Strain Name:

B6.Cg-Terctm1Rdp Dmdmdx-4Cv/BlauJ

Stock Number:



On Hold

Use Restrictions Apply, see Terms of Use
Register Interest
Common Names: B6.mdx/mTR;     mdx/mTRKO;    
The mdx/mTRKO mouse model combines dystrophin-deficiency with telomere dysfunction/shortening, and may be a superior Duchenne muscular dystrophy model as it better recapitulates several of the human characteristics of DMD myopathology (progressive muscle weakness and damage, skeletal muscle fibrosis, diminished muscle stem cell regenerative capacity, dilated cardiomyopathy, heart failure and shortened life-span).


Strain Information

Type Chemically Induced Mutation; Congenic; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
Visit our online Nomenclature tutorial.
Additional information on Congenic nomenclature.
Mating SystemSee Breeding & Husbandry under the Health & Care tab         (Female x Male)   04-APR-14
Specieslaboratory mouse
GenerationF?+pN1F2 (17-JUN-15)
Generation Definitions
Donating Investigator Helen M Blau,   Stanford University School of Medicine

Duchenne muscular dystrophy (DMD) is a progressive muscular disorder caused by an imbalance between muscle degeneration and regeneration resulting in muscle degeneration, necrosis, accumulation of fat and fibrosis, and insufficient regeneration/loss of myofibers. The genetic cause of DMD are mutations of the dystrophin muscular dystrophy gene (DMD) on the X chromosome. Both the Dmdmdx (termination codon in exon 23) and Dmdmdx-4Cv (nonsense point mutation in exon 53) mutations in mice are predicted to express a truncated protein. Females heterozygous for either mutation are viable and fertile with no gross phenotypic abnormalities. Homozygous females and hemizygous males are viable and fertile with myopathic features of DMD; although the myopathology is both less severe than the human disease course and variable by mouse strain genetic background.
Specifically, the muscle pathology observed for C57BL/10ScSn-Dmdmdx mice (C57BL/10.mdx ; Stock No. 001801) and B6Ros.Cg-Dmdmdx-4Cv mice (B6.mdx-4Cv ; Stock No. 002378) includes active fiber necrosis, cellular infiltration, a wide range of fiber sizes, and numerous centrally nucleated regenerating fibers. However, despite the absence of dystrophin in skeletal and cardiac muscles, adult C57BL/10.mdx and B6.mdx-4Cv mice fail to exhibit several of features of DMD, including severe muscle weakness, progressive cardiomyopathy and shortened lifespan. In addition, these animals do not show other skeletal muscle characteristics of DMD (such as smaller number of myofibers, accumulation of fat and fibrosis, insufficient myofiber regeneration, and loss of muscle weight).
Differences between the two mutations exist. The Dmdmdx-4Cv allele has very low frequency of reversion to the wildtype allele in skeletal muscle (~10-fold lower frequency than the Dmdmdx mutation). In addition, the Dmdmdx-4Cv mutation affects more of the transcripts arising from alternative promoter usage within the dystrophin gene compared to the Dmdmdx mutation.

While telomere shortening is normally observed over time in mitotically active tissues, muscle tissue exhibits a lower proliferation rate and less telomere shortening with age. However, increased telomere shortening is associated with dystrophic human muscle cells and DMD patients. C57BL/6J mice homozygous for the telomerase RNA component null allele (C57BL/6J.mTR-/- ; Stock No. 004132) lack telomerase activity. Early generation homozygous mice have intact telomeres and appear grossly unaffected and healthy. However, telomere length is progressively shortened with successive generations of breeding mTR-/- mice together; resulting in dysfunction of the reproductive and hematopoietic systems, but little or no skeletal muscle abnormalities.

To investigate how telomere dysfunction affects the severity of muscular dystrophy seen in dystrophin-deficient mice, Dr. Helen M. Blau (Stanford University School of Medicine) created the double mutant mdx/mTR colony (Stock No. 023535) by breeding C57BL/6J-congenic mTR+/- mice with C57BL/6J-congenic Dmdmdx-4Cv mice. Males homozygous for the mTR null allele and hemizygous for the X-linked Dmdmdx-4Cv allele (mTR-/-;Dmdmdx-4Cv/Y), and females homozygous for both alleles (mTR-/-;Dmdmdx-4Cv/mdx-4Cv), are referred to as mdx/mTRKO. When compared to C57BL/10.mdx and B6.mdx-4Cv animals, the mdx/mTRKO mice exhibit additional features of severe human muscular dystrophy: including profound loss of muscle force, poor performance on a treadmill, increased serum creatine kinase levels, accumulation of fibrosis and calcium deposits within skeletal muscle tissues, kyphosis, dilated cardiomyopathy (ventricular dilation), cardiac contractile and conductance dysfunction, heart failure and shortened life-span. The severity of muscle wasting is concomitant with a decline in muscle stem cell regenerative capacity. mdx/mTRKO mice also exhibit telomere erosion (in cardiomyocytes, but not in other heart muscle cells), mitochondrial fragmentation and increased oxidative stress. The dystrophy phenotype becomes more severe with each successive generation of breeding mdx/mTRKO mice together (because such breeding results in progressively shorter telomere lengths with each generation). Specifically, mdx/mTRKO mice bred together for one generation (G1) exhibit cardiac dysfunction by ~80 weeks of age with death first occurring at ~30 weeks of age (~50% survival at 120 weeks of age). mdx/mTRKO G2 mice exhibit cardiac dysfunction by ~32 weeks of age with death first occurring at ~19 weeks of age (~50% survival at 80 weeks of age). mdx/mTRKO G3 mice exhibit cardiac dysfunction by ~8 weeks of age.

