Overview

Also Known As: CsnK1a1^fl

These CsnK1a1^fl floxed mice allow Cre recombinase-inducible knockout of casein kinase Ia (CKIα) for studying multiple cellular processes (Wnt pathway, cell cycle regulation, DNA damage response, KRAS-MEK-ERK mitogenic signaling, β-catenin-destruction complex) in cancer and senescence-associated inflammatory response (SIR)/para-inflammation suppression.

Donating Investigator

Yinon Ben-Neriah, The Hebrew University of Jerusalem

Genetic overview

Genetic Background	Generation

Csnk1a1^tm1.1Ybn

Allele Type	Gene Symbol	Gene Name
Targeted (Conditional ready (e.g. floxed), No functional change)	Csnk1a1	casein kinase 1, alpha 1

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Research Applications

Immunology, Inflammation and Autoimmunity Research
Research Tools
Cell Biology Research
Cancer Research
Neurobiology Research

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Base Price

Starting at:

$2,854.50 Domestic price Cryo Recovery

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Details

Detailed Description

The CsnK1a1^fl (also called Slc6a8^fl) conditional allele has loxP sites flanking exons 1-2 of the casein kinase Ia gene (CKIα). When bred to mice that express Cre recombinase, the resulting offspring will have the floxed sequences deleted in the cre-expressing tissues. Homozygous mice (CsnK1a1^flox/flox) are viable and fertile with no reported abnormalities. When CsnK1a1^fl mice are bred to the germline Cre-deleter strain Pgk1-Cre (e.g., Stock No. 020811), the resulting CsnK1a1 pan-deletion homozygotes die before embryonic day (E)6.5.

These CsnK1a1^fl mice are a Cre-lox tool for generating tissue-specific CsnK1a1 deletions, and may be useful for studying cancer, tumorigenesis and multiple cellular processes including Wnt pathway, cell cycle regulation, DNA damage response and β-catenin-destruction complex.

For example, breeding CsnK1a1^fl to mice expressing Cre recombinase in intestinal tissue (e.g., Vil1-Cre; Stock No. 021504) results in intestinal CsnK1a1 ablation mice. Such mice recapitulate many features of human colorectal tumors (including Wnt hyperinduction, induction of the DNA damage response and cellular senescence), as well as widespread cyclin D1 expression and substantial p53 expression, all in the absence of tumorigenesis (absence of Wnt-associated excessive proliferation or tumorigenesis; gut homeostasis is maintained).
Subsequent breeding to p53^flox (Stock No. 008462) or p21-/- (Stock No. 003263) allow further investigation into the factors initiating highly invasive carcinoma.

Development

A targeting vector was designed by Dr. Yinon Ben-Neriah (The Hebrew University of Jerusalem) to place loxP sites flanking exons 1-2 of the casein kinase 1, alpha 1 gene (Csnk1a1 or CKIα) on chromosome 18. This also inserted a loxP-flanked neomycin cassette. The construct was electroporated into (129X1/SvJ x 129S1/Sv)F1-Kitl⁺-derived R1 embryonic stem (ES) cells. Next, ES cells were transiently transfected with the pCA-NLS-Cre vector. The resulting ES cells with the CsnK1a1^fl genotype (retaining the floxed exons 1-2 with deletion of the neo cassette) were identified and used for aggregation with CD1-derived morulae. Chimeric mice were bred to CD1 for germline transmission. The donating investigator reported that the CsnK1a1^fl colony was bred with C57BL/6 inbred mice (a mixture of C57BL/6JOlaHsd and C57BL/6J) for at least ten generations (see SNP results below). During backcrossing, the Y chromosome may not have been fixed to the C57BL/6 genetic background. In 2015, CsnK1a1^fl males were sent to The Jackson Laboratory Repository. Upon arrival, sperm was cryopreserved. To generate the living CsnK1a1^fl colony, an aliquot of the frozen sperm was used to fertilize oocytes from C57BL/6J female mice (Stock No. 000664). The CsnK1a1^fl colony was then maintained by breeding heterozygous or homozygous mice together.

In 2015, a 32 SNP (single nucleotide polymorphism) panel analysis, with 27 markers covering all 19 chromosomes and the X chromosome, as well as 5 markers that distinguish between the C57BL/6J and C57BL/6N substrains, was performed on all 14 heterozygous mice from the first generation rederived living colony at The Jackson Laboratory Repository. All 26 markers on somatic chromosomes throughout the genome suggest a C57BL/6 genetic background. All heterozygous females, but none of the heterozygous males, had one marker on the X chromosome [~66.9 Mbp] segregating for C57BL/6 and 129 allele-type.

