Description

Strain Information

Type Spontaneous Mutation; Additional information on Genetically Engineered Mutant Mice. Type Inbred Strain; Additional information on Inbred Strains. Species laboratory mouse Generation F39

Appearance
muted brown shade, possible head tilt
Related Genotype: A/A Muted^mu +/Muted^mu ?

agouti, unaffected
Related Genotype: A/A + ?/? + or A/A Foxc1^ch +/+ Muted^mu

Important Note
This strain is heterozygous for Foxc1^ch and Muted^mu maintained in repulsion.

Description
Mice homozygous for the congenital hydrocephalus (Foxc1^ch) spontaneous mutation die at birth, probably from inability to breathe. Homozygous mutant mice have bulging hemorrhagic cerebral hemispheres and open eyelids, urogenital abnormalities, and severely abnormal skull, cervical vertebrae, sternum, laryngeal cartilages, and hyoid bone. The hydrocephalus may trace to lack of formation of subarachnoid space, which is first detectable in 11-day embryos. Most of the defects in the head region are probably secondary to the severe displacements created by the hydrocephalus. Mice homozygous for the muted spontaneous mutation (Muted^mu), maintained in repulsion with congenital hydrocephalus, have light eyes at birth and their fur is a muted brown shade, often with white underfur. Some have a balance defect, similar to that of pallid (Pldn^pa). Homozygous mutant mice show head-tilting and loss of postural reflexes, due to absence of otoliths from the sacculus and utriculus of one or both ears. The bony labyrinth is normal; the mice are not deaf and do not circle. Mutant mice have prolonged bleeding times and a platelet storage pool deficiency (SPD) associated with abnormalities of the dense granules of the blood platelets.

Control Information

	Control
	? +/+ ? untested from colony
Considerations for Choosing Controls

Related Strains

Strains carrying   Muted^mu allele

000505

B6C3 Aw-J/A-Mutedmu/J

View Strains carrying   Muted^mu     (1 strain)

Additional Web Information

Genetic Quality Control Annual Report

Phenotype

Phenotype Information

View Mammalian Phenotype Terms

Mammalian Phenotype Terms

      assigned by genotype

Foxc1^ch/Foxc1⁺

        CHMU/Le

• vision/eye phenotype
• *normal* vision/eye phenotype (MGI Ref ID J:61775)
  • despite these abnormalities intraocular pressure is rarely increased
• abnormal anterior eye segment morphology (MGI Ref ID J:61775)
  • 48 of 51 had clinically detectable abnormalities with 40 mice having bilateral abnormalities
• abnormal ciliary body morphology (MGI Ref ID J:61775)
  • some eyes have a focally hypoplastic ciliary body with short and thin ciliary processes
• abnormal iridocorneal angle (MGI Ref ID J:61775)
  • most eyes contain morphologically normal and abnormal regions of the iridocorneal angle
  • abnormalities include large blood vessels and iris strands
• abnormal canal of Schlemm morphology (MGI Ref ID J:61775)
  • small or absent
• abnormal trabecular meshwork morphology (MGI Ref ID J:61775)
  • areas may be hypoplastic or absent
  • in some places the trabecular meshwork appears compressed
  • some areas where the trabecular meshwork is absent contain cells that resemble mesenchymal precursor cells
• cataracts (MGI Ref ID J:61775)
  • seen in about 25% of mice and the incidence increase with age
• corneal adhesion to iris (MGI Ref ID J:61775)
  • tend to be more severe than in Foxc1^tm1Blh heterozygotes on a C57BL/6J containing background
• corneal vascularization (MGI Ref ID J:61775)
  • present in some older mice
• large pupils (MGI Ref ID J:61775)
  • some have very large pupils resembling the phenotype associated with aniridia