These mdx/mTR mice harbor two mutations; the mTR null allele (Terctm1Rdp) and the X-linked muscular dystrophy mutation (Dmdmdx-4Cv).

The mTR null allele was designed by Dr. Ronald DePinho (Albert Einstein College of Medicine) with a neomycin cassette replacing the entire telomerase RNA component gene on chromosome 3. C57BL/6J-congenic mice harboring the mTR null allele are described and available from The Jackson Laboratory Repository as Stock No. 004132. Dr. Helen M. Blau (Stanford University School of Medicine) obtained heterozygous mTR mutant mice on a C57BL/6 genetic background from Dr. DePinho, and then bred them with C57BL/6J wildtype mice for six more generations. The resulting "C57BL6 mTRHet" mice (B6J.mTRHet) were used as described below.

The Dmdmdx-4Cv mutation was created in the laboratory of Dr. Verne M. Chapman (Roswell Park Memorial Institute) by N-ethyl-N-nitrosourea (ENU) treatment. Dmdmdx-4Cv has as a C-to-T transition (resulting in a termination codon) at position 7916 within exon 53 of the dystrophin muscular dystrophy gene (Dmd) on the X chromosome. B6Ros.Cg-Dmdmdx-4Cv mice are described and available from The Jackson Laboratory Repository as Stock No. 002378. Dr. Helen M. Blau (Stanford University School of Medicine) obtained Dmdmdx-4Cv mice on a C57BL/6 genetic background from Jeffrey S. Chamberlain (University of Washington), and then bred them with C57BL/6J wildtype mice for six generations. The resulting "C57BL6 mdx4cv" mice (B6J.mdx4cv) were used as described below.

To generate the double mutant line, Dr. Blau bred B6J.mTRHet mice with B6J.mdx4cv mice. Males heterozygous for the mTR null allele and hemizygous for the mdx4cv allele (called mdx4cv/mTRHet or mdx/mTRHet) were sent to The Jackson Laboratory Repository in 2013. Upon arrival, males were used to cryopreserve sperm. To establish our living mdx/mTR mouse colony, an aliquot of the frozen sperm was used to fertilize oocytes from C57BL/6J inbred females (Stock No. 000664). See the "Health & Care" section for more details on strain maintenance.

Control Information

   See control note: Depending upon the nature of the experiment, the following mouse line(s) may be appropriate controls:
C57BL/6J.mTR-/- (Stock No. 004132: B6.Cg-Terctm1Rdp/J)
and/or B6.mdx-4Cv (Stock No. 002378: B6Ros.Cg-Dmdmdx-4Cv/J)
   000664 C57BL/6J
  Considerations for Choosing Controls

Related Strains

Strains carrying   Dmdmdx-4Cv allele
002378   B6Ros.Cg-Dmdmdx-4Cv/J
View Strains carrying   Dmdmdx-4Cv     (1 strain)

Strains carrying   Terctm1Rdp allele
004132   B6.Cg-Terctm1Rdp/J
018915   STOCK Terctm1Rdp Dmdmdx/J
View Strains carrying   Terctm1Rdp     (2 strains)

View Strains carrying other alleles of Dmd     (11 strains)


Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI
- Model with phenotypic similarity to human disease where etiologies involve orthologs. Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).
Muscular Dystrophy, Duchenne Type; DMD
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.
Cardiomyopathy, Dilated, 3b; CMD3B   (DMD)
Dyskeratosis Congenita, Autosomal Dominant, 1; DKCA1   (TERC)
Muscular Dystrophy, Becker Type; BMD   (DMD)
Pulmonary Fibrosis and/or Bone Marrow Failure, Telomere-Related, 2;   (TERC)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Dmdmdx-4Cv/Dmdmdx-4Cv Terctm1Rdp/Terctm1Rdp

