Overview

Also Known As: Ts65Dn

Ts65Dn mice are trisomic for about two-thirds of the genes orthologous to human chromosome 21 and are a well-characterized model for studying Down Syndrome.

Genetic overview

Genetic Background	Generation
	N?+N6+N27 (2019-06-17 00:00:00)

Ts(17¹⁶)65Dn

Allele Type	Gene Symbol	Gene Name
Radiation induced	Ts(17¹⁶)65Dn	trisomy, Chr 16 translocation to Chr 17, Davisson 65

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Research Applications

Neurobiology Research
Mouse/Human Gene Homologs

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Base Price

Starting at:

$247.50 Domestic price for female 4-week

408.00 Domestic price for breeder pair

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Details

Important Note

Pde6b^rd1, the recessive retinal degeneration 1 mutation, is segregating in this colony. Animals that are homozygous for rd1 will be blind. Stock No. 005252 is an alternative strain, with a virtually identical genetic background except that it is wild-type for Pde6b^rd1.

Detailed Description

Segmentally trisomic Ts(17¹⁶)65Dn mice provide a postnatal model for Down syndrome. Ts65Dn mice have three copies of most of the genes on mouse Chr 16 that are homologues of human Chr 21 genes. These extra genes, along with the centromere and about 5% of proximal Chr 17 are contained in a small extra chromosome derived from a reciprocal translocation.

Neural cognitive deficits and behavioral abnormalities have been noted in Ts65Dn mice. They have spatial learning and memory defects as assessed in the Morris water maze and the radial arm maze, show developmental delay in sensorimotor milestones, and exhibit locomotor hyperactivity, lack of behavioral inhibition, and stereotypic behavior. They perform similar to controls in visual placing, balance, prehensile reflex and traction on a horizontal bar, motor coordination, swimming ability and olfaction orienting. They also show altered noradrenergic transmission in the hippocampus and cerebral cortex and degeneration of basal forebrain cholinergic neurons by 6 months of age. Trisomic females are smaller and produce fewer, smaller litters than euploid females while trisomic males are effectively sterile with hypospermia.

The precise locations of the Chr 16 and Chr 17 breakpoints are 84,351,351 bp and 9,426,822 bp, respectively. The Chr 16 segment contains about two thirds of the human Chr 21 homologues in the mouse, from mitochondrial ribosomal protein L39 (Mrpl39) gene to the distal telomere. These data were used to generate a PCR genotyping assay for Ts65Dn (Reinholdt et al., 2011), replacing the previous methods of chromosome analysis or qPCR. For comparison of segments conserved in human Chr 21 with mouse Chrs 16, 17, 10 and genetic definition of Ts65Dn, see the Human - Mouse Orthology Map. Northern and Western blotting, enzyme activity assays and reverse phase protein arrays (RPPA) demonstrate that some but not all genes in the translocation product are expressed at elevated levels in segmentally trisomic animals. RPPA shows a loss of correlation among some brain proteins (Ahmed et al., 2012). The Clcc1^m1J spontaneous mutation, which causes increased sensitivity to endoplasmic reticulum stress in the cerebellum, is a homozygous strain characteristic of C3H/HeSnJ (Jia et al., 2015) so is segregating in this strain.

Please see the Down Syndrome and Cytogenetics Models Resource for more information.

Development

Cesium irradiation was used to produce a reciprocal translocation, T (16;17) 65Dn. One of the translocation chromosomes is a small marker chromosome, comprised of the centromere and proximal end of Chr 17 (~9.5Mb) and the distal end of mouse Chr 16 (~34Mb). Translocation heterozygous females produced progeny trisomic for this small translocation product and a stock was established in which Ts65Dn mice are trisomic for the genes carried in the small translocation chromosome, symbolized Ts(1716)65Dn.

Control Suggestions

Wild-type from the colony

Additional Information

Considerations for Choosing Controls

Selected References

Reinholdt LG; Ding Y; Gilbert GT; Czechanski A; Solzak JP; Roper RJ; Johnson MT; Donahue LR; Lutz C; Davisson MT. 2011. Molecular characterization of the translocation breakpoints in the Down syndrome mouse model Ts65Dn. Mamm Genome 22(11-12):685-91PubMed: 21953412 MGI: J:178871
Ahmed MM; Sturgeon X; Ellison M; Davisson MT; Gardiner KJ. 2012. Loss of Correlations among Proteins in Brains of the Ts65Dn Mouse Model of Down Syndrome. J Proteome Res 11(2):1251-63PubMed: 22214338 MGI: J:180732
Reeves RH; Irving NG; Moran TH; Wohn A; Kitt C; Sisodia SS; Schmidt C; Bronson RT; Davisson MT. 1995. A mouse model for Down syndrome exhibits learning and behaviour deficits [see comments] Nat Genet 11(2):177-84PubMed: 7550346 MGI: J:29232

