

Donating Investigator

Bradford B. Lowell, Beth Israel Deaconess Med Cntr (Harvard)

Genetic overview

Genetic Background	Generation
	?+N1pN1F26 (2019-03-01 00:00:00)

Mc4r^tm1Lowl

Allele Type	Gene Symbol	Gene Name
Targeted (Conditional ready (e.g. floxed), Null/Knockout)	Mc4r	melanocortin 4 receptor

View Genetics

Research Applications

Research Tools
Diabetes and Obesity Research
Neurobiology Research

View All Research Applications

Base Price

Starting at:

$270.00 Domestic price for female 4-week

540.00 Domestic price for breeder pair

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Details

Detailed Description

The mice have a loxp-flanked transcriptional blocking (loxTB) sequence that prevents normal endogenous gene transcription and translation from the endogenous locus. As such, homozygous mice are devoid of functional mRNA in all tested regions of the brain. Homozygous mice exhibit obesity, accompanied by hyperphagia, increased snout-anus length and hyperinsulinemia. In 2018, The Jackson Laboratory colony, on the mixed B6;129S4 background and maintained on standard chow diet, shows that homozygous mice are significantly heavier than sex-matched wildtype controls by approximately 6-8 weeks of age (more obvious for female homozygotes at a younger age), and obesity (30g) is apparent at approximate 7 weeks of age for homozygous males and approximately 10 weeks of age for homozygous females. The function of this disrupted allele can be restored by the enzymatic activity of Cre-recombinase. These mutant mice may be useful in studies of neurobiology, obesity, diabetes, hunger/appetite, and fat and energy metabolism.

When bred to a strain expressing Cre recombinase in the hypothalamus see Stock No. 006395 for example), this mutant mouse strain exhibits as intermediate phenotype in comparison to homozygous null mice.

When crossed to STOCK Slc32a1^tm2(cre)Lowl/J (see Stock No. 016962) Cre recombinase expression in inhibitory GABAergic neuron cell bodies results in offspring that exhibit obesity.

When crossed to B6;129S-Oxt^{tm1.1(cre)Dolsn}/J (see Stock No. 024234) Cre recombinase expression in oxytocin-expressing cells results in offspring that exhibit obesity.

Development

A targeting vector was designed to insert a loxp-flanked transcriptional blocker sequence (loxTB) between the transcriptional start site and ATG of the endogenous gene. The blocker sequence contains an SV40 enhancer, neomycin resistance gene, two HSV-TK polyA sequences, and an additional transcriptional pause signal from the pGL3-control vector. The construct was electroporated into 129S4/SvJae-derived embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6 blastocysts. Chimeric mice were bred to C57BL/6 mice. Mutant mice heterozygous for the "loxTB Mc4r" allele were bred together and maintained as such prior to arrival at The Jackson Laboratory.

Control Suggestions

Wild-type from the colony

Approximate Controls

101045 B6129SF2/J

Additional Information

Considerations for Choosing Controls

Selected References

Balthasar N; Dalgaard LT; Lee CE; Yu J; Funahashi H; Williams T; Ferreira M; Tang V; McGovern RA; Kenny CD; Christiansen LM; Edelstein E; Choi B; Boss O; Aschkenasi C; Zhang CY; Mountjoy K; Kishi T; Elmquist JK; Lowell BB. 2005. Divergence of melanocortin pathways in the control of food intake and energy expenditure. Cell 123(3):493-505PubMed: 16269339 MGI: J:115192

View All References

Genetics

Mc4r^tm1Lowl

Allele Symbol: Mc4r^tm1Lowl

Allele Name	targeted mutation 1, Bradford B Lowell
Allele Type	Targeted (Conditional ready (e.g. floxed), Null/Knockout)
Allele Synonym(s)	targeted mutation 1, Bradford B Lowell; Mc4r^tm1Lowl
Gene Symbol and Name	Mc4r, melanocortin 4 receptor
Gene Synonym(s)	Glu3; Fatboy; glucose 3; pork chop; Pkcp; Pkcp; BMIQ20
Strain of Origin	129S4/SvJae
Chromosome	18
Molecular Note	A loxP flanked PGK-neomycin selection marker inserted in the 5' UTR created a null allele. Cre recombinase deletes the selection marker, restoring normal activity of the allele. Mice fail to respond to MC4R agonist MTII. This is a null allele that can be "reactivated" by cre recombinase.
Mutations Made By	Bradford Lowell, Beth Israel Deaconess Med Cntr (Harvard)