        B6.Cg-Terctm1Rdp Dmdmdx-4Cv
  • cardiovascular system phenotype
  • abnormal myocardial fiber morphology
    • cardiomyocyte nuclear area is moderately reduced in hearts of second generation (G2) 32 week old males as compared to controls   (MGI Ref ID J:200365)
    • cardiomyocyte diameter is smaller in hearts of 32 week old G2 males   (MGI Ref ID J:200365)
    • hearts from G2 males exhibit a loss of thick and thin myofilaments   (MGI Ref ID J:200365)
  • cardiac fibrosis
    • ventricular fibrosis is observed by 32 weeks in hearts of G2 males   (MGI Ref ID J:200365)
  • decreased ventricle muscle contractility
    • 32 week old G2 males exhibit reduced ventricular contractility as assessed by a reduction in fractional shortening as compared to controls   (MGI Ref ID J:200365)
  • dilated cardiomyopathy
    • reduced cardiac function is observed in older G1 males (80 weeks), but is not observed at 32 weeks   (MGI Ref ID J:200365)
    • cardiac dysfunction is observed at 8 weeks in third generation males   (MGI Ref ID J:200365)
    • cardiac dysfunction can be induced by angiotension II infusion in younger second generation males   (MGI Ref ID J:200365)
  • dilated heart left ventricle
    • increased chamber size is observed in 32 week old G2 males as compared to controls   (MGI Ref ID J:200365)
    • left ventricular transverse area is increased in diastole and systole in G2 males   (MGI Ref ID J:200365)
  • increased heart left ventricle size
    • left ventricle enlargement is observed by 32 weeks in hearts of G2 males as compared to controls   (MGI Ref ID J:200365)
  • prolonged QRS complex duration
    • wide QRS interval is observed in both G1 and G2 males as compared to controls   (MGI Ref ID J:200365)
  • ventricular cardiomyopathy   (MGI Ref ID J:200365)
  • cellular phenotype
  • abnormal mitochondrial shape
    • extensive mitochondrial fragmentation observed in cardiac muscle of second generation mice   (MGI Ref ID J:200365)
  • abnormal telomere length
    • 50% reduction in telomere length in G2 cardiomyocytes as compared to controls   (MGI Ref ID J:200365)
    • telomere lengths are similar to controls in vascular smooth muscle cells   (MGI Ref ID J:200365)
  • decreased mitochondria size
    • mitochondria size is decreaseed in cardiac muscle of second generation mice   (MGI Ref ID J:200365)
  • disorganized mitochondrial cristae
    • lack of well-defined cristae observed in cardiac muscle of second generation mice   (MGI Ref ID J:200365)
  • increased mitochondria number
    • moderately increased number of mitochondria is observed in cardiac muscle of second generation mice   (MGI Ref ID J:200365)
  • oxidative stress
    • an increased number of 8-OHdg-positive nuclei, a marker of oxidative damage, is observed in G2 hearts as compared to controls   (MGI Ref ID J:200365)
  • mortality/aging
  • premature death
    • death occurs as early as 30 weeks in first generation males, T50 is 120 weeks   (MGI Ref ID J:200365)
    • death occurs as early as 19 weeks in second generation males, T50 is 80 weeks   (MGI Ref ID J:200365)
  • muscle phenotype
  • abnormal myocardial fiber morphology
    • cardiomyocyte nuclear area is moderately reduced in hearts of second generation (G2) 32 week old males as compared to controls   (MGI Ref ID J:200365)
    • cardiomyocyte diameter is smaller in hearts of 32 week old G2 males   (MGI Ref ID J:200365)
    • hearts from G2 males exhibit a loss of thick and thin myofilaments   (MGI Ref ID J:200365)
  • decreased ventricle muscle contractility
    • 32 week old G2 males exhibit reduced ventricular contractility as assessed by a reduction in fractional shortening as compared to controls   (MGI Ref ID J:200365)
  • dilated cardiomyopathy
    • reduced cardiac function is observed in older G1 males (80 weeks), but is not observed at 32 weeks   (MGI Ref ID J:200365)
    • cardiac dysfunction is observed at 8 weeks in third generation males   (MGI Ref ID J:200365)
    • cardiac dysfunction can be induced by angiotension II infusion in younger second generation males   (MGI Ref ID J:200365)
  • ventricular cardiomyopathy   (MGI Ref ID J:200365)
View Research Applications

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

Cancer Research
Genes Regulating Growth and Proliferation
      DNA Repair
Tumor Suppressor Genes

Cardiovascular Research
Heart Abnormalities

Cell Biology Research
Channel and Transporter Defects
DNA Damage Response
Protein Processing
Signal Transduction

Developmental Biology Research
Internal/Organ Defects
      hematopoietic defects
Lymphoid Tissue Defects
      hematopoietic defects
Mesodermal Defects
      Myogenesis Defects

Hematological Research
Hematopoietic Defects
Immunological Defects

Internal/Organ Research
Heart Abnormalities

Neurobiology Research
Ataxia (Movement) Defects
Channel and Transporter Defects
Muscular Dystrophy
      Duchenne type

Reproductive Biology Research
Developmental Defects Affecting Gonads
      germ cell deficient

Research Tools
Cardiovascular Research
Cell Biology Research
Genetics Research
Hematological Research
Reproductive Biology Research

Dmdmdx-4Cv related

Neurobiology Research
Muscular Dystrophy
      Duchenne type

Terctm1Rdp related

Cancer Research
Genes Regulating Growth and Proliferation
      DNA Repair
Tumor Suppressor Genes

