Description

The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.

Strain Information

Type Mutant Strain; Targeted Mutation; Additional information on Genetically Engineered and Mutant Mice. Visit our online Nomenclature tutorial. Species laboratory mouse Generation F?+1   Donating Investigator Philippe Soriano,   Fred Hutchinson Cancer Research Center

Description
Mice homozygous for disruption of the csk gene die in utero at 9 - 10 days of gestation, exhibiting defects in neurulation. Mutant embryos are anatomically indistinguishable from normal or heterozygous littermates at E8.5, but are identifiable at E9.5 by their smaller size, failure to 'turn' (reverse orientation of germ layers) and failure to close their cephalic neural folds. The allantois of these mutant embryos is also abnormal and does not connect with the chorion, preventing formation of the umbilical cord and placenta. The kinase Csk plays a role in negative regulation of the Src family tyrosine kinases by phosphorylating a key carboxy-terminal tyrosine residue. Expression of csk in normal embryos is detectable at low levels beginning at E8.5, and is at its highest level of expression at E9.5.

Control Information

	Control
	Wild-type from the colony
Considerations for Choosing Controls

Additional Web Information

New 129 Nomenclature Bulletin

Phenotype

Phenotype Information

View Mammalian Phenotype Terms

Mammalian Phenotype Terms

      assigned by genotype

The following phenotype information may relate to a genetic background differing from this JAX^® Mice strain.

Csk^tm1Sor/Csk^tm1Sor

        either: (involves: 129S7/SvEvBrd) or (involves: 129S7/SvEvBrd * C57BL/6J)

• lethality-prenatal/perinatal
• embryonic lethality during organogenesis (MGI Ref ID J:12622)
  • most homozygotes die between E9.5 and E10.5
  • no homozygotes are recovered at or after E11.5
• embryogenesis phenotype
• abnormal allantois morphology (MGI Ref ID J:12622)
  • at E9.5, the allantois is often abnormal and either resorbing or tuberous
• enlarged allantois (MGI Ref ID J:12622)
  • allantois is often overgrown with a "bleb" at its extremity
• absent notochord (MGI Ref ID J:12622)
  • at E8.5, the mutant notochord is consistently smaller or even absent
• caudal body truncation (MGI Ref ID J:12622)
  • at E9.5, homozygotes exhibit a small and underdeveloped caudal portion
• decreased embryo size (MGI Ref ID J:12622)
  • at E9.5, most homozygous mutant embryos are ~25% to ~50% the size of wild-type embryos
• incomplete cephalic closure (MGI Ref ID J:12622)
  • at E9.5, homozygotes fail to close their cephalic neural folds
• incomplete embryo turning (MGI Ref ID J:12622)
  • at E9.5, most homozygous mutant embryos remain unturned
• open neural tube (MGI Ref ID J:12622)
  • at E9.5, the mutant neural tube is closed at the level of the otic vesicle but remains open beyond the midbrain-forebrain boundary
  • abnormal folding of the neuroectoderm is noted at the level of the cephalic folds and of the neural tube
• wavy neural tube (MGI Ref ID J:12622)
  • at E9.5, homozygotes exhibit a wavy and disorganized neural tube
  • in addition, the neural tube is often curved and infiltrated with pyknotic cells
• nervous system phenotype
• incomplete cephalic closure (MGI Ref ID J:12622)
  • at E9.5, homozygotes fail to close their cephalic neural folds
• open neural tube (MGI Ref ID J:12622)
  • at E9.5, the mutant neural tube is closed at the level of the otic vesicle but remains open beyond the midbrain-forebrain boundary
  • abnormal folding of the neuroectoderm is noted at the level of the cephalic folds and of the neural tube
• wavy neural tube (MGI Ref ID J:12622)
  • at E9.5, homozygotes exhibit a wavy and disorganized neural tube
  • in addition, the neural tube is often curved and infiltrated with pyknotic cells
• growth/size phenotype
• decreased embryo size (MGI Ref ID J:12622)
  • at E9.5, most homozygous mutant embryos are ~25% to ~50% the size of wild-type embryos
• cardiovascular system phenotype
• poor circulation (MGI Ref ID J:12622)
  • at E9.5, blood circulation is essentially absent in the visceral yolk sac and in mutant embryos
  • however, all homozygotes at this stage show normal decidual sizes and normal beating of the heart
• craniofacial phenotype
• megacephaly (MGI Ref ID J:12622)
  • at E9.5, homozygotes display a disproportionately bulky and dilated head