Muted^mu/Muted^mu

        CHMU/Le

• hematopoietic system phenotype
• *normal* hematopoietic system phenotype (MGI Ref ID J:29151)
  • normal platelet counts
• abnormal platelet dense granule morphology (MGI Ref ID J:29151)
  • although a normal number of dense granules stain with mepacrine, UV flashing is reduced by more than fivefold indicating an abnormal intragranular environment
• abnormal platelet dense granule number (MGI Ref ID J:29151)
• abnormal platelet physiology (MGI Ref ID J:29151)
  • decreased aggregation both in the presence of high or low concentrations of collagen
• decreased platelet serotonin level (MGI Ref ID J:29151)
  • platelet serotonin levels are less than 8% those of normal
• platelet storage pool deficiency (MGI Ref ID J:29151)
  • platelets nearly absent of dense granules and very little releasable ATP is detected when low or high levels of collagen are added to platelets from homozygotes
• homeostasis/metabolism phenotype
• abnormal platelet physiology (MGI Ref ID J:29151)
  • decreased aggregation both in the presence of high or low concentrations of collagen
• decreased platelet serotonin level (MGI Ref ID J:29151)
  • platelet serotonin levels are less than 8% those of normal
• increased bleeding time (MGI Ref ID J:29151)
  • bleed time is greater than 15 minutes
• platelet storage pool deficiency (MGI Ref ID J:29151)
  • platelets nearly absent of dense granules and very little releasable ATP is detected when low or high levels of collagen are added to platelets from homozygotes
• cellular phenotype
• decreased lysosomal enzyme secretion (MGI Ref ID J:29151)
  • lysosomal enzyme levels are increased in kidneys and there is an associated decrease in secretion into the urine
  • thrombin induced release of glucuronidase from platelets is decreased, although to a lesser degree than in mocha homozygotes, and thrombin induced release of galactosidase is 60% to 70% of normal
• pigmentation phenotype
• abnormal retinal pigment epithelium morphology (MGI Ref ID J:29151)
  • although homozygotes do not have the giant granules that are found in the retinal pigment epithelial cells of beige mice, they do have enlarged retinal pigment granules
• vision/eye phenotype
• abnormal retinal pigment epithelium morphology (MGI Ref ID J:29151)
  • although homozygotes do not have the giant granules that are found in the retinal pigment epithelial cells of beige mice, they do have enlarged retinal pigment granules
• renal/urinary system phenotype
• abnormal proximal convoluted tubule morphology (MGI Ref ID J:29151)
  • higher than normal autofluorescence, typical of ceroid-like pigment, is found in proximal tubules

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

Foxc1^ch/Foxc1⁺

        involves: CBA * STOCK Tyr^c f

• nervous system phenotype
• *normal* nervous system phenotype (MGI Ref ID J:5191)
  • unlike homozygotes, no cases of hydrocephalus are seen
• renal/urinary system phenotype
• abnormal urinary system morphology (MGI Ref ID J:5191)
  • at 4 weeks of age about 1/6 of mice have urogenital abnormalities
• abnormal kidney vasculature (MGI Ref ID J:5191)
  • abnormal arrangement of the renal arteries and veins may be seen at P0 but with a lower incidence compared to homozygotes
  • at 4 weeks of age about 50% of mice have an abnormal right renal artery
• hydronephrosis (MGI Ref ID J:5191)
  • incidence is less than that in homozygotes
• hydroureter (MGI Ref ID J:5191)
  • incidence is less than that in homozygotes
• reproductive system phenotype
• abnormal reproductive system morphology (MGI Ref ID J:5191)
  • at 4 weeks of age about 1/6 of mice have urogenital abnormalities
• abnormal ovary morphology (MGI Ref ID J:5191)
  • may be located more anteriorly than in controls
  • this occurs with a lower incidence compared to homozygotes
• abnormal testis morphology (MGI Ref ID J:5191)
  • may be located more anteriorly than in controls
  • this occurs with a lower incidence compared to homozygotes
• skeleton phenotype
• abnormal cervical atlas morphology (MGI Ref ID J:5191)
  • the neural canal is wider and more rounded at its ventral border and the lateral vertebral foramin is often open dorsolaterally
• abnormal occipital bone morphology (MGI Ref ID J:5191)
  • the border of the foramen magnum at the suture between the supraoccipital and exoccipital is slightly concave rather than straight or slightly convex as in controls
• abnormal sternum morphology (MGI Ref ID J:5191)
  • in some mice at 4 weeks of age, the anterior and posterior halves of the sternum consist of separate bones
• abnormal thyroid cartilage morphology (MGI Ref ID J:5191)
  • may have defects on the ventral side
• craniofacial phenotype
• abnormal occipital bone morphology (MGI Ref ID J:5191)
  • the border of the foramen magnum at the suture between the supraoccipital and exoccipital is slightly concave rather than straight or slightly convex as in controls
• respiratory system phenotype
• abnormal thyroid cartilage morphology (MGI Ref ID J:5191)
  • may have defects on the ventral side
• endocrine/exocrine gland phenotype
• abnormal ovary morphology (MGI Ref ID J:5191)
  • may be located more anteriorly than in controls
  • this occurs with a lower incidence compared to homozygotes
• abnormal testis morphology (MGI Ref ID J:5191)
  • may be located more anteriorly than in controls
  • this occurs with a lower incidence compared to homozygotes
• cardiovascular system phenotype
• abnormal kidney vasculature (MGI Ref ID J:5191)
  • abnormal arrangement of the renal arteries and veins may be seen at P0 but with a lower incidence compared to homozygotes
  • at 4 weeks of age about 50% of mice have an abnormal right renal artery

