Strain Detail Sheet

Strain Name    :

C.129P2(Cg)-Cftrtm1Unc/Mmnc

Stock Number :

029585-UNC

Gene Information

Gene Details [Including genotyping protocols]

(provided by MGI)
Allele Symbol: Cftrtm1Unc
Name: targeted mutation 1, University of North Carolina
Alteration at locus: Knockout
Gene Symbol: Cftr
Name: cystic fibrosis transmembrane conductance regulator
Chromosome: 6
Alteration at locus: Knockout

Genetic Alterations:
A neomycin cassette was inserted into exon 10. This resulted in a truncation mutation. Low levels of the truncated CFTR mRNA can be detected.

Genotype Determination:

  • Donor's Protocol
  • Center protocol and contact for technical support will be shipped with mice.

ES Cell Line: E14TG2a derived from 129P2/OlaHsd

Strain Description [Including phenotype, strain background, strain development and suggested control mice]

Phenotype

Homozygous phenotype: Homozygous mice display many features common to human cystic fibrosis patients, including failure to thrive, meconium ileus, alteration of mucous and serous glands, and obtstruction of glandlike structures with inspissated eosinophilic material. Death resulting from intestinal obstruction usually occurs before 40 days of age, if mice are not supplemented with colyte.

Heterozygous phenotype: Heterozygous mice are normal and fertile.


Mammalian Phenotype Terms:(provided by MGI)      Extend all MPTs
      assigned by genotype