Disease/Phenotype

Disease Terms

Models with phenotypic similarity to human diseases where etiology is unknown or involving genes where ortholog is unknown.

fatty liver disease

Research Areas By Genotype

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

Research Tools
- Cre-lox System
  - loxP-flanked Sequences
- Metabolism Research
- Neurobiology Research
- Diabetes and Obesity Research
  - loxP
Diabetes and Obesity Research
- Obesity Without Diabetes
- Obesity With Diabetes
- Hyperinsulinemia
Neurobiology Research
- Metabolic Defects

Mammalian Phenotype Terms by Genotype

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

Genotype: Mc4r^tm1Lowl/Mc4r^tm1Lowl Tg(Sim1-cre)1Lowl/0
involves: 129S4/SvJae * C57BL/6J * FVB

behavior/neurological phenotype

abnormal food intake
- when treated with MTII an Mc4r inhibitor, wild-type mice show a 50% reduction in food intake, while transgenic mice display no effect on intake

growth/size/body region phenotype

increased body weight
- transgenic mice have increased fat mass compared with wild-type littermates, but significantly decreased fat mass compared to Mc4r^tm1Lowl littermates

increased lean body mass
- transgenic mice have increased lean mass compared with wild-type littermates, but significantly decreased lean mass compared to Mc4r^tm1Lowl littermates

obese
- at 12 weeks of age, male and female mutants have only 37% and 46% respectively, of the obesity observed in mice homozygous for Mc4r disruption

homeostasis/metabolism phenotype

abnormal oxygen consumption
- mice do not show an increase in oxygen consumption from stimulation by MTII as wild-type mice do

decreased oxygen consumption
- oxygen consumption is reduced in the dark and light cycles compared to wild-type and is similar to Mc4r^tm1Lowl homozygotes

mammalian phenotype

behavior/neurological phenotype
- Normal - transgenic mice are obese, yet show food intake comparable to wild-type mice at 11 weeks of age

growth/size/body region phenotype
- Normal - at 12 weeks, transgenic mice and wild-type littermates have the same snout-anus length, compared to increased length observed in nontransgenic Mc4r^tm1Lowl mice

Genotype: Mc4r^tm1Lowl/Mc4r^tm1Lowl Tg(Nes-cre)1Kln/0
involves: 129S4/SvJae * C57BL/6 * SJL

normal phenotype

no abnormal phenotype detected
- Normal - mice homozygous for reactivated Mc4r in neurons show normal body weights and rescue of the increased snout-anus length observed in Mc4r^tm1Lowl homozygotes

Genotype: Mc4r^tm1Lowl/Mc4r^tm1Lowl Tg(Zp3-cre)3Mrt/0
involves: 129S4/SvJae * C57BL/6J * FVB/N

normal phenotype

no abnormal phenotype detected
- mice homozygous for reactivated Mc4r in neurons show normal body weights and rescue of the increased snout-anus length observed in Mc4r homozygotes
- Normal - mice homozygous for reactivated Mc4r in the germline show normal body weights and rescue of the increased snout-anus length observed in Mc4r^tm1Lowl homozygotes

Genotype: Mc4r^tm1Lowl/Mc4r^tm1Lowl
involves: 129S4/SvJae

growth/size/body region phenotype

obese
- become obese but not hypertensive

Genotype: Mc4r^tm1Lowl/Mc4r^tm1Lowl Slc17a6^tm2(cre)Lowl/Slc17a6⁺
involves: 129S4/SvJaeSor * 129S6/SvEvTac * C57BL/6 * FVB/N

mammalian phenotype

growth/size/body region phenotype
- Normal - rescue of the increased weight gain, of the fat stores, of hyperphagia and of the increased linear length seen in single Mc4r homozygotes

homeostasis/metabolism phenotype
- Normal - mice show normalization of the hyperglycemia and hyperinsulinemia that is seen in single Mc4r homozygotes

respiratory system phenotype
- Normal - rescue of the depressed respiratory exchange ratio seen in single Mc4r homozygotes