View All References

Genetics

Ts(17¹⁶)65Dn

Allele Symbol: Ts(17¹⁶)65Dn

Allele Name	trisomy, Chr 16 translocation to Chr 17, Davisson 65
Allele Type	Radiation induced
Allele Synonym(s)	trisomy, Chr 16 translocation to Chr 17, Davisson 65; Ts(17¹⁶)65Dn
Gene Symbol and Name	Ts(17¹⁶)65Dn, trisomy, Chr 16 translocation to Chr 17, Davisson 65
Gene Synonym(s)	trisomy 16; Ts65Dn
Strain of Origin	DBA/2J
Chromosome	16
Molecular Note	About 15% of the distal end of chromosome 16 is fused to less than 10% of the centromeric end of chromosome 17 to form a small translocation chromosome. The translocation breaks mouse Chr 16 just proximal to the amyloid precursor protein ( App ) gene and contains the HSA21-homologous genes from App to the telomere. The translocation chromosome also contains the centromere and a small portion (~5%) of Chr 17. Northern and Western blotting and enzyme activity assays demonstrate that genes on the translocation product are expressed at elevated levels in segmentally trisomic animals.

Disease/Phenotype

Disease Terms

Characteristics of this human disease are associated with transgenes and other mutation types in the mouse.

Down syndrome

Research Areas By Genotype

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

Neurobiology Research
- Down syndrome
Mouse/Human Gene Homologs
- Down syndrome

Mammalian Phenotype Terms by Genotype

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

Genotype: Ts(17¹⁶)65Dn/0
involves: C3H/HeSnJ * C57BL/6JEi * DBA/2J

cellular phenotype

abnormal male germ cell morphology
- significantly more sperm with head abnormalities

decreased sperm progressive motility
- significantly reduced frequencies of sperm with progressive motility

oligozoospermia
- sperm concentration was significantly reduced below controls

nervous system phenotype

abnormal cerebellar granule cell morphology
- dendritic spine density on granule cells is decreased on average by 17% compared to in wild-type mice

abnormal CNS synapse formation
- 18% of dendritic spines are enlarged and display irregular heads or a globular shape
- average synapse length is increased 34% in the hippocampus and 25% in the cortex
- glutamatergic synapses are distributed 33% on the dendritic shaft (compared to 51% in wild-type mice) and 67% (compared to 49% in wild-type mice) on the heads or necks of the dendritic spines
- in young and old mice alike, small presynaptic boutons are decreased and large presynaptic boutons are increased in the fascia dentate and motor cortex with the average diameter of a presynaptic bouton increased by 40% in the cortex
- the area of presynaptic elements (p38+) is increased in the fascia dentate and motor cortex

abnormal dendrite morphology
- 18% of spines are enlarged and display irregular heads or a globular shape
- basal dentritic spine density in CA1 is increased
- dendritic spine density on granule cells is decreased on average by 17% compared to in wild-type mice

abnormal neuron morphology
- in fascia dentate, spine density is significantly decreased on dendrites of granule cells; dendritic spines are significantly enlarged; dendritic width is similar to controls

reproductive system phenotype

abnormal male germ cell morphology
- significantly more sperm with head abnormalities

abnormal Sertoli cell morphology
- only a few Sertoli cells are visible; germ cells appear to be detached from the remaining Sertoli cells

abnormal spermatogenesis
- spermatocytes beyond pachytene stage and round spermatids are significantly reduced in number, while elongated spermatids are rare and remaining spermatids have deformed nuclei

abnormal testis morphology
- Leydig cells are clustered loosely in expanded interstitial compartment

arrest of male meiosis
- many tubules contain germ cells in arrested at meiotic metaphase 1

decreased sperm progressive motility
- significantly reduced frequencies of sperm with progressive motility

decreased testis weight
- significantly smaller testes than controls
- testes are 37.9% of control testes weights

male infertility
- fail to produce a vaginal plug
- presence of an intact extra chromosome interferes with chromosome pairing in meiosis
- produced no progeny

oligozoospermia
- sperm concentration was significantly reduced below controls

endocrine/exocrine gland phenotype

abnormal Sertoli cell morphology
- only a few Sertoli cells are visible; germ cells appear to be detached from the remaining Sertoli cells

abnormal testis morphology
- Leydig cells are clustered loosely in expanded interstitial compartment