View Research Applications

Research Applications

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

Foxc1^ch related

Developmental Biology Research
Craniofacial and Palate Defects (hydrocephaly: severely abnormal skull)
Neurodevelopmental Defects
Skeletal Defects (hydrocephaly)

Neurobiology Research
Neurodevelopmental Defects

Sensorineural Research
Eye Defects

Muted^mu related

Dermatology Research
Color and White Spotting Defects

Neurobiology Research
Vestibular and Hearing Defects

Sensorineural Research
Vestibular and Hearing Defects

Genes & Alleles

Gene & Allele Information

Allele Symbol		Foxc1ch
Allele Name		congenital hydrocephalus
Allele Type		Spontaneous
Common Name(s)		ch; mf1ch;
Strain of Origin		CBA x STOCK Tyr f
Gene Symbol and Name		Foxc1, forkhead box C1
Chromosome		13
Gene Common Name(s)		ARA; FKHL7; FREAC-3; FREAC3; Fkh1; IGDA; IHG1; IRID1; Mf1; Mf4; ch; congenital hydrocephalus; fkh-1; forkhead homolog 1, (Drosophila); frkhda; mesoderm/mesenchyme forkhead 1; mesoderm/mesenchyme forkhead 4;
Molecular Note		A transition point mutation at nucleotide 366 altered a C to a T in the coding region. This results in a stop codon in the sequences encoding the third helix of the WH domain, and the authors predict that a truncated protein would be generated lacking DNA binding activity. [MGI Ref ID J:48079]
Allele Symbol		Mutedmu
Allele Name		muted
Allele Type		Spontaneous
Common Name(s)		mu;
Strain of Origin		STOCK t
Gene Symbol and Name		Muted, muted
Chromosome		13
Gene Common Name(s)		1810074A19Rik; BLOC-1 subunit; DKFZp686E2287; MU; RIKEN cDNA 1810074A19 gene; mu;
Molecular Note		An early transposon (Etn) insertion has been identified as the mutation underlying the phenotype in muted mice. Analysis of genomic DNA revealed an insertion into the third intron. 183 bp of Etn sequence has been incorporated into the mRNA , likely by the activation of cryptic splice sites within the Etn. This results in an in-frame insertion into the translated protein at position 106, predicting a 246 amino acid protein. A significant reduction in mRNA levels is observed. [MGI Ref ID J:75830]

Genotyping

Genotyping Information

This strain will not have a genotyping protocol or one is not currently available.

Helpful Links

Optimizing PCR Protocols

References

References

Selected Reference(s)

Lyon MF; Meredith R. 1969. Muted, a new mutant affecting coat colour and otoliths of the mouse, and its position in linkage group XIV. Genet Res 14(2):163-6. [PubMed: 5367369]  [MGI Ref ID J:5145]

Additional References

Green MC. 1970. The developmental effects of congenital hydrocephalus (ch) in the mouse. Dev Biol 23(4):585-608. [PubMed: 5500588]  [MGI Ref ID J:5191]

Jones SM; Erway LC; Johnson KR; Yu H; Jones TA. 2004. Gravity receptor function in mice with graded otoconial deficiencies. Hear Res 191(1-2):34-40. [PubMed: 15109702]  [MGI Ref ID J:89392]

Kume T; Deng K; Hogan BL. 2000. Murine forkhead/winged helix genes Foxc1 (Mf1) and Foxc2 (Mfh1) are required for the early organogenesis of the kidney and urinary tract. Development 127(7):1387-95. [PubMed: 10704385]  [MGI Ref ID J:60834]