In addition, 3 of 5 markers that determine C57BL/6J from C57BL/6N were found to be segregating in all tested mice (chromosomes 8 [~15.2 Mbp], 15 [~57.6 Mbp] and 19 [~49.9 Mbp]), and some mice had one marker segregating on chromosome 13 [~41.0 Mbp]. These data suggest that the mice sent to The Jackson Laboratory Repository were on a mixed C57BL/6N;C57BL/6J genetic background, or alternatively, the C57BL/6JOlaHsd contributions may have similar SNPs as C57BL/6N.

Control Suggestions

Approximate Controls

Additional Information

Considerations for Choosing Controls

Selected References

Elyada E; Pribluda A; Goldstein RE; Morgenstern Y; Brachya G; Cojocaru G; Snir-Alkalay I; Burstain I; Haffner-Krausz R; Jung S; Wiener Z; Alitalo K; Oren M; Pikarsky E; Ben-Neriah Y. 2011. CKIalpha ablation highlights a critical role for p53 in invasiveness control. Nature 470(7334):409-13PubMed: 21331045 MGI: J:204886

View All References

Genetics

Csnk1a1^tm1.1Ybn

Allele Symbol: Csnk1a1^tm1.1Ybn

Allele Name	targeted mutation 1.1, Yinon Ben-Neriah
Allele Type	Targeted (Conditional ready (e.g. floxed), No functional change)
Allele Synonym(s)	Csnk1a1^tm1.1Ybn; targeted mutation 1.1, Yinon Ben-Neriah
Gene Symbol and Name	Csnk1a1, casein kinase 1, alpha 1
Gene Synonym(s)	5430427P18Rik; 4632404G05Rik; CKIa; 2610208K14Rik; RIKEN cDNA 4632404G05 gene; RIKEN cDNA 5430427P18 gene; 2610208K14Rik; 5430427P18Rik; HEL-S-77p; HLCDGP1; PRO2975; 4632404G05Rik; CK1; CK1a; RIKEN cDNA 2610208K14 gene
Strain of Origin	(129X1/SvJ x 129S1/Sv)F1-Kitl⁺
Chromosome	18
Molecular Note	A floxed neomycin resistance cassette was inserted upstream of exon 1. An additional loxP site was inserted downstream of exon 2. Cre-mediated recombination removed the neomycin resistance cassette and left exons 1 and 2 floxed.

Disease/Phenotype

Disease Terms

Research Areas By Genotype

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

Immunology, Inflammation and Autoimmunity Research
- Intracellular Signaling Molecules
- Growth Factors/Receptors/Cytokines
Research Tools
- Cancer Research
  - anti-tumor activity
  - tumor immunology
  - Cre-lox System
- Genetics Research
  - Mutagenesis and Transgenesis: Cre-lox System
- Reproductive Biology Research
  - Cre-lox System
- Immunology, Inflammation and Autoimmunity Research
- Cardiovascular Research
  - Cre-lox System
- Cre-lox System
  - loxP-flanked Sequences
- Developmental Biology Research
  - Cre-lox System
Cell Biology Research
- Cell Cycle Regulation
- Signal Transduction
Cancer Research
- Cre-lox System
  - loxP-flanked Sequences
- Oncogenes
- Tumor Suppressor Genes
- Tumor Resistance
Neurobiology Research
- Cre-lox System
  - loxP-flanked Sequences

Mammalian Phenotype Terms by Genotype

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

Genotype: Csnk1a1^tm1.1Ybn/Csnk1a1^tm1.1Ybn Tg(KRT14-cre/ERT)20Efu/0
involves: 129S1/Sv * 129X1/SvJ * CD-1

cellular phenotype

decreased cellular sensitivity to ultraviolet irradiation
- 24 h after exposure to a high, sunburn-inducing dose of UVB, hyperpigmented tails of tamoxifen-treated mice show absence of skin swelling and significantly fewer TUNEL+ apoptotic keratinocytes in the tail skin than similarly-treated control mice, indicating protection from UV (sunburn) damage

increased apoptosis
- tamoxifen-injected mice show increased apoptosis in the epidermis, as shown by increased cleaved-caspase 3 expression

limbs/digits/tail phenotype

increased tail pigmentation
- hyperpigmentation of the tail at 1 month after tamoxifen i.p. treatment
- topical treatment with 4HT for 14 days induces skin hyperpigmentation on the tail, esp. at >3 weeks after induction

mammalian phenotype

neoplasm
- Normal - no skin tumor formation is observed for at least 9 months after tamoxifen i.p. treatment

craniofacial phenotype

increased ear pigmentation
- hyperpigmentation of the ears at 1 month after tamoxifen i.p. treatment
- topical treatment with 4HT for 14 days induces skin hyperpigmentation on the ear, esp. at >3 weeks after induction

