This Df(10)5Yey/+ mutant strain contains one copy of mouse Chromosome 10 with the targeted sequence deleted between, and including, the protein arginine N-methyltransferase 2 (Prmt2) gene and the pyridoxal (pyridoxine, vitamin B6) kinase (Pdxk) gene. Heterozygous mice are viable and fertile. This deleted region on the mouse chromosome is one of two regions orthologous to a deleted copy of human Chromosome 21 (Hsa21) which has been implicated in developmental cognitive disabilities like Down Syndrome (DS) and Monosomy 21. Dp(10)5Yey/+ lacks 41 genes on Chromosome 10 which are syntenic to the distal part of human 21q22.3, and is orthologous to genes on Hsa21. These mice exhibit Monosomy 21 related phenotypic defects including impaired contextual conditioning behavior, abnormal spatial learning, and abnormal motor coordination and balance. These mice may be useful for understanding developmental and cognitive disabilities associated with Monosomy 21.

Development

Chromosome-engineering cassettes were inserted into mouse Chromosome 10 of 129S7/SvEvBrd-Hprt1^b-m2-derived AB2.2 embryonic stem (ES) cells, bracketing a span of approximately 2.3 Mb between, and including, the protein arginine N-methyltransferase 2 (Prmt2) gene and pyridoxal (pyridoxine, vitamin B6) kinase (Pdxk) gene. The cassette placed at the proximal locus was targeted upstream of Prmt2 and contained an agouti transgene, a 3' portion of an HPRT minigene, a loxP site and puromycin resistance gene. The cassette placed at the distal locus was targeted downstream of the Pdxk gene and contained a neomycin resistance gene, a loxP site, a 5' portion of an HPRT minigene, and a tyrosinase minigene. Double-targeted ES cells were transiently transfected with the cre recombinase expression vector pOG231. After subsequent selection of recombinants by using hypoxanthine aminopterin thymidine (HAT) media, correctly targeted ES cells, containing one copy of mouse Chromosome 10 with the targeted sequence deleted (Del), were injected into C57BL/6J-Tyr^c-Brd blastocysts. The resulting chimeric males were mated to 129/SvEv females to produce a colony of Df(10)5Yey/+ mice. Upon arrival at The Jackson Laboratory these mice were bred to 129S1/SvImJ mice (Stock No. 002448) for at least one generation.

Selected References

Yu T; Clapcote SJ; Li Z; Liu C; Pao A; Bechard AR; Carattini-Rivera S; Matsui S; Roder JC; Baldini A; Mobley WC; Bradley A; Yu YE. 2010. Deficiencies in the region syntenic to human 21q22.3 cause cognitive deficits in mice. Mamm Genome 21(5-6):258-67. PubMed: 20512340 MGI: J:161398

View All References

Genetics

Del(10Prmt2-Pdxk)4Yey

Allele Symbol: Del(10Prmt2-Pdxk)4Yey

Allele Name	deletion, Chr 10, Y Eugene Yu 4
Allele Type	Targeted (Null/Knockout)
Allele Synonym(s)	Del(10)1Yey; Del(10Prmt2-Pdxk)1Yey; Del5Yey; Df(10)1Yey; Df(Prmt2-Pdxk)1Yey
Gene Symbol and Name	Del(10Prmt2-Pdxk)4Yey, deletion, Chr 10, Y Eugene Yu 4
Gene Synonym(s)	Del(10Prmt2-Pdxk)1Yey; Del(10Prmt2-Pdxk)1Yey; deletion, Chr 10, Y Eugene Yu 1
Strain of Origin	129S7/SvEvBrd-Hprt
Chromosome	10
Molecular Note	Cre mediated chromosomal rearrangement between loxP sites in regions proximal to Prmt2 and distal to Pdxk resulted in deletion of the genes, including Prmt2 and Pdxk, in this approximately 2.3 Mb region that is syntenic with the distal part of human 21q22.3.

Disease/Phenotype

Disease Terms

Research Areas By Genotype

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

Neurobiology Research
- Ataxia (Movement) Defects
- Behavioral and Learning Defects

Mammalian Phenotype Terms by Genotype

Genotype: Del(10Prmt2-Pdxk)4Yey/+
129S/SvEv-Del(10Prmt2-Pdxk)129S/SvEv-Del(10Prmt2-Pdxk)4Yey

behavior/neurological phenotype

abnormal motor coordination/ balance
- mice swim faster than wild-type mice

abnormal spatial learning
- after training, mice take longer to find the hidden platform than wild-type mice

behavior/neurological phenotype
- mice exhibit normal cued conditioning and pain sensitivity

impaired contextual conditioning behavior
- mice exhibit reduced freezing in a 72-h context test compared with wild-type mice

References

Yu T; Clapcote SJ; Li Z; Liu C; Pao A; Bechard AR; Carattini-Rivera S; Matsui S; Roder JC; Baldini A; Mobley WC; Bradley A; Yu YE. 2010. Deficiencies in the region syntenic to human 21q22.3 cause cognitive deficits in mice. Mamm Genome 21(5-6):258-67. PubMed: 20512340 MGI: J:161398

Pricing & Availability

Cryo Recovery

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Cryorecovery - Not-For-Profit & Academic Pricing

Service	Genotype	Price
	Heterozygous or wildtype for Del(10Prmt2-Pdxk)4Yey

Progeny testing is not required

The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. 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. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 10 and 14 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.

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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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