decreased testis weight
- significantly smaller testes than controls
- testes are 37.9% of control testes weights

growth/size/body region phenotype

decreased body size
- mice are ~20% smaller in size compared to normal littermates postnatally

decreased body weight

Genotype: Ts(17¹⁶)65Dn/0
involves: C3H/HeJ * C57BL/6 * DBA/2J

behavior/neurological phenotype

abnormal spatial learning
- mice show impairment in a Morris water maze test

growth/size/body region phenotype

decreased body weight

nervous system phenotype

abnormal cerebellar granule cell morphology
- granule cell density is reduced to 76% of that in control mice

decreased Purkinje cell number
- Purkinje cell density is reduced to 90% of that in control mice

increased brain size

small cerebellum
- cerebellar volume is reduced to 88% of that in control mice

Genotype: Ts(17¹⁶)65Dn/0
involves: DBA/2J

craniofacial phenotype

enlarged neurocranium
- cranial vault is enlarged

small cranium
- size difference was most pronounced along the rostralcaudal axis

small mandible
- mice show a Down's Syndrome-like pattern of mandible reduction

limbs/digits/tail phenotype

short femur

skeleton phenotype

enlarged neurocranium
- cranial vault is enlarged

short femur

small cranium
- size difference was most pronounced along the rostralcaudal axis

small mandible
- mice show a Down's Syndrome-like pattern of mandible reduction

Genotype: Ts(17¹⁶)65Dn/0
involves: C3H * C57BL/6 * DBA/2J

craniofacial phenotype

abnormal incisor morphology
- mice exhibit a reduction in the height of the incisive alveolar segment compared to in wild-type mice

abnormal mandibular angle morphology
- reduced in size compared to in wild-type mice

decreased cranium height
- mice exhibit a more generalized shortening of the skull along the anterior posterior axis compared to in Ts(12¹⁶)1Cje mice

small mandible

small mandibular coronoid process
- reduced in size compared to in wild-type mice

growth/size/body region phenotype

abnormal incisor morphology
- mice exhibit a reduction in the height of the incisive alveolar segment compared to in wild-type mice

skeleton phenotype

abnormal incisor morphology
- mice exhibit a reduction in the height of the incisive alveolar segment compared to in wild-type mice

abnormal mandibular angle morphology
- reduced in size compared to in wild-type mice

decreased cranium height
- mice exhibit a more generalized shortening of the skull along the anterior posterior axis compared to in Ts(12¹⁶)1Cje mice

small mandible

small mandibular coronoid process
- reduced in size compared to in wild-type mice

Genotype: Ts(17¹⁶)65Dn/0
involves: C3H/HeJ * C57BL/6JEi * DBA/2J

nervous system phenotype

abnormal Purkinje cell morphology
- Purkinje cell linear density is decreased compared to in wild-type mice

Genotype: Ts(17¹⁶)65Dn/0
involves: C3H/HeJ * C57BL/6J * DBA/2J

hematopoietic system phenotype

abnormal spleen B cell follicle morphology
- splenic white pulp contains follicles that are larger and more irregular in shape than normal follicles and are often fused with adjacent follicles

abnormal spleen red pulp morphology
- splenic red pulp is largely obliterated

immune system phenotype

abnormal spleen B cell follicle morphology
- splenic white pulp contains follicles that are larger and more irregular in shape than normal follicles and are often fused with adjacent follicles

abnormal spleen red pulp morphology
- splenic red pulp is largely obliterated

neoplasm

increased follicular lymphoma incidence
- splenic architecture is replaced by proliferated immature mononuclear cells arranged in follicular aggregates indicating follicular lymphoma

increased lymphoma incidence
- malignant lymphoma in the spleen and lymph nodes is observed in some mutants
- megakaryocytes are numerous is some spleens, suggesting a relation to megakaryocytic leukemia

increased malignant tumor incidence
- some mutants exhibit malignant tumors of liver, colon, or lung