Rice R; Rice DP; Olsen BR; Thesleff I. 2003. Progression of calvarial bone development requires Foxc1 regulation of Msx2 and Alx4. Dev Biol 262(1):75-87. [PubMed: 14512019]  [MGI Ref ID J:85739]

Smith RS; Zabaleta A; Kume T; Savinova OV; Kidson SH; Martin JE; Nishimura DY; Alward WL; Hogan BL; John SW. 2000. Haploinsufficiency of the transcription factors FOXC1 and FOXC2 results in aberrant ocular development. Hum Mol Genet 9(7):1021-32. [PubMed: 10767326]  [MGI Ref ID J:61775]

Swank RT; Reddington M; Howlett O; Novak EK. 1991. Platelet storage pool deficiency associated with inherited abnormalities of the inner ear in the mouse pigment mutants muted and mocha. Blood 78(8):2036-44. [PubMed: 1912584]  [MGI Ref ID J:29151]

Zhang Q; Li W; Novak EK; Karim A; Mishra VS; Kingsmore SF; Roe BA; Suzuki T; Swank RT. 2002. The gene for the muted (mu) mouse, a model for Hermansky-Pudlak syndrome, defines a novel protein which regulates vesicle trafficking. Hum Mol Genet 11(6):697-706. [PubMed: 11912185]  [MGI Ref ID J:75830]

Foxc1^ch related

Breen M; Richardson R; Bondareff W; Weinstein HG. 1973. Acidic glycosaminoglycans in developing sterno-costal cartilage of the hydrocephalic (ch+-ch+) mouse. Biochim Biophys Acta 304(3):828-36. [PubMed: 4269479]  [MGI Ref ID J:5368]

Green MC. 1970. The developmental effects of congenital hydrocephalus (ch) in the mouse. Dev Biol 23(4):585-608. [PubMed: 5500588]  [MGI Ref ID J:5191]

Gruneberg H. 1943. Congenital hydrocephalus in the mouse, a case of spurious pleiotropism J Genet 45(1):1-21.  [MGI Ref ID J:75733]

Gruneberg H. 1971. Exocrine glands and the Chievitz organ of some mouse mutants. J Embryol Exp Morphol 25(2):247-61. [PubMed: 5088022]  [MGI Ref ID J:140462]

Gruneberg H. 1953. Genetical studies on the skeleton of the mouse. VII. Congenital hydrocephalus J Genet 51:327-58.  [MGI Ref ID J:14980]

Gruneberg H; Wickramaratne GA. 1974. A re-examination of two skeletal mutants of the mouse, vestigial-tail (vt) and congenital hydrocephalus (ch). J Embryol Exp Morphol 31(1):207-22. [PubMed: 4819561]  [MGI Ref ID J:5431]

Hong HK; Lass JH; Chakravarti A. 1999. Pleiotropic skeletal and ocular phenotypes of the mouse mutation congenital hydrocephalus (ch/Mf1) arise from a winged helix/forkhead transcriptionfactor gene. Hum Mol Genet 8(4):625-37. [PubMed: 10072431]  [MGI Ref ID J:54407]

Kume T; Deng K; Hogan BL. 2000. Murine forkhead/winged helix genes Foxc1 (Mf1) and Foxc2 (Mfh1) are required for the early organogenesis of the kidney and urinary tract. Development 127(7):1387-95. [PubMed: 10704385]  [MGI Ref ID J:60834]

Kume T; Deng KY; Winfrey V; Gould DB; Walter MA; Hogan BL. 1998. The forkhead/winged helix gene Mf1 is disrupted in the pleiotropic mouse mutation congenital hydrocephalus. Cell 93(6):985-96. [PubMed: 9635428]  [MGI Ref ID J:48079]

Raimondi AJ; Bailey OT; McLone DG; Lawson RF; Echeverry A. 1973. The pathophysiology and morphology of murine hydrocephalus in Hy-3 and Ch mutants. Surg Neurol 1(1):50-5. [PubMed: 4784576]  [MGI Ref ID J:5426]

Rice R; Rice DP; Olsen BR; Thesleff I. 2003. Progression of calvarial bone development requires Foxc1 regulation of Msx2 and Alx4. Dev Biol 262(1):75-87. [PubMed: 14512019]  [MGI Ref ID J:85739]