Cell Biology Research
DNA Damage Response

Research Tools
Cell Biology Research
Genetics Research

Genes & Alleles

Gene & Allele Information provided by MGI

Allele Symbol Dmdmdx-4Cv
Allele Name X linked muscular dystrophy 4, Verne Chapman
Allele Type Chemically induced (ENU)
Common Name(s) mdx4cv; mdx4cv; mdx4cv; mdxCv4;
Mutation Made ByDr. Verne Chapman (deceased),   Roswell Park Memorial Institute
Strain of OriginC3Ha.Cg-Hprt Pgk1
Gene Symbol and Name Dmd, dystrophin, muscular dystrophy
Chromosome X
Gene Common Name(s) BMD; CMD3B; DXS142; DXS164; DXS206; DXS230; DXS239; DXS268; DXS269; DXS270; DXS272; Dp427; Dp71; Duchenne muscular dystrophy; MRX85; X-linked muscular dystrophy; dys; mdx; pke; pyruvate kinase expression;
Molecular Note A C to T transition in exon 53 at position 7916 creates a premature stop codon. [MGI Ref ID J:34517]
Allele Symbol Terctm1Rdp
Allele Name targeted mutation 1, Ronald DePinho
Allele Type Targeted (Null/Knockout)
Common Name(s) TR-; Terc-; mTR-; mTerc-;
Mutation Made ByDr. Carol Greider,   Johns Hopkins Univ School of Medicine
Strain of OriginSTOCK 129/Sv and C57BL/6J and SJL
ES Cell Line NameWW6
ES Cell Line StrainSTOCK 129/Sv and C57BL/6J and SJL
Gene Symbol and Name Terc, telomerase RNA component
Chromosome 3
Gene Common Name(s) mTER; mTR;
Molecular Note Replacement of the entire gene with a neomycin cassette. [MGI Ref ID J:43517]


Genotyping Information

Genotyping Protocols

Dmdmdx-4Cv, Pyrosequencing
Terctm1Rdpalternate2, MELT

Helpful Links

Genotyping resources and troubleshooting


References provided by MGI

Selected Reference(s)

Mourkioti F; Kustan J; Kraft P; Day JW; Zhao MM; Kost-Alimova M; Protopopov A; DePinho RA; Bernstein D; Meeker AK; Blau HM. 2013. Role of telomere dysfunction in cardiac failure in Duchenne muscular dystrophy. Nat Cell Biol 15(8):895-904. [PubMed: 23831727]  [MGI Ref ID J:200365]

Sacco A; Mourkioti F; Tran R; Choi J; Llewellyn M; Kraft P; Shkreli M; Delp S; Pomerantz JH; Artandi SE; Blau HM. 2010. Short telomeres and stem cell exhaustion model Duchenne muscular dystrophy in mdx/mTR mice. Cell 143(7):1059-71. [PubMed: 21145579]  [MGI Ref ID J:167294]

Additional References

Dmdmdx-4Cv related

Adamo CM; Dai DF; Percival JM; Minami E; Willis MS; Patrucco E; Froehner SC; Beavo JA. 2010. Sildenafil reverses cardiac dysfunction in the mdx mouse model of Duchenne muscular dystrophy. Proc Natl Acad Sci U S A 107(44):19079-83. [PubMed: 20956307]  [MGI Ref ID J:166234]

Aigner B; Rathkolb B; Klaften M; Sedlmeier R; Klempt M; Wagner S; Michel D; Mayer U; Klopstock T; de Angelis MH; Wolf E. 2009. Generation of N-ethyl-N-nitrosourea-induced mouse mutants with deviations in plasma enzyme activities as novel organ-specific disease models. Exp Physiol 94(4):412-21. [PubMed: 19151073]  [MGI Ref ID J:187875]

Arpke RW; Darabi R; Mader TL; Zhang Y; Toyama A; Lonetree CL; Nash N; Lowe DA; Perlingeiro RC; Kyba M. 2013. A New Immuno- Dystrophin-Deficient Model, the NSG-Mdx Mouse, Provides Evidence for Functional Improvement Following Allogeneic Satellite Cell Transplantation. Stem Cells :. [PubMed: 23606600]  [MGI Ref ID J:199729]

Banks GB; Combs AC; Chamberlain JR; Chamberlain JS. 2008. Molecular and cellular adaptations to chronic myotendinous strain injury in mdx mice expressing a truncated dystrophin. Hum Mol Genet 17(24):3975-86. [PubMed: 18799475]  [MGI Ref ID J:142565]

Chapman VM; Miller DR; Armstrong D; Caskey CT. 1989. Recovery of induced mutations for X chromosome-linked muscular dystrophy in mice. Proc Natl Acad Sci U S A 86(4):1292-6. [PubMed: 2919177]  [MGI Ref ID J:9638]

Chretien F; Dreyfus PA; Christov C; Caramelle P; Lagrange JL; Chazaud B; Gherardi RK. 2005. In vivo fusion of circulating fluorescent cells with dystrophin-deficient myofibers results in extensive sarcoplasmic fluorescence expression but limited dystrophin sarcolemmal expression. Am J Pathol 166(6):1741-8. [PubMed: 15920159]  [MGI Ref ID J:98788]

Claeys KG; Sozanska M; Martin JJ; Lacene E; Vignaud L; Stockholm D; Laforet P; Eymard B; Kichler A; Scherman D; Voit T; Israeli D. 2010. DNAJB2 expression in normal and diseased human and mouse skeletal muscle. Am J Pathol 176(6):2901-10. [PubMed: 20395441]  [MGI Ref ID J:161160]

Cordani N; Pisa V; Pozzi L; Sciorati C; Clementi E. 2014. Nitric oxide controls fat deposition in dystrophic skeletal muscle by regulating fibro-adipogenic precursor differentiation. Stem Cells 32(4):874-85. [PubMed: 24170326]  [MGI Ref ID J:210190]

Danko I; Chapman V; Wolff JA. 1992. The frequency of revertants in mdx mouse genetic models for Duchenne muscular dystrophy. Pediatr Res 32(1):128-31. [PubMed: 1635838]  [MGI Ref ID J:23502]

