Overview

The Mark3 (MAP/microtubule affinity-regulating kinase) targeted in this strain is associated with the Cdc25c cell division cycle 25 homolog C) gene. Western blot analysis confirms that expression of this targeted gene is eliminated in brain, spleen, thymus, white and brown adipose tissue, large and small intestines, stomach, kidney and liver. A phenotype has not as yet been detected.

Donating Investigator

Dr. Helen Piwnica-Worms, MD Anderson Cancer Center

Genetic overview

Genetic Background	Generation

Mark3^tm1Hpw

Allele Type	Gene Symbol	Gene Name
Targeted (Null/Knockout)	Mark3	MAP/microtubule affinity regulating kinase 3

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Research Applications

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Base Price

Starting at:

$2,854.50 Domestic price Cryo Recovery

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Details

Detailed Description

The protein kinase targeted in this strain is associated with the Cdc25c cell division cycle 25 homolog C) gene. Western blot analysis confirms that expression of this targeted gene is eliminated in brain, spleen, thymus, white and brown adipose tissue, large and small intestines, stomach, kidney and liver. A phenotype has not as yet been detected.

Development

A 1.6 kb fragment of the gene was disrupted by the insertion of a neomycin resistance cassette. Exon 2 (hosting the ATP binding site) and the 5' slice site of intron 2/3 were shifted out of frame. The mutation was created using 129X1/SvJ-derived RW-4 embryonic stem (ES) cells. This line was backcrossed nine times to C57BL/6 by the donating investigator.

Genetics

Mark3^tm1Hpw

Allele Symbol: Mark3^tm1Hpw

Allele Name	targeted mutation 1, Helen Piwnica-Worms
Allele Type	Targeted (Null/Knockout)
Allele Synonym(s)	cTak KO; Par-1a^-
Gene Symbol and Name	Mark3, MAP/microtubule affinity regulating kinase 3
Gene Synonym(s)
Strain of Origin	129X1/SvJ
Chromosome	12
Molecular Note	A 1.9 kb fragment of the gene was disrupted by the insertion of a neomycin resistance cassette. Exon 2 (hosting the ATP binding site) and the 5' slice site of intron 2/3 were shifted out of frame. Multi-tissue Western blotting confirmed ablation of this gene in all tissues of homozygous null-mice.
Mutations Made By	Dr. Helen Piwnica-Worms, MD Anderson Cancer Center

Disease/Phenotype

Disease Terms

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: Mark3^tm1Hpw/Mark3^tm1Hpw
involves: 129X1/SvJ * C57BL/6

homeostasis/metabolism phenotype

improved glucose tolerance
- mice exhibit improved glucose tolerance on a high-fat diet compared to wild-type mice on the same diet
- Normal - normal glucose sensitivity on a regular diet
- mutants on a high-fat diet are normoglycemic

abnormal metabolism
- Normal - however, body temperature, food intake and activity levels are similar to wild-type mice
- males on a regular diet exhibit higher oxygen consumption, with an approximate 9% increase in the total metabolic rate

decreased circulating insulin level
- Normal - however, normal serum insulin levels when fed a regular diet
- mice on a high-fat diet exhibit lower serum insulin levels during the first 60 min of the glucose tolerance test

decreased liver glycogen level
- decrease in glycogen deposition in the liver
- overnight starvation leads to complete hepatic glycogen depletion compared to partial depletion in wild-type liver and absence of restoration of hepatic glycogen content

increased energy expenditure
- males on a regular diet exhibit 10% increase in total energy expenditure

decreased susceptibility to diet-induced obesity
- mice are protected against high-fat-diet induced obesity, showing weight gain that is delayed and at a reduced rate; mice require 7 additional weeks of high-fat diet to reach the original weight of the wild-type mice

increased circulating adiponectin level
- males on a regular diet show a 1.6-fold higher level of serum adiponectin

hypoglycemia
- overnight starvation leads to complete hepatic glycogen depletion, associated with hypoketotic hypoglycemia

liver/biliary system phenotype

abnormal liver physiology
- overnight starvation results in increased hepatocellular autophagy (increase in autophagic vacuoles in the liver) and increased glycogen synthase levels

decreased liver glycogen level
- decrease in glycogen deposition in the liver
- overnight starvation leads to complete hepatic glycogen depletion compared to partial depletion in wild-type liver and absence of restoration of hepatic glycogen content