Rice R; Rice DP; Thesleff I. 2005. Foxc1 integrates Fgf and Bmp signalling independently of twist or noggin during calvarial bone development. Dev Dyn 233(3):847-852. [PubMed: 15906377]  [MGI Ref ID J:98808]

Smith RS; Zabaleta A; Kume T; Savinova OV; Kidson SH; Martin JE; Nishimura DY; Alward WL; Hogan BL; John SW. 2000. Haploinsufficiency of the transcription factors FOXC1 and FOXC2 results in aberrant ocular development. Hum Mol Genet 9(7):1021-32. [PubMed: 10767326]  [MGI Ref ID J:61775]

Vivatbutsiri P; Ichinose S; Hytonen M; Sainio K; Eto K; Iseki S. 2008. Impaired meningeal development in association with apical expansion of calvarial bone osteogenesis in the Foxc1 mutant. J Anat 212(5):603-11. [PubMed: 18422524]  [MGI Ref ID J:137357]

Muted^mu related

Bossi G; Booth S; Clark R; Davis EG; Liesner R; Richards K; Starcevic M; Stinchcombe J; Trambas C; Dell'Angelica EC; Griffiths GM. 2005. Normal lytic granule secretion by cytotoxic T lymphocytes deficient in BLOC-1, -2 and -3 and myosins Va, VIIa and XV. Traffic 6(3):243-51. [PubMed: 15702992]  [MGI Ref ID J:105404]

Falcon-Perez JM; Starcevic M; Gautam R; Dell'Angelica EC. 2002. BLOC-1, a novel complex containing the pallidin and muted proteins involved in the biogenesis of melanosomes and platelet-dense granules. J Biol Chem 277(31):28191-9. [PubMed: 12019270]  [MGI Ref ID J:88019]

Jones SM; Erway LC; Johnson KR; Yu H; Jones TA. 2004. Gravity receptor function in mice with graded otoconial deficiencies. Hear Res 191(1-2):34-40. [PubMed: 15109702]  [MGI Ref ID J:89392]

Lyon MF; Meredith R. 1965. Muted, mu Mouse News Lett 32:38.  [MGI Ref ID J:29164]

McGarry MP; Reddington M; Novak EK; Swank RT. 1999. Survival and lung pathology of mouse models of Hermansky-Pudlak syndrome and Chediak-Higashi syndrome. Proc Soc Exp Biol Med 220(3):162-8. [PubMed: 10193444]  [MGI Ref ID J:53228]

Moriyama K; Bonifacino JS. 2002. Pallidin is a component of a multi-protein complex involved in the biogenesis of lysosome-related organelles. Traffic 3(9):666-77. [PubMed: 12191018]  [MGI Ref ID J:88020]

Nguyen T; Wei ML. 2004. Characterization of melanosomes in murine Hermansky-Pudlak syndrome: mechanisms of hypopigmentation. J Invest Dermatol 122(2):452-60. [PubMed: 15009730]  [MGI Ref ID J:88797]

Silvers WK. 1979. The Coat Colors of Mice; A Model for Mammalian Gene Action and Interaction. In: The Coat Colors of Mice. Springer-Verlag, New York.  [MGI Ref ID J:78801]

Swank RT; Reddington M; Howlett O; Novak EK. 1991. Platelet storage pool deficiency associated with inherited abnormalities of the inner ear in the mouse pigment mutants muted and mocha. Blood 78(8):2036-44. [PubMed: 1912584]  [MGI Ref ID J:29151]

Zhang Q; Li W; Novak EK; Karim A; Mishra VS; Kingsmore SF; Roe BA; Suzuki T; Swank RT. 2002. The gene for the muted (mu) mouse, a model for Hermansky-Pudlak syndrome, defines a novel protein which regulates vesicle trafficking. Hum Mol Genet 11(6):697-706. [PubMed: 11912185]  [MGI Ref ID J:75830]