pigmentation phenotype

abnormal epidermal melanocyte morphology
- a slow but significant increase of melanocyte numbers is noted in the tail epidermis during the first 14 days after topical 4HT induction, followed by a rapid increase thererafter; however, the number of dermal melanocytes is not significantly altered
- after topical 4HT induction, epidermal melanocytes become progressively larger and more dendritic, indicating melanocytic differentiation
- intradermal injection of ACK2 (a Kit-neutralizing antibody) reduces the number of melanocytes in the epidermis at days 7 and 14 after 4HT induction relative to vehicle-treated control mice
- many dendritic melanocytes containing black melanin pigment are observed around p53+ keratinocytes at day 28 after tamoxifen i.p. treatment
- melanocyte number is increased in the dorsal epidermis at day 28 after tamoxifen i.p. treatment
- treatment of 4HT-induced mice with oral imatinib (a Kit inhibitor) results in decreased melanocyte numbers in the epidermis at day P28 relative to vehicle-treated control mice

abnormal epidermal pigmentation
- increased melanin content in the dorsal epidermis at day 28 after tamoxifen i.p. treatment
- increased melanin content in the ear epidermis at day 28 after topical 4-hydroxytamoxife (4HT) induction

abnormal eumelanosome eumelanin content
- amount of eumelanin is significantly increased in the epidermis at day 28 after topical 4HT induction
- Normal - amount of pheomelanin remains unchanged during topical 4HT induction
- treatment of tamoxifen-injected mice with oral imatinib (a Kit inhibitor) results in severe reduction of eumelanin production relative to vehicle-treated control mice at day 28

hyperpigmentation
- at 1 month after tamoxifen i.p. treatment, mice show skin hyperpigmentation on the ears, paws, tail, mouth, and trunk relative to heterozygous control mice
- skin hyperpigmentation is accompanied by beta-catenin and p53 stabilization, preferential induction of p53 target genes, and p53-dependent up-regulation of Kit ligand
- treatment with ACK2 (a Kit-neutralizing antibody) or imatinib (a Kit inhibitor) abolishes the induction of hyperpigmentation, indicating that it requires the KitL/Kit pathway

increased ear pigmentation
- hyperpigmentation of the ears at 1 month after tamoxifen i.p. treatment
- topical treatment with 4HT for 14 days induces skin hyperpigmentation on the ear, esp. at >3 weeks after induction

increased foot pigmentation
- hyperpigmentation of the paws at 1 month after tamoxifen i.p. treatment

increased melanocyte number
- a slow but significant increase of melanocyte numbers is noted in the tail epidermis during the first 14 days after topical 4HT induction, followed by a rapid increase thererafter
- intradermal injection of ACK2 (a Kit-neutralizing antibody) reduces the number of melanocytes in the epidermis at days 7 and 14 after 4HT induction relative to vehicle-treated control mice
- melanocyte number is increased in the dorsal epidermis at day 28 after tamoxifen i.p. treatment
- treatment of 4HT-induced mice with oral imatinib (a Kit inhibitor) results in decreased melanocyte numbers in the epidermis at day P28 relative to vehicle-treated control mice

increased tail pigmentation
- hyperpigmentation of the tail at 1 month after tamoxifen i.p. treatment
- topical treatment with 4HT for 14 days induces skin hyperpigmentation on the tail, esp. at >3 weeks after induction

growth/size/body region phenotype

increased ear pigmentation
- hyperpigmentation of the ears at 1 month after tamoxifen i.p. treatment
- topical treatment with 4HT for 14 days induces skin hyperpigmentation on the ear, esp. at >3 weeks after induction

hearing/vestibular/ear phenotype

increased ear pigmentation
- hyperpigmentation of the ears at 1 month after tamoxifen i.p. treatment
- topical treatment with 4HT for 14 days induces skin hyperpigmentation on the ear, esp. at >3 weeks after induction

integument phenotype

abnormal epidermal melanocyte morphology
- a slow but significant increase of melanocyte numbers is noted in the tail epidermis during the first 14 days after topical 4HT induction, followed by a rapid increase thererafter; however, the number of dermal melanocytes is not significantly altered
- after topical 4HT induction, epidermal melanocytes become progressively larger and more dendritic, indicating melanocytic differentiation
- intradermal injection of ACK2 (a Kit-neutralizing antibody) reduces the number of melanocytes in the epidermis at days 7 and 14 after 4HT induction relative to vehicle-treated control mice
- many dendritic melanocytes containing black melanin pigment are observed around p53+ keratinocytes at day 28 after tamoxifen i.p. treatment
- melanocyte number is increased in the dorsal epidermis at day 28 after tamoxifen i.p. treatment
- treatment of 4HT-induced mice with oral imatinib (a Kit inhibitor) results in decreased melanocyte numbers in the epidermis at day P28 relative to vehicle-treated control mice