Genotype: Mc4r^tm1Lowl/Mc4r^tm1Lowl Slc32a1^tm2(cre)Lowl/Slc32a1⁺
involves: 129S4/SvJaeSor * 129S6/SvEvTac * C57BL/6 * FVB/N

growth/size/body region phenotype

obese

Genotype: Mc4r^tm1Lowl/Mc4r^tm1Lowl Oxt^{tm1.1(cre)Dolsn}/Oxt⁺
involves: 129S4/SvJaeSor * 129S6/SvEvTac * C57BL/6

growth/size/body region phenotype

obese

The following phenotype relates to a compound genotype created using this strain

Genotype: Mc4r^tm1Lowl/Mc4r^tm1Lowl
involves: 129S4/SvJae * C57BL/6J

adipose tissue phenotype

adipose tissue inflammation
- white adipose tissue of mutants fed the high-fat diet for 8 weeks exhibits increased macrophage infiltration and pro-inflammatory cytokine expression compared to wild-type white adipose tissue

increased total body fat amount
- mutants fed the high-fat diet also exhibit increased adiposity, but only up to 8 weeks of high-fat feeding with no further increase after 8 weeks
- mutants fed the standard diet exhibit increased adiposity compared to wild-type mice on the same diet

homeostasis/metabolism phenotype

abnormal oxygen consumption
- mice do not show an increase in oxygen consumption from stimulation by MTII as wild-type mice do

decreased circulating adiponectin level
- mutants fed the high-fat diet exhibit decreased serum adiponectin levels compared to wild-type mice on the same diet

decreased oxygen consumption
- oxygen consumption is reduced in the dark and light cycles compared to wild-type and is similar to mutants also expressing Tg(Sim1-cre)1Lowl

increased circulating alanine transaminase level
- mutants fed the high-fat diet show increased serum alanine aminotransferase concentrations compared to wild-type mice

increased circulating free fatty acid level
- mutants fed the high-fat diet show an increase in serum free fatty acid concentrations relative to wild-type mice

increased circulating insulin level
- hyperinsulinemia is displayed by homozygotes

increased circulating interleukin-6 level
- mutants fed the high-fat diet exhibit increased serum IL-6 levels compared to wild-type mice on the same diet

increased circulating leptin level
- mutants fed the high-fat diet exhibit increased serum leptin levels compared to wild-type mice on the same diet

increased liver triglyceride level
- livers of mutants fed the high-fat diet exhibit increased triglyceride secretion compared to wild-type livers
- mutants exhibit increased hepatic triglyceride content compared to wild-type mice on either the standard or high-fat diet

increased susceptibility to diet-induced obesity
- mutants exhibit increased weight gain compared to wild-type mice when fed a high-fat diet

immune system phenotype

adipose tissue inflammation
- white adipose tissue of mutants fed the high-fat diet for 8 weeks exhibits increased macrophage infiltration and pro-inflammatory cytokine expression compared to wild-type white adipose tissue

increased circulating interleukin-6 level
- mutants fed the high-fat diet exhibit increased serum IL-6 levels compared to wild-type mice on the same diet

liver inflammation
- livers from mutants fed the high-fat diet exhibit ballooning degeneration and massive infiltration of inflammatory cells
- livers from mutants fed the high-fat diet exhibit increased inflammatory cell infiltration compared to wild-type livers

liver/biliary system phenotype

hepatic steatosis
- mutants fed the high-fat diet develop liver steatosis faster (by 8 weeks of high-fat diet) than wild-type mice (by 20 weeks of high-fat diet)
- mutants fed the high-fat diet for 8 weeks exhibit massive microvesicular steatosis in the centrilobular and portal areas while wild-type mice only have minimal lipid accumulation in the liver

increased hepatocellular carcinoma incidence
- mutants fed the high-fat diet, but not the standard diet, for a year develop liver tumors
- tumors resemble hepatocellular carcinoma

increased liver triglyceride level
- livers of mutants fed the high-fat diet exhibit increased triglyceride secretion compared to wild-type livers
- mutants exhibit increased hepatic triglyceride content compared to wild-type mice on either the standard or high-fat diet

increased liver weight
- mutants exhibit increased liver weight compared to wild-type mice on either the standard or high-fat diet

liver fibrosis
- livers from mutants fed the high-fat diet exhibit increased pericellular fibrosis compared to wild-type mice at 8 and 20 weeks of high-fat feeding

liver inflammation
- livers from mutants fed the high-fat diet exhibit ballooning degeneration and massive infiltration of inflammatory cells
- livers from mutants fed the high-fat diet exhibit increased inflammatory cell infiltration compared to wild-type livers

neoplasm

increased hepatocellular carcinoma incidence
- mutants fed the high-fat diet, but not the standard diet, for a year develop liver tumors
- tumors resemble hepatocellular carcinoma

behavior/neurological phenotype

abnormal food intake
- unlike wild-type mice, mutants do not exhibit a reduction in food intake after treatment with the Mc4r inhibitor, MTII

polyphagia
- obesity is accompanied by polyphagia

growth/size/body region phenotype

increased body length
- at 12 weeks, homozygotes show increased snout-anus length