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	Repository-Cryopreserved. Must Be Recovered. Please refer to pricing and supply notes for further information.
Supply Notes	Cryorecovery of Strains Needing Progeny Testing. The recovery process begins when a signed agreement form is returned to the Customer Service Department after order placement. Although results vary by strain, at least two untested males and two untested females (two pairs) will be recovered, typically within 15 weeks of our receipt of the signed agreement form. If the first recovery attempt is unsuccessful or only one pair is recovered, a second recovery will be done, extending the overall recovery time to approximately 25 weeks. However, all pups recovered will be sent. Progeny testing is required to identify the genotype of mice of this strain, as a genotyping assay is not available. This type of testing involves breeding the recovered animals and assessing the phenotype of the offspring in order to identify animals carrying the mutation of interest. We can perform the progeny testing for you as a service or we can ship all recovered animals (at least two untested pairs) to you for progeny testing at your facility. If you perform the progeny testing, there is NO guarantee that a carrier will be identified. If we perform progeny testing as a service, additional breeding time will be required. In this case, when a male and female (one pair) are identified that carry the mutation, they and their offspring will be shipped. Delivery time for strains requiring progeny testing often exceeds 25 weeks and may take 12 months or more due to the difficulties in breeding some strains. The progeny testing cost is in addition to the recovery cost and is based on the number of boxes used and the time taken to produce the mice identified as carrying the mutation. Please note that identified pairs may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation of the strain. Mating schemes are sometimes modified for successful cryopreservation. Please contact Customer Service for more information on the cost of progeny testing for a strain: Tel: 1-800-422-6423 or 1-207-288-5845. Cryorecovery to establish a Dedicated Supply for greater quantities of mice One to two pairs will be recovered to establish a Dedicated Supply of mice. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 or 1-207-288-5845. This strain is included in the Mouse Mutant Resource collection. Genomic DNA is available for this strain from the Mouse DNA Resource.
Important Note	This strain is heterozygous for Foxc1ch and Mutedmu maintained in repulsion.

Control Information

	Control
	? +/+ ? untested from 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.

General Terms and Conditions

See Terms of Use

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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Ordering and Purchasing Information

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Tel: 800.422.6423 or 207.288.5845
Fax: 207.288.6150
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Terms of Use

Terms of Use

General Terms and Conditions

Contact information

General inquiries

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phone:	207-288-6470
fax:	207-288-6655

JAX^® Mice & Services Conditions of Use

“Each recipient institution, including its employees and other researchers under its control (RECIPIENT), of mice or services using mice from The Jackson Laboratory (TJL) agrees that such mice, descendants of those mice derived by inbreeding or crossbreeding, including unmodified derivatives of those mice or their descendants (“MICE”) shall not be: (i) used for any purpose other than the internal research of the RECIPIENT, (ii) sold or otherwise provided to any third party for any use, or (iii) provided to any agent or other third party to provide breeding or other services with respect to MICE. Acceptance of MICE from TJL shall be deemed agreement by RECIPIENT to these conditions, and departure from these conditions requires The Jackson Laboratory’s prior written authorization.”

In case of dissatisfaction for a valid reason and claimed in writing by a purchaser within ninety (90) days of receipt of MICE, products or services, The Jackson Laboratory will, at its option, provide credit or replacement for the MICE or product received or the services provided.

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In no event shall The Jackson Laboratory, its trustees, directors, officers, employees, and affiliates be liable for any causes of action or damages, including any direct, indirect, special, or consequential damages, arising out of the provision of MICE, products or services, including economic damage or injury to property and lost profits, and including any damage arising from acts or negligence on the part of The Jackson Laboratory, its agents or employees. In purchasing or receiving MICE, products or services from The Jackson Laboratory, purchaser or recipient, or any party claiming by or through them, expressly releases and discharges The Jackson Laboratory from all such causes of action or damages, and further agrees to defend and indemnify The Jackson Laboratory from any costs or damages arising out of any third party claims.

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The foregoing represents the General Terms and Conditions applicable to The Jackson Laboratory’s MICE, products and services. In addition, special terms and conditions of sale of certain MICE, products and services may be set forth separately in The Jackson Laboratory web pages, catalogs, price lists, contracts, and/or other documents, and these special terms and conditions shall also govern the sale of these MICE, products and services by The Jackson Laboratory, and by its licensees and distributors.

Acceptance of delivery of MICE, products or services shall be deemed agreement to these terms and conditions. No purchase order or other document transmitted by purchaser or recipient that may modify the terms and conditions hereof, shall be in any way binding on The Jackson Laboratory, and instead the terms and conditions set forth herein, including any special terms and conditions set forth separately, shall govern the sale of MICE, products services by The Jackson Laboratory.