Genotype: Ts(17¹⁶)65Dn/0
involves: C3H/HeH * C3H/HeSn * C57BL/6Ei * C57BL/6J * DBA/2J

cardiovascular system phenotype

abnormal heart electrocardiography waveform feature
- flecainide-treated mice exhibit a specific electrophysiologic signature as compare to wild-type mice

abnormal heart morphology
- great vessel and cardiac malformation in 1 of 18 mice that died postnatally

abnormal QRS complex
- fragmented time-course with decreased S wave amplitude

decreased heart rate

decreased P wave amplitude
- in the frontal plane

decreased QRS amplitude

prolonged PR interval

prolonged QRS complex duration

prolonged QT interval
- larger QT and QTc

prolonged RR interval

retroesophageal right subclavian artery
- aberrant right subclavian artery arising from the distal part of the aortic arch

ventricular septal defect
- 1 in 18 newborns exhibit an upper communication of the ventricles, indication a septation defect of the ventricles

mortality/aging

postnatal lethality, incomplete penetrance

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

Genotype: Ts(17¹⁶)65Dn/0
B6EiC3Sn.BLiA-Ts(17<16>)65Dn/DnJ

behavior/neurological phenotype

abnormal learning/memory/conditioning
- in 22 degree water there is increased latency of acquisition of the hidden platform in the Morris water maze test

abnormal spatial learning

decreased grip strength
- output of a grip strength meter shows reduced grip force relative to controls

hyperactivity
- although activity during the light cycle is not different from that of controls, during the dark cycle the total activity is significantly greater than in background controls

impaired contextual conditioning behavior

impaired cued conditioning behavior

increased stereotypic behavior
- significantly increased dark cycle horizontal and vertical stereotypic activity

increased vertical activity
- significantly increased dark cycle rearing

growth/size/body region phenotype

decreased body length
- the length from the nost to the tip of the tail is shorter than in background controls, although the length from the nose to the base of the tail does not have a statistically significant difference

decreased body weight

References

Reinholdt LG; Ding Y; Gilbert GT; Czechanski A; Solzak JP; Roper RJ; Johnson MT; Donahue LR; Lutz C; Davisson MT. 2011. Molecular characterization of the translocation breakpoints in the Down syndrome mouse model Ts65Dn. Mamm Genome 22(11-12):685-91PubMed: 21953412 MGI: J:178871
Ahmed MM; Sturgeon X; Ellison M; Davisson MT; Gardiner KJ. 2012. Loss of Correlations among Proteins in Brains of the Ts65Dn Mouse Model of Down Syndrome. J Proteome Res 11(2):1251-63PubMed: 22214338 MGI: J:180732
Reeves RH; Irving NG; Moran TH; Wohn A; Kitt C; Sisodia SS; Schmidt C; Bronson RT; Davisson MT. 1995. A mouse model for Down syndrome exhibits learning and behaviour deficits [see comments] Nat Genet 11(2):177-84PubMed: 7550346 MGI: J:29232

Additional References

Liu DP; Schmidt C; Billings T; Davisson MT. 2003. Quantitative PCR genotyping assay for the Ts65Dn mouse model of Down syndrome. Biotechniques 35(6):1170-4, 1176, 1178 passimPubMed: 14682051 MGI: J:112549
Davisson M; Akeson E; Schmidt C; Harris B; Farley J; Handel MA. 2007. Impact of trisomy on fertility and meiosis in male mice. Hum Reprod 22(2):468-76PubMed: 17050550 MGI: J:117029
Belichenko NP; Belichenko PV; Kleschevnikov AM; Salehi A; Reeves RH; Mobley WC. 2009. The 'Down syndrome critical region' is sufficient in the mouse model to confer behavioral, neurophysiological, and synaptic phenotypes characteristic of Down syndrome. J Neurosci 29(18):5938-48PubMed: 19420260 MGI: J:148478
Holtzman DM; Santucci D; Kilbridge J; Chua-Couzens J; Fontana DJ; Daniels SE; Johnson RM; Chen K; Sun Y; Carlson E; Alleva E; Epstein CJ; Mobley WC. 1996. Developmental abnormalities and age-related neurodegeneration in a mouse model of Down syndrome. Proc Natl Acad Sci U S A 93(23):13333-8PubMed: 8917591 MGI: J:36555
Dierssen M; Vallina IF; Baamonde C; Garcia-Calatayud S; Lumbreras MA; Florez J. 1997. Alterations of central noradrenergic transmission in Ts65Dn mouse, a model for Down syndrome. Brain Res 749(2):238-44PubMed: 9138724 MGI: J:39408
Davisson MT; Bechtel LJ; Akeson EC; Fortna A; Slavov D; Gardiner K. 2001. Evolutionary breakpoints on human chromosome 21. Genomics 78(1/2):99-106PubMed: 11707078 MGI: J:69673
Hill JM; Ades AM; McCune SK; Sahir N; Moody EM; Abebe DT; Crnic LS; Brenneman DE. 2003. Vasoactive intestinal peptide in the brain of a mouse model for Down syndrome. Exp Neurol 183(1):56-65PubMed: 12957488 MGI: J:85337