increased susceptibility to diet-induced obesity
- mutants exhibit increased weight gain compared to wild-type mice when fed a high-fat diet

increased susceptibility to weight gain
- mutants exhibit increased weight gain compared to wild-type mice when fed either the standard diet or a high-fat diet

obese
- male and female homozygotes display severe early-onset obesity

Genotype: Mc4r^tm1Lowl/Mc4r⁺
involves: 129S4/SvJae * C57BL/6

growth/size/body region phenotype

obese

References

Balthasar N; Dalgaard LT; Lee CE; Yu J; Funahashi H; Williams T; Ferreira M; Tang V; McGovern RA; Kenny CD; Christiansen LM; Edelstein E; Choi B; Boss O; Aschkenasi C; Zhang CY; Mountjoy K; Kishi T; Elmquist JK; Lowell BB. 2005. Divergence of melanocortin pathways in the control of food intake and energy expenditure. Cell 123(3):493-505PubMed: 16269339 MGI: J:115192

Additional References

Clemmensen C; Jall S; Kleinert M; Quarta C; Gruber T; Reber J; Sachs S; Fischer K; Feuchtinger A; Karlas A; Simonds SE; Grandl G; Loher D; Sanchez-Quant E; Keipert S; Jastroch M; Hofmann SM; Nascimento EBM; Schrauwen P; Ntziachristos V; Cowley MA; Finan B; Muller TD; Tschop MH. 2018. Coordinated targeting of cold and nicotinic receptors synergistically improves obesity and type 2 diabetes. Nat Commun 9(1):4304PubMed: 30353008 MGI: J:267780
Singha AK; Yamaguchi J; Gonzalez NS; Ahmed N; Toney GM; Fujikawa T. 2019. Glucose-Lowering by Leptin in the Absence of Insulin Does Not Fully Rely on the Central Melanocortin System in Male Mice. Endocrinology 160(3):651-663PubMed: 30698681 MGI: J:271662

Additional - Mc4r^tm1Lowl related

Technical Support

Contact Technical Support

Genotyping Protocols
- Melt Curve Analysis: Mc4r^tm1Lowl Alternate 1
- Standard PCR: Mc4r^tm1Lowl
- Genotyping resources and troubleshooting
Dietary Information
- LabDiet® 5K52 formulation (6% fat)
Breeding Considerations

Although homozygous mice are viable and fertile, the donating investigator breeds heterozygous mice together to generate homozygous, heterozygous, and wildtype mice. Of note: In 2018, The Jackson Laboratory colony, on the mixed B6;129S4 background and maintained on standard chow diet, shows that homozygous mice are significantly heavier than sex-matched wildtype controls by approximately 6-8 weeks of age (more obvious for female homozygotes at a younger age), and obesity (30g) is apparent at approximate 7 weeks of age for homozygous males and approximately 10 weeks of age for homozygous females.
- Additional Breeding and Husbandry Support
Mating System
- Heterozygote x Heterozygote
Citation
When using the loxTB Mc4r mouse strain in a publication, please cite the originating article(s) and include JAX stock #006414 in your Materials and Methods section.

Animal Health Reports

Facility Barrier Level Descriptions

AX12 (Maximum)

Pricing & Availability

Available

Domestic
International

Live Mouse

Age

Genotype

Price

weeks

Breeder Pair

Sex

Genotype

Price

Female
Male

Cryorecovery - Pricing

Service	Genotype	Price
	Heterozygous or Wild-type for Mc4r<tm1Lowl>

We will fulfill your order by providing at least two carriers for each strain ordered. The total number, sex, and genotypes provided will vary, although typically 8 or more animals are provided. Please check genotypes which will be recovered. While the genotypes of all animals produced will be communicated to you prior to scheduling shipment, the genotypes of animals provided may not reflect the mating scheme and genotypes described in the strain description. Animals are typically ready to ship in 11-14 weeks. If a second recovery is required to produce the minimum number of animals, then delivery time would increase to approximately 25 weeks. If we fail to produce animals of the correct genotype, you will not be charged. We 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.

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Also Known As: loxTB Mc4r

Donating Investigator

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Control Suggestions

Approximate Controls

Additional Information

Selected References

Mc4rtm1Lowl

Allele Symbol: Mc4rtm1Lowl

Disease Terms

Models with phenotypic similarity to human diseases where etiology is unknown or involving genes where ortholog is unknown.