Gayraud-Morel B; Chretien F; Flamant P; Gomes D; Zammit PS; Tajbakhsh S. 2007. A role for the myogenic determination gene Myf5 in adult regenerative myogenesis. Dev Biol 312(1):13-28. [PubMed: 17961534]  [MGI Ref ID J:128921]

Howard PL; Dally GY; Wong MH; Ho A; Weleber RG; Pillers DA; Ray PN. 1998. Localization of dystrophin isoform Dp71 to the inner limiting membrane of the retina suggests a unique functional contribution of Dp71 in the retina. Hum Mol Genet 7(9):1385-91. [PubMed: 9700191]  [MGI Ref ID J:115134]

Im WB; Phelps SF; Copen EH; Adams EG; Slightom JL; Chamberlain JS. 1996. Differential expression of dystrophin isoforms in strains of mdx mice with different mutations. Hum Mol Genet 5(8):1149-53. [PubMed: 8842734]  [MGI Ref ID J:34517]

Judge LM; Arnett AL; Banks GB; Chamberlain JS. 2011. Expression of the dystrophin isoform Dp116 preserves functional muscle mass and extends lifespan without preventing dystrophy in severely dystrophic mice. Hum Mol Genet 20(24):4978-90. [PubMed: 21949353]  [MGI Ref ID J:177877]

Judge LM; Haraguchiln M; Chamberlain JS. 2006. Dissecting the signaling and mechanical functions of the dystrophin-glycoprotein complex. J Cell Sci 119(Pt 8):1537-46. [PubMed: 16569668]  [MGI Ref ID J:107808]

Khouzami L; Bourin MC; Christov C; Damy T; Escoubet B; Caramelle P; Perier M; Wahbi K; Meune C; Pavoine C; Pecker F. 2010. Delayed cardiomyopathy in dystrophin deficient mdx mice relies on intrinsic glutathione resource. Am J Pathol 177(3):1356-64. [PubMed: 20696779]  [MGI Ref ID J:163690]

Laure L; Suel L; Roudaut C; Bourg N; Ouali A; Bartoli M; Richard I; Daniele N. 2009. Cardiac ankyrin repeat protein is a marker of skeletal muscle pathological remodelling. FEBS J 276(3):669-84. [PubMed: 19143834]  [MGI Ref ID J:147891]

Li D; Shin JH; Duan D. 2011. iNOS Ablation Does Not Improve Specific Force of the Extensor Digitorum Longus Muscle in Dystrophin-Deficient mdx4cv Mice. PLoS One 6(6):e21618. [PubMed: 21738735]  [MGI Ref ID J:174763]

Li D; Yue Y; Duan D. 2008. Preservation of muscle force in mdx3cv mice correlates with low-level expression of a near full-length dystrophin protein. Am J Pathol 172(5):1332-41. [PubMed: 18385524]  [MGI Ref ID J:134272]

Li D; Yue Y; Lai Y; Hakim CH; Duan D. 2011. Nitrosative stress elicited by nNOSmicro delocalization inhibits muscle force in dystrophin-null mice. J Pathol 223(1):88-98. [PubMed: 21125668]  [MGI Ref ID J:167308]

Li S; Kimura E; Ng R; Fall BM; Meuse L; Reyes M; Faulkner JA; Chamberlain JS. 2006. A highly functional mini-dystrophin/GFP fusion gene for cell and gene therapy studies of Duchenne muscular dystrophy. Hum Mol Genet 15(10):1610-22. [PubMed: 16595609]  [MGI Ref ID J:144130]

Nguyen-Tran DH; Hait NC; Sperber H; Qi J; Fischer K; Ieronimakis N; Pantoja M; Hays A; Allegood J; Reyes M; Spiegel S; Ruohola-Baker H. 2014. Molecular mechanism of sphingosine-1-phosphate action in Duchenne muscular dystrophy. Dis Model Mech 7(1):41-54. [PubMed: 24077965]  [MGI Ref ID J:208735]

Pillers DA; Weleber RG; Green DG; Rash SM; Dally GY; Howard PL ; Powers MR ; Hood DC ; Chapman VM ; Ray PN ; Woodward WR. 1999. Effects of dystrophin isoforms on signal transduction through neural retina: genotype-phenotype analysis of duchenne muscular dystrophy mouse mutants. Mol Genet Metab 66(2):100-10. [PubMed: 10068512]  [MGI Ref ID J:53822]

Shin JH; Hakim CH; Zhang K; Duan D. 2011. Genotyping mdx, mdx3cv, and mdx4cv mice by primer competition polymerase chain reaction. Muscle Nerve 43(2):283-6. [PubMed: 21254096]  [MGI Ref ID J:169288]

Stuelsatz P; Shearer A; Li Y; Muir LA; Ieronimakis N; Shen QW; Kirillova I; Yablonka-Reuveni Z. 2015. Extraocular muscle satellite cells are high performance myo-engines retaining efficient regenerative capacity in dystrophin deficiency. Dev Biol 397(1):31-44. [PubMed: 25236433]  [MGI Ref ID J:218053]