View Research Applications

Research Applications

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

Csk^tm1Sor related

Cancer Research
Genes Regulating Growth and Proliferation

Cell Biology Research
Genes Regulating Growth and Proliferation

Developmental Biology Research
Embryonic Lethality (Homozygous)
Neural Tube Defects
Postnatal Mortality

Neurobiology Research
Neural Tube Defects

Genes & Alleles

Gene & Allele Information

Allele Symbol		Csktm1Sor
Allele Name		targeted mutation 1, Philippe Soriano
Allele Type		Targeted (knock-out)
Common Name(s)		Csk-;
Mutation Made By		Philippe Soriano,   Fred Hutchinson Cancer Research Center
Strain of Origin		129S7/SvEvBrd-Hprt1<+>
ES Cell Line Name		AB1
ES Cell Line Strain		129S7/SvEvBrd-Hprt1<+>
Gene Symbol and Name		Csk, c-src tyrosine kinase
Chromosome		9
Gene Common Name(s)		AW212630; MGC112926; MGC117393; expressed sequence AW212630;
Molecular Note		Deletion of all coding sequences and replacement with a neomycin cassette. [MGI Ref ID J:12622]

Genotyping

Genotyping Information

Genotyping Protocols

Csk^tm1Sor, Standard PCR
NEOTD (Generic Neo), Standard PCR

Helpful Links

Genotyping resources and troubleshooting

References

References

Selected Reference(s)

Imamoto A; Soriano P. 1993. Disruption of the csk gene, encoding a negative regulator of Src family tyrosine kinases, leads to neural tube defects and embryonic lethality in mice. Cell 73(6):1117-24. [PubMed: 7685657]  [MGI Ref ID J:12622]

Additional References

Csk^tm1Sor related

Duan LJ; Imamoto A; Fong GH. 2004. Dual roles of the C-terminal Src kinase (Csk) during developmental vascularization. Blood 103(4):1370-2. [PubMed: 14576066]  [MGI Ref ID J:115663]

Thomas SM; Soriano P; Imamoto A. 1995. Specific and redundant roles of Src and Fyn in organizing the cytoskeleton. Nature 376(6537):267-71. [PubMed: 7617039]  [MGI Ref ID J:113005]

Health & husbandry

Health & Colony Maintenance Information

Currently there no information available for this strain. This may be due to the supply level of this strain.

Purchasing information

Pricing, Supply Level & Notes, Controls, General Terms & Conditions

Pricing

Supply Details

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). This strain is included in the Induced Mutant Resource Colony collection. Genomic DNA is available for this strain from the Mouse DNA Resource.

Control Information

	Control
	Wild-type from the colony
Considerations for Choosing Controls
USA, Canada and Mexico - Control Pricing Information for Genetically Engineered Mutant Strains.
International - Control Pricing Information for Genetically Engineered Mutant Strains.

Payment Terms and Conditions

Terms are granted by individual review and stated on the customer invoice(s) and account statement. These transactions are payable in U.S. currency within the granted terms. Payment for services, products, shipping containers, and shipping costs that are rendered are expected within the payment terms indicated on the invoice or stated by contract. Invoices and account balances in arrears of stated terms may result in The Jackson Laboratory pursuing collection activities including but not limited to outside agencies and court filings.

See Terms of Use tab for General Terms and Conditions

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.

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Contact Information
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Terms of Use

Terms of Use

General Terms and Conditions

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Contact information

General inquiries

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fax:	207-288-6655

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