Research Areas By Genotype

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

Mammalian Phenotype Terms by Genotype

Genotype: Mc4rtm1Lowl/Mc4rtm1Lowl Tg(Sim1-cre)1Lowl/0involves: 129S4/SvJae * C57BL/6J * FVB

behavior/neurological phenotype

growth/size/body region phenotype

homeostasis/metabolism phenotype

mammalian phenotype

Genotype: Mc4rtm1Lowl/Mc4rtm1Lowl Tg(Nes-cre)1Kln/0involves: 129S4/SvJae * C57BL/6 * SJL

normal phenotype

Genotype: Mc4rtm1Lowl/Mc4rtm1Lowl Tg(Zp3-cre)3Mrt/0involves: 129S4/SvJae * C57BL/6J * FVB/N

normal phenotype

Genotype: Mc4rtm1Lowl/Mc4rtm1Lowlinvolves: 129S4/SvJae

growth/size/body region phenotype

Genotype: Mc4rtm1Lowl/Mc4rtm1Lowl Slc17a6tm2(cre)Lowl/Slc17a6+involves: 129S4/SvJaeSor * 129S6/SvEvTac * C57BL/6 * FVB/N

mammalian phenotype

Genotype: Mc4rtm1Lowl/Mc4rtm1Lowl Slc32a1tm2(cre)Lowl/Slc32a1+involves: 129S4/SvJaeSor * 129S6/SvEvTac * C57BL/6 * FVB/N

growth/size/body region phenotype

Genotype: Mc4rtm1Lowl/Mc4rtm1Lowl Oxttm1.1(cre)Dolsn/Oxt+involves: 129S4/SvJaeSor * 129S6/SvEvTac * C57BL/6

growth/size/body region phenotype

Genotype: Mc4rtm1Lowl/Mc4rtm1Lowlinvolves: 129S4/SvJae * C57BL/6J

adipose tissue phenotype

homeostasis/metabolism phenotype

immune system phenotype

liver/biliary system phenotype

neoplasm

behavior/neurological phenotype

growth/size/body region phenotype

Genotype: Mc4rtm1Lowl/Mc4r+involves: 129S4/SvJae * C57BL/6

growth/size/body region phenotype

References

Additional References

Additional - Mc4rtm1Lowl related

Genotyping Protocols

Dietary Information

Breeding Considerations

Mating System

Citation

Animal Health Reports

Live Mouse

Breeder Pair

Cryorecovery - Pricing

Related Products and Services

Payment Terms and Conditions

The Jackson Laboratory's Genotype Promise

Terms of Use

Additional Use Restrictions Apply

Licensing Information

JAX® Mice, Products & Services Conditions of Use

No Warranty

Credit for PRODUCTS or SERVICES

Animal Care and Use for SERVICES

No Liability

Mc4r^tm1Lowl

Allele Symbol: Mc4r^tm1Lowl

Genotype: Mc4r^tm1Lowl/Mc4r^tm1Lowl Tg(Sim1-cre)1Lowl/0
involves: 129S4/SvJae * C57BL/6J * FVB

Genotype: Mc4r^tm1Lowl/Mc4r^tm1Lowl Tg(Nes-cre)1Kln/0
involves: 129S4/SvJae * C57BL/6 * SJL

Genotype: Mc4r^tm1Lowl/Mc4r^tm1Lowl Tg(Zp3-cre)3Mrt/0
involves: 129S4/SvJae * C57BL/6J * FVB/N

Genotype: Mc4r^tm1Lowl/Mc4r^tm1Lowl
involves: 129S4/SvJae

Genotype: Mc4r^tm1Lowl/Mc4r^tm1Lowl Slc17a6^tm2(cre)Lowl/Slc17a6⁺
involves: 129S4/SvJaeSor * 129S6/SvEvTac * C57BL/6 * FVB/N

Genotype: Mc4r^tm1Lowl/Mc4r^tm1Lowl Slc32a1^tm2(cre)Lowl/Slc32a1⁺
involves: 129S4/SvJaeSor * 129S6/SvEvTac * C57BL/6 * FVB/N

Genotype: Mc4r^tm1Lowl/Mc4r^tm1Lowl Oxt^{tm1.1(cre)Dolsn}/Oxt⁺
involves: 129S4/SvJaeSor * 129S6/SvEvTac * C57BL/6

Genotype: Mc4r^tm1Lowl/Mc4r^tm1Lowl
involves: 129S4/SvJae * C57BL/6J

Genotype: Mc4r^tm1Lowl/Mc4r⁺
involves: 129S4/SvJae * C57BL/6

Additional - Mc4r^tm1Lowl related