Swiderski K; Shaffer SA; Gallis B; Odom GL; Arnett AL; Scott Edgar J; Baum DM; Chee A; Naim T; Gregorevic P; Murphy KT; Moody J; Goodlett DR; Lynch GS; Chamberlain JS. 2014. Phosphorylation within the cysteine-rich region of dystrophin enhances its association with beta-dystroglycan and identifies a potential novel therapeutic target for skeletal muscle wasting. Hum Mol Genet 23(25):6697-711. [PubMed: 25082828]  [MGI Ref ID J:216212]

Tanaka KK; Hall JK; Troy AA; Cornelison DD; Majka SM; Olwin BB. 2009. Syndecan-4-expressing muscle progenitor cells in the SP engraft as satellite cells during muscle regeneration. Cell Stem Cell 4(3):217-25. [PubMed: 19265661]  [MGI Ref ID J:149919]

Vignier N; Amor F; Fogel P; Duvallet A; Poupiot J; Charrier S; Arock M; Montus M; Nelson I; Richard I; Carrier L; Servais L; Voit T; Bonne G; Israeli D. 2013. Distinctive serum miRNA profile in mouse models of striated muscular pathologies. PLoS One 8(2):e55281. [PubMed: 23418438]  [MGI Ref ID J:199417]

Terctm1Rdp related

Akbay EA; Contreras CM; Perera SA; Sullivan JP; Broaddus RR; Schorge JO; Ashfaq R; Saboorian H; Wong KK; Castrillon DH. 2008. Differential roles of telomere attrition in type I and II endometrial carcinogenesis. Am J Pathol 173(2):536-44. [PubMed: 18599611]  [MGI Ref ID J:138286]

Allsopp RC; Morin GB; DePinho R; Harley CB; Weissman IL. 2003. Telomerase is required to slow telomere shortening and extend replicative lifespan of HSCs during serial transplantation. Blood 102(2):517-20. [PubMed: 12663456]  [MGI Ref ID J:115695]

Argilla D; Chin K; Singh M; Hodgson JG; Bosenberg M; de Solorzano CO; Lockett S; DePinho RA; Gray J; Hanahan D. 2004. Absence of telomerase and shortened telomeres have minimal effects on skin and pancreatic carcinogenesis elicited by viral oncogenes. Cancer Cell 6(4):373-85. [PubMed: 15488760]  [MGI Ref ID J:94774]

Armanios M; Alder JK; Parry EM; Karim B; Strong MA; Greider CW. 2009. Short telomeres are sufficient to cause the degenerative defects associated with aging. Am J Hum Genet 85(6):823-32. [PubMed: 19944403]  [MGI Ref ID J:158466]

Artandi SE; Chang S; Lee SL; Alson S; Gottlieb GJ; Chin L; DePinho RA. 2000. Telomere dysfunction promotes non-reciprocal translocations and epithelial cancers in mice [see comments] Nature 406(6796):641-5. [PubMed: 10949306]  [MGI Ref ID J:63843]

Autexier C. 2008. POT of gold: modeling dyskeratosis congenita in the mouse. Genes Dev 22(13):1731-6. [PubMed: 18593874]  [MGI Ref ID J:137424]

Begus-Nahrmann Y; Hartmann D; Kraus J; Eshraghi P; Scheffold A; Grieb M; Rasche V; Schirmacher P; Lee HW; Kestler HA; Lechel A; Rudolph KL. 2012. Transient telomere dysfunction induces chromosomal instability and promotes carcinogenesis. J Clin Invest 122(6):2283-8. [PubMed: 22622037]  [MGI Ref ID J:190483]

Begus-Nahrmann Y; Lechel A; Obenauf AC; Nalapareddy K; Peit E; Hoffmann E; Schlaudraff F; Liss B; Schirmacher P; Kestler H; Danenberg E; Barker N; Clevers H; Speicher MR; Rudolph KL. 2009. p53 deletion impairs clearance of chromosomal-instable stem cells in aging telomere-dysfunctional mice. Nat Genet 41(10):1138-43. [PubMed: 19718028]  [MGI Ref ID J:155011]

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Sarin KY; Cheung P; Gilison D; Lee E; Tennen RI; Wang E; Artandi MK; Oro AE; Artandi SE. 2005. Conditional telomerase induction causes proliferation of hair follicle stem cells. Nature 436(7053):1048-52. [PubMed: 16107853]  [MGI Ref ID J:100644]

Satyanarayana A; Wiemann SU; Buer J; Lauber J; Dittmar KE; Wustefeld T; Blasco MA; Manns MP; Rudolph KL. 2003. Telomere shortening impairs organ regeneration by inhibiting cell cycle re-entry of a subpopulation of cells. EMBO J 22(15):4003-13. [PubMed: 12881434]  [MGI Ref ID J:84928]

Schaetzlein S; Kodandaramireddy NR; Ju Z; Lechel A; Stepczynska A; Lilli DR; Clark AB; Rudolph C; Kuhnel F; Wei K; Schlegelberger B; Schirmacher P; Kunkel TA; Greenberg RA; Edelmann W; Rudolph KL. 2007. Exonuclease-1 deletion impairs DNA damage signaling and prolongs lifespan of telomere-dysfunctional mice. Cell 130(5):863-77. [PubMed: 17803909]  [MGI Ref ID J:129929]

Schaetzlein S; Lucas-Hahn A; Lemme E; Kues WA; Dorsch M; Manns MP; Niemann H; Rudolph KL. 2004. Telomere length is reset during early mammalian embryogenesis. Proc Natl Acad Sci U S A 101(21):8034-8. [PubMed: 15148368]  [MGI Ref ID J:90665]