The following phenotype information may relate to one or more alleles on a genetic background differing from this MMRRC strain.
Cftrtm1Unc/Cftr+
        involves: 129P2/OlaHsd
  • reproductive system phenotype
    • asthenozoospermia (MGI Ref ID J:122297)
      • male heterozygotes show a significant reduction in sperm motility with compromised forward movement parameters relative to wild-type controls
    • decreased litter size (MGI Ref ID J:122297)
      • when crossed to wild-type females, male heterozygotes yield a reduced litter size relative to wild-type males (on average 4.20 +/- 1.09 vs 6.22 +/- 0.67, respectively)
    • impaired fertilization (MGI Ref ID J:122297)
      • in vitro fertilizing capacity of heterozygous mutant sperm is significantly lower than that of wild-type sperm (16% vs 48.5%, respectively)
      • in addition, heterozygous mutant sperm show reduced binding and penetration of zona pellucida-free eggs relative to wild-type sperm
    • impaired sperm capacitation (MGI Ref ID J:122297)
      • after 2-hr incubation in capacitation-inducing medium, the % of capacitated sperm (B pattern) in male heterozygotes is significantly lower than that of wild-type controls, as shown by CTC staining
      • reduced sperm capacitation is associated with defective HCO3_ transport, including a reduction in the magnitude of HCO3_ -induced membrane hyperpolarization and a decrease in HCO3_ -induced cAMP production relative to wild-type controls
    • reduced male fertility (MGI Ref ID J:122297)
      • only 5 of 9 male heterozygotes mated with wild-type females produce offspring
Cftrtm1Unc/Cftr+
        involves: BALB/cJ * C57BL/6J
  • reproductive system phenotype
    • transmission ratio distortion (MGI Ref ID J:125558)
      • excess BALB/cJ alleles in 3-week old non-cystic fibrosis affected females
Cftrtm1Unc/Cftrtm1Unc
        B6.129P2-Cftr<tm1Unc>
  • mortality/aging
    • partial postnatal lethality (MGI Ref ID J:44904)
      • increased relative to homozygotes on a mixed 129P2/OlaHsd and C57BL/6J background
      • at P20 survival is 6.4% of all live births
      • death usually occurs with 3 days of birth mostly from intestinal disease
  • digestive/alimentary phenotype
    • abnormal intestine morphology (MGI Ref ID J:44904)
      • intestinal disease involving the colon and distal ileum is a common cause of death
  • respiratory system phenotype
    • abnormal bronchus morphology (MGI Ref ID J:44904)
      • at 6 months of age many bronchiolar surfaces are covered with a thick layer of material that is not seen in wild-type mice or in homozygotes on a mixed 129P2/OlaHsd and C57BL/6J background
      • increase in the amount of acidic mucopolysacharides in material lining the airways compared to wild-type mice and homozygotes on a mixed 129P2/OlaHsd and C57BL/6J background
      • age dependent increase in the relative proportion of non-ciliated cells in the airway epithelium with proliferation of endoplasmic reticulum and increase in the number of secretory granules in these cells; however, this increase is not seen in mice on a mixed 129P2/OlaHsd and C57BL/6J background
    • abnormal pulmonary alveolus morphology (MGI Ref ID J:44904)
      • as early as P30, patchy lesions consisting of acinar dilation with interstitial thickening and accumulation of inflammatory cells and connective tissue in the alveolar walls are seen consistent with obstructive small airway disease
      • at 6 months of age many alveolar surfaces are covered with a thick layer of material that is not seen in wild-type mice or in homozygotes on a mixed 129P2/OlaHsd and C57BL/6J background
    • abnormal respiratory system physiology (MGI Ref ID J:44904)
      • elevated negative basal nasal potential difference and absence of response to imposition of a luminally directed Cl- gradient
      • increased lung compliance (MGI Ref ID J:44904)
        • lung compliance corrected for body weight is increased compared to wild-type mice or homozygous mice on a mixed 129P2/OlaHsd and C57BL/6J background
      • lung inflammation (MGI Ref ID J:44904)
        • as early as P30, patchy lesions consisting of acinar dilation with interstitial thickening and accumulation of inflammatory cells and connective tissue in the alveolar walls are seen consistent with obstructive small airway disease
        • this pathology becomes more severe with age
        • however, no infection with any pulmonary pathogens is detected
    • pulmonary interstitial fibrosis (MGI Ref ID J:44904)
      • increased deposition of collagen and other fibrillar material with age
  • growth/size phenotype
    • postnatal growth retardation (MGI Ref ID J:44904)
      • more severe than in homozygous mice on a mixed 129P2/OlaHsd and C57BL/6J background
  • immune system phenotype
    • lung inflammation (MGI Ref ID J:44904)
      • as early as P30, patchy lesions consisting of acinar dilation with interstitial thickening and accumulation of inflammatory cells and connective tissue in the alveolar walls are seen consistent with obstructive small airway disease
      • this pathology becomes more severe with age
      • however, no infection with any pulmonary pathogens is detected
Cftrtm1Unc/Cftrtm1Unc
        B6.129P2-Cftr<tm1Unc>/J
  • homeostasis/metabolism phenotype
    • homeostasis/metabolism phenotype (MGI Ref ID J:145380)
      • although mutant FSH levels are slightly increased relative to wild-type levels, cir culating levels of both FSH and LH still remain within normal range at proestrus
      • abnormal phospholipid level (MGI Ref ID J:58571)
        • homozygotes exhibit a membrane lipid imbalance characterized by an increase in phospholipid-bound arachidonic acid (AA) and a decrease in phospholipid-bound docosahexaenoic acid (DHA), that is most pronounced in the pancreas, lung and ileum, organs affected in cystic fibrosis, and in the heart
        • oral administration of DHA reverses the membrane lipid imbalance
  • digestive/alimentary phenotype
    • abnormal pancreatic acinus morphology (MGI Ref ID J:58571)
      • massive luminal dilatation
      • oral administration of DHA reverses the pancreatic phenotype
      • pancreatic acinar cell zymogen granule accumulation (MGI Ref ID J:58571)
        • zymogen granule accumulation at the apical pole of the acinar cells
    • ileum hypertrophy (MGI Ref ID J:58571)
      • ileal hypertrophy; villus height is increased
      • oral administration of DHA restores villus height to normal
    • intestinal obstruction (MGI Ref ID J:112450)
      • develop intestinal blockage when fed a normal (solid) diet
  • respiratory system phenotype
    • abnormal respiratory system physiology (MGI Ref ID J:112450)
      • abnormal nasal potential difference
      • lung inflammation (MGI Ref IDs J:112450, J:58571)
        • increased inflammatory response to chronic Pseudomonas aeruginosa infection (MGI Ref ID J:112450)
        • homozygotes exposed to Pseudomonas LPS daily for 3 days exhibit enhanced lung inflammation, as indicated by a significant increase in neutrophil concentration compared to wild-type (MGI Ref ID J:58571)
        • oral administration of DHA blocks the enhanced neutrophil infiltration in response to Pseudomonas LPS (MGI Ref ID J:58571)
  • growth/size phenotype
    • decreased body weight (MGI Ref ID J:112450)
      • reduced at 7, 14, and 21 days of age relative to wild-type mice
    • decreased body weight (MGI Ref ID J:145380)
      • at 6-8 and 14-16 weeks of age, total body weight is reduced by only 15% and 12%, respectively, thus not explaining the larger differences noted in average weight of reproductive organs (~50% and 36%, respectively)
  • immune system phenotype
    • lung inflammation (MGI Ref IDs J:112450, J:58571)
      • increased inflammatory response to chronic Pseudomonas aeruginosa infection (MGI Ref ID J:112450)
      • homozygotes exposed to Pseudomonas LPS daily for 3 days exhibit enhanced lung inflammation, as indicated by a significant increase in neutrophil concentration compared to wild-type (MGI Ref ID J:58571)
      • oral administration of DHA blocks the enhanced neutrophil infiltration in response to Pseudomonas LPS (MGI Ref ID J:58571)
  • endocrine/exocrine gland phenotype
    • abnormal pancreatic acinus morphology (MGI Ref ID J:58571)
      • massive luminal dilatation
      • oral administration