Additional - Ts(17¹⁶)65Dn related

Technical Support

Contact Technical Support

Genotyping Protocols
- QPCR:Ts(17¹⁶)65Dn
- Separated PCR:Clcc1^m1J
- Standard PCR:Pde6b^rd1
- Separated PCR:Ts(17¹⁶)65Dn
- Standard PCR:Ts(17¹⁶)65Dn
- Standard PCR:Ts(17¹⁶)65Dn
- Standard PCR:Pde6b^rd1
- Probe:Pde6b^rd1
- Genotyping resources and troubleshooting
Dietary Information
- LabDiet® 5K52 formulation (6% fat)
Breeding Considerations

Male carriers are sterile.
- Additional Breeding and Husbandry Support
Mating System
- Ts65Dn trisomic females x B6EiC3SnF1/J (001875) males
  See Colony Maintenance for Ts65Dn for additional details
Citation
When using the Ts65Dn mouse strain in a publication, please cite the originating article(s) and include JAX stock #001924 in your Materials and Methods section.

Animal Health Reports

Facility Barrier Level Descriptions

AX11 (Maximum)

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Price

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Male

Cryorecovery - Pricing

Service	Genotype	Price
	Heterozygous Females and Wildtype males for Ts(17<16>)65Dn

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.

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Also Known As: Ts65Dn

Genetic overview

Research Applications

Base Price

Important Note

Detailed Description

Development

Control Suggestions

Additional Information

Selected References

Ts(1716)65Dn

Allele Symbol: Ts(1716)65Dn

Disease Terms

Characteristics of this human disease are associated with transgenes and other mutation types in the mouse.

Research Areas By Genotype

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

Mammalian Phenotype Terms by Genotype

Genotype: Ts(1716)65Dn/0involves: C3H/HeSnJ * C57BL/6JEi * DBA/2J

cellular phenotype

nervous system phenotype

reproductive system phenotype

endocrine/exocrine gland phenotype

growth/size/body region phenotype

Genotype: Ts(1716)65Dn/0involves: C3H/HeJ * C57BL/6 * DBA/2J

behavior/neurological phenotype

growth/size/body region phenotype

nervous system phenotype

Genotype: Ts(1716)65Dn/0involves: DBA/2J

craniofacial phenotype

limbs/digits/tail phenotype

skeleton phenotype

Genotype: Ts(1716)65Dn/0involves: C3H * C57BL/6 * DBA/2J

craniofacial phenotype

growth/size/body region phenotype

skeleton phenotype

Genotype: Ts(1716)65Dn/0involves: C3H/HeJ * C57BL/6JEi * DBA/2J

nervous system phenotype

Genotype: Ts(1716)65Dn/0involves: C3H/HeJ * C57BL/6J * DBA/2J

hematopoietic system phenotype

immune system phenotype

neoplasm

Genotype: Ts(1716)65Dn/0involves: C3H/HeH * C3H/HeSn * C57BL/6Ei * C57BL/6J * DBA/2J

cardiovascular system phenotype

mortality/aging

Genotype: Ts(1716)65Dn/0B6EiC3Sn.BLiA-Ts(17<16>)65Dn/DnJ

behavior/neurological phenotype

growth/size/body region phenotype

References

Additional References

Additional - Ts(1716)65Dn related

Genotyping Protocols

Dietary Information

Breeding Considerations

Mating System

Citation

Animal Health Reports

Live Mouse

Breeder Pair

Cryorecovery - Pricing

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

Ts(17¹⁶)65Dn

Allele Symbol: Ts(17¹⁶)65Dn

Genotype: Ts(17¹⁶)65Dn/0
involves: C3H/HeSnJ * C57BL/6JEi * DBA/2J

Genotype: Ts(17¹⁶)65Dn/0
involves: C3H/HeJ * C57BL/6 * DBA/2J

Genotype: Ts(17¹⁶)65Dn/0
involves: DBA/2J

Genotype: Ts(17¹⁶)65Dn/0
involves: C3H * C57BL/6 * DBA/2J

Genotype: Ts(17¹⁶)65Dn/0
involves: C3H/HeJ * C57BL/6JEi * DBA/2J

Genotype: Ts(17¹⁶)65Dn/0
involves: C3H/HeJ * C57BL/6J * DBA/2J

Genotype: Ts(17¹⁶)65Dn/0
involves: C3H/HeH * C3H/HeSn * C57BL/6Ei * C57BL/6J * DBA/2J

Genotype: Ts(17¹⁶)65Dn/0
B6EiC3Sn.BLiA-Ts(17<16>)65Dn/DnJ

Additional - Ts(17¹⁶)65Dn related