Schoeftner S; Blanco R; de Silanes IL; Munoz P; Gomez-Lopez G; Flores JM; Blasco MA. 2009. Telomere shortening relaxes X chromosome inactivation and forces global transcriptome alterations. Proc Natl Acad Sci U S A 106(46):19393-8. [PubMed: 19887628]  [MGI Ref ID J:154764]

Schoeftner S; Blasco MA. 2008. Developmentally regulated transcription of mammalian telomeres by DNA-dependent RNA polymerase II. Nat Cell Biol 10(2):228-36. [PubMed: 18157120]  [MGI Ref ID J:132362]

Sebastian C; Herrero C; Serra M; Lloberas J; Blasco MA; Celada A. 2009. Telomere shortening and oxidative stress in aged macrophages results in impaired STAT5a phosphorylation. J Immunol 183(4):2356-64. [PubMed: 19605693]  [MGI Ref ID J:151571]

Siegl-Cachedenier I; Munoz P; Flores JM; Klatt P; Blasco MA. 2007. Deficient mismatch repair improves organismal fitness and survival of mice with dysfunctional telomeres. Genes Dev 21(17):2234-47. [PubMed: 17785530]  [MGI Ref ID J:125218]

Song Z; Wang J; Guachalla LM; Terszowski G; Rodewald HR; Ju Z; Rudolph KL. 2010. Alterations of the systemic environment are the primary cause of impaired B and T lymphopoiesis in telomere-dysfunctional mice. Blood 115(8):1481-9. [PubMed: 19965646]  [MGI Ref ID J:157779]

Song Z; Zhang J; Ju Z; Rudolph KL. 2012. Telomere dysfunctional environment induces loss of quiescence and inherent impairments of hematopoietic stem cell function. Aging Cell 11(3):449-55. [PubMed: 22284665]  [MGI Ref ID J:216115]

Sperka T; Song Z; Morita Y; Nalapareddy K; Guachalla LM; Lechel A; Begus-Nahrmann Y; Burkhalter MD; Mach M; Schlaudraff F; Liss B; Ju Z; Speicher MR; Rudolph KL. 2011. Puma and p21 represent cooperating checkpoints limiting self-renewal and chromosomal instability of somatic stem cells in response to telomere dysfunction. Nat Cell Biol 14(1):73-9. [PubMed: 22138576]  [MGI Ref ID J:178922]

Stout GJ; Blasco MA. 2013. Telomere length and telomerase activity impact the UV sensitivity syndrome xeroderma pigmentosum C. Cancer Res 73(6):1844-54. [PubMed: 23288511]  [MGI Ref ID J:196907]

Tanemura K; Ogura A; Cheong C; Gotoh H; Matsumoto K; Sato E; Hayashi Y; Lee HW; Kondo T. 2005. Dynamic rearrangement of telomeres during spermatogenesis in mice. Dev Biol 281(2):196-207. [PubMed: 15893973]  [MGI Ref ID J:98586]

Tao S; Tang D; Morita Y; Sperka T; Omrani O; Lechel A; Sakk V; Kraus J; Kestler HA; Kuhl M; Rudolph KL. 2015. Wnt activity and basal niche position sensitize intestinal stem and progenitor cells to DNA damage. EMBO J 34(5):624-40. [PubMed: 25609789]  [MGI Ref ID J:219566]

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Tuo B; Ju Z; Riederer B; Engelhardt R; Manns MP; Rudolph KL; Seidler U. 2012. Telomere shortening is associated with reduced duodenal HCOFormula secretory but normal gastric acid secretory capacity in aging mice. Am J Physiol Gastrointest Liver Physiol 303(12):G1312-21. [PubMed: 23019197]  [MGI Ref ID J:193657]

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Wang J; Sun Q; Morita Y; Jiang H; Gross A; Lechel A; Hildner K; Guachalla LM; Gompf A; Hartmann D; Schambach A; Wuestefeld T; Dauch D; Schrezenmeier H; Hofmann WK; Nakauchi H; Ju Z; Kestler HA; Zender L; Rudolph KL. 2012. A differentiation checkpoint limits hematopoietic stem cell self-renewal in response to DNA damage. Cell 148(5):1001-14. [PubMed: 22385964]  [MGI Ref ID J:190258]

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Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Room Number           AX11

Colony Maintenance

Breeding & HusbandryThe Dmdmdx-4Cv mutation is X-linked; therefore mdx-deficient mice are Dmdmdx-4Cv/mdx-4Cv females and Dmdmdx-4Cv/Y males. Telomere length is progressively shortened with successive generations of breeding homozygous mTR null mice (mTR-/-) together.

To replicate the findings in Mourkioti et al. 2013 Nat Cell Biol 15:895, Dr. Helen M. Blau suggests following their specific breeding scheme in Supplementary Fig. S1a of that publication. This scheme places emphasis on starting with the parental generation for every cohort of G0, G1, G2, etc., and using non-sibling matings only as a means of reducing the likelihood of spontaneous mutations influencing experimental outcome. Investigators wishing to recapitulate Dr. Blau's exact breeding scheme may wish to contract with JAX Breeding Services.