abnormal epidermal pigmentation
- increased melanin content in the dorsal epidermis at day 28 after tamoxifen i.p. treatment
- increased melanin content in the ear epidermis at day 28 after topical 4-hydroxytamoxife (4HT) induction

abnormal epidermis stratum basale morphology
- at day 28 after tamoxifen i.p. treatment, BrdU+ (proliferating) cells and beta-catenin nuclear staining are increased in the basal layer of the epidermis

abnormal skin physiology
- tamoxifen-injected mice show induction of the DNA-damage response, as shown by increased gamma-H2AX staining in the epidermis

epidermal hyperplasia
- after tamoxifen i.p. treatment, the epidermis becomes hyperplastic with increased melanin deposition
- treatment of tamoxifen-injected mice with oral imatinib (a Kit inhibitor) induces thinning of the epidermis with decreased melanin levels in the epidermis relative to vehicle-treated control mice

increased ear pigmentation
- hyperpigmentation of the ears at 1 month after tamoxifen i.p. treatment
- topical treatment with 4HT for 14 days induces skin hyperpigmentation on the ear, esp. at >3 weeks after induction

increased foot pigmentation
- hyperpigmentation of the paws at 1 month after tamoxifen i.p. treatment

increased tail pigmentation
- hyperpigmentation of the tail at 1 month after tamoxifen i.p. treatment
- topical treatment with 4HT for 14 days induces skin hyperpigmentation on the tail, esp. at >3 weeks after induction

thick epidermis
- increased epidermal thickness in the ears 28 days after topical 4HT induction

References

Elyada E; Pribluda A; Goldstein RE; Morgenstern Y; Brachya G; Cojocaru G; Snir-Alkalay I; Burstain I; Haffner-Krausz R; Jung S; Wiener Z; Alitalo K; Oren M; Pikarsky E; Ben-Neriah Y. 2011. CKIalpha ablation highlights a critical role for p53 in invasiveness control. Nature 470(7334):409-13PubMed: 21331045 MGI: J:204886

Additional - Csnk1a1^tm1.1Ybn related

Technical Support

Contact Technical Support

Genotyping Protocols
- Standard PCR:Csnk1a1^tm1.1Ybn
- Genotyping resources and troubleshooting
Breeding Considerations

When maintaining a live colony, heterozygous mice may be bred together, to wildtype mice from the colony, or to C57BL/6J inbred mice (Stock No. 000664). Alternatively, homozygous mice may be bred together.
- Additional Breeding and Husbandry Support
Citation
When using the CsnK1a1^fl mouse strain in a publication, please cite the originating article(s) and include JAX stock #025398 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

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Genotype

Price

weeks

Cryorecovery - Pricing

Service	Genotype	Price
	Heterozygous for Csnk1a1<tm1.1Ybn>

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.

Related Products and Services

Frozen Mouse Embryo	B6.129(Cg)-Csnk1a1<tm1.1Ybn>/J Frozen Embryo	$2595.00
Frozen Mouse Embryo	B6.129(Cg)-Csnk1a1<tm1.1Ybn>/J Frozen Embryo	$2595.00
Frozen Mouse Embryo	B6.129(Cg)-Csnk1a1<tm1.1Ybn>/J Frozen Embryo	$3373.50
Frozen Mouse Embryo	B6.129(Cg)-Csnk1a1<tm1.1Ybn>/J Frozen Embryo	$3373.50

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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.

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Also Known As: CsnK1a1fl

Donating Investigator

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Control Suggestions

Approximate Controls

Additional Information

Selected References

Csnk1a1tm1.1Ybn

Allele Symbol: Csnk1a1tm1.1Ybn

Disease Terms

Research Areas By Genotype

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

Mammalian Phenotype Terms by Genotype

Genotype: Csnk1a1tm1.1Ybn/Csnk1a1tm1.1Ybn Tg(KRT14-cre/ERT)20Efu/0involves: 129S1/Sv * 129X1/SvJ * CD-1

cellular phenotype

limbs/digits/tail phenotype

mammalian phenotype

craniofacial phenotype

pigmentation phenotype

growth/size/body region phenotype

hearing/vestibular/ear phenotype

integument phenotype

References

Additional - Csnk1a1tm1.1Ybn 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

Licensing Information

JAX® Mice, Products & Services Conditions of Use

No Warranty

Credit for PRODUCTS or SERVICES

Animal Care and Use for SERVICES

No Liability

Also Known As: CsnK1a1^fl

Csnk1a1^tm1.1Ybn

Allele Symbol: Csnk1a1^tm1.1Ybn

Genotype: Csnk1a1^tm1.1Ybn/Csnk1a1^tm1.1Ybn Tg(KRT14-cre/ERT)20Efu/0
involves: 129S1/Sv * 129X1/SvJ * CD-1

Additional - Csnk1a1^tm1.1Ybn related