decreased susceptibility to hepatic steatosis
- mice show resistance to hepatic steatosis after chronic exposure to a high-fat diet, however hepatic glucose uptake is not altered

decreased susceptibility to diet-induced hepatic steatosis
- mice show resistance to hepatic steatosis after chronic exposure to a high-fat diet, however hepatic glucose uptake is not altered

mortality/aging

postnatal lethality
- only 17% of the expected 25% of pups were observed

adipose tissue phenotype

decreased total body fat amount
- on a regular diet, adiposity is reduced with unaltered glucose handling and normal insulin sensitivity
- however when fed a high-fat diet, mice show a similar increase in overall adiposity as controls

decreased white adipose tissue amount
- white adipose tissue from gonadal fat pads is disproportionately smaller in mice on a regular diet

decreased brown adipose tissue amount
- brown adipose tissue is disproportionally smaller in mice on a regular diet

abnormal adipocyte glucose uptake
- on a regular diet, mice exhibit a decrease in white adipose tissue (WAT) glucose uptake, however on a high-fat diet, uptake is increased so that the difference of glucose uptake in comparison to wild-type on a high-fat diet is eliminated

cellular phenotype

abnormal adipocyte glucose uptake
- on a regular diet, mice exhibit a decrease in white adipose tissue (WAT) glucose uptake, however on a high-fat diet, uptake is increased so that the difference of glucose uptake in comparison to wild-type on a high-fat diet is eliminated

growth/size/body region phenotype

decreased body weight
- decrease in body weight is observed at 32 weeks of age but not at 6 weeks of age
- 9% reduction in body weight at 32 weeks of age when fed a regular diet

decreased susceptibility to diet-induced obesity
- mice are protected against high-fat-diet induced obesity, showing weight gain that is delayed and at a reduced rate; mice require 7 additional weeks of high-fat diet to reach the original weight of the wild-type mice

References

Additional - Mark3^tm1Hpw related

Technical Support

CONTACT TECHNICAL SUPPORT

Genotyping Protocols
- Separated PCR:Mark3
- Genotyping resources and troubleshooting
Breeding Considerations

When maintained as a live colony, homozygotes or heterozygotes may be bred.
- Additional Breeding and Husbandry Support
Citation
When using the B6.129X1-Mark3^tm1Hpw/J mouse strain in a publication, please cite the originating article(s) and include JAX stock #009366 in your Materials and Methods section.

Animal Health Reports

Facility Barrier Level Descriptions

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

Pricing & Availability

Cryo Recovery

Domestic
International

Live Mouse

Age

Genotype

Price

weeks

Cryorecovery - Pricing

Service/Product	Description	Price
> >	Heterozygous or Wild-Type for Mark3<tm1Hpw>

Related Products and Services

Frozen Mouse Embryo	B6.129X1-Mark3<tm1Hpw>/J Frozen Embryo	$2595.00
Frozen Mouse Embryo	B6.129X1-Mark3<tm1Hpw>/J Frozen Embryo	$2595.00
Frozen Mouse Embryo	B6.129X1-Mark3<tm1Hpw>/J Frozen Embryo	$3373.50
Frozen Mouse Embryo	B6.129X1-Mark3<tm1Hpw>/J Frozen Embryo	$3373.50

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The Jackson Laboratory's Genotype Promise

The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project. We do not guarantee breeding performance and therefore suggest that investigators order more than one breeding pair to avoid delays in their research.

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Use of MICE by companies or for-profit entities requires a license prior to shipping.

Licensing Information

Phone: 207-288-6470

Email: TechTran@jax.org

Donating Investigator

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Mark3tm1Hpw

Allele Symbol: Mark3tm1Hpw

Disease Terms

Research Areas By Phenotype

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

Mammalian Phenotype Terms by Genotype

Genotype: Mark3tm1Hpw/Mark3tm1Hpwinvolves: 129X1/SvJ * C57BL/6

homeostasis/metabolism phenotype

liver/biliary system phenotype

mortality/aging

adipose tissue phenotype

cellular phenotype

growth/size/body region phenotype

References

Additional - Mark3tm1Hpw related

Genotyping Protocols

Breeding Considerations

Citation

Animal Health Reports

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

Live Mouse

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

Mark3^tm1Hpw

Allele Symbol: Mark3^tm1Hpw

Genotype: Mark3^tm1Hpw/Mark3^tm1Hpw
involves: 129X1/SvJ * C57BL/6

Additional - Mark3^tm1Hpw related