The Jackson Laboratory Repository colony began by using Dmdmdx-4Cv/Y;mTR+/- males (G0 males) from Dr. Blau to fertilize oocytes from C57BL/6J inbred females (Stock No. 000664). Next, mice were bred together that were heterozygous or homozygous for Dmdmdx-4Cv and wildtype or heterozygous (not homozygous) for mTR- to obtain animals with G0 genotype. Thereafter, for routine maintenance of the living mdx/mTR colony at The Jackson Laboratory Repository (Stock No. 023535), we bred non-sibling G0 mice together. By this method, the animals with the genotypes listed in part A (i-vi) may be available from The Jackson Laboratory Repository:

A) G0 animals are dystrophin-deficient and heterozygous for mTR. G0 animals have the same phenotype as C57BL/6J-congenic Dmdmdx-4Cv homozygous mice (Stock No. 002378). Breeding G0 animals together (Dmdmdx-4Cv/mdx-4Cv;mTR+/- females and Dmdmdx-4Cv/Y;mTR+/- males) results in the following offspring:
i) Dmdmdx-4Cv/mdx-4Cv;mTR+/+ females
ii) Dmdmdx-4Cv/Y;mTR+/+ males
iii) Dmdmdx-4Cv/mdx-4Cv;mTR+/- females (G0 females)
iv) Dmdmdx-4Cv/Y;mTR+/- males (G0 males)
v) Dmdmdx-4Cv/mdx-4Cv;mTR-/- females (G1 females)
vi) Dmdmdx-4Cv/Y;mTR-/- males (G1 males)

B) G1 animals are the first generation of mice deficient in both dystrophin and mTR. G1 animals have enhanced DMD myopathology. Breeding G1 animals together (Dmdmdx-4Cv/mdx-4Cv;mTR-/- females and Dmdmdx-4Cv/Y;mTR-/- males) results in the following offspring:
i) Dmdmdx-4Cv/mdx-4Cv;mTR-/- females (G2 females)
ii) Dmdmdx-4Cv/Y;mTR-/- males (G2 males)

C) G2 animals are the second generation of mice deficient in both mdx and mTR. G2 animals have enhanced DMD myopathology that is more severe than G1 animals. Breeding G2 animals together results in G3 offspring.
Note that G2, G3, etc. animals may be obtained by contract with JAX Breeding Services.

Mating SystemSee Breeding & Husbandry under the Health & Care tab         (Female x Male)   04-APR-14

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls


This strain is currently On Hold.
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Live Mice

Price per mouse (US dollars $)GenderGenotypes Provided
Individual Mouse $239.00MaleHeterozygous for Terctm1Rdp, Hemizygous for Dmdmdx-4Cv  
$239.00FemaleHeterozygous for Terctm1Rdp, Homozygous for Dmdmdx-4Cv  
Individual Mouse $239.00MaleHomozygous for Terctm1Rdp , Hemizygous for Dmdmdx-4Cv  
$239.00FemaleHomozygous for Terctm1Rdp, Homozygous for Dmdmdx-4Cv  
Individual Mouse $239.00MaleWild-type for Terctm1Rdp, Hemizygous for Dmdmdx-4Cv  
$239.00FemaleWild-type for Terctm1Rdp, Homozygous for Dmdmdx-4Cv  
Price per Pair (US dollars $)Pair Genotype
$478.00Heterozygous for Terctm1Rdp, Homozygous for Dmdmdx-4Cv x Heterozygous for Terctm1Rdp, Hemizygous for Dmdmdx-4Cv  

Standard Supply

This strain is currently on HOLD - Contact Customer Service for more information.

Pricing for International shipping destinations View USA Canada and Mexico Pricing

Live Mice

Price per mouse (US dollars $)GenderGenotypes Provided
Individual Mouse $310.70MaleHeterozygous for Terctm1Rdp, Hemizygous for Dmdmdx-4Cv  
$310.70FemaleHeterozygous for Terctm1Rdp, Homozygous for Dmdmdx-4Cv  
Individual Mouse $310.70MaleHomozygous for Terctm1Rdp , Hemizygous for Dmdmdx-4Cv  
$310.70FemaleHomozygous for Terctm1Rdp, Homozygous for Dmdmdx-4Cv  
Individual Mouse $310.70MaleWild-type for Terctm1Rdp, Hemizygous for Dmdmdx-4Cv  
$310.70FemaleWild-type for Terctm1Rdp, Homozygous for Dmdmdx-4Cv  
Price per Pair (US dollars $)Pair Genotype
$621.40Heterozygous for Terctm1Rdp, Homozygous for Dmdmdx-4Cv x Heterozygous for Terctm1Rdp, Hemizygous for Dmdmdx-4Cv  

Standard Supply

This strain is currently on HOLD - Contact Customer Service for more information.

View USA Canada and Mexico Pricing View International Pricing

Standard Supply

This strain is currently on HOLD - Contact Customer Service for more information.

Control Information

   See control note: Depending upon the nature of the experiment, the following mouse line(s) may be appropriate controls:
C57BL/6J.mTR-/- (Stock No. 004132: B6.Cg-Terctm1Rdp/J)
and/or B6.mdx-4Cv (Stock No. 002378: B6Ros.Cg-Dmdmdx-4Cv/J)
   000664 C57BL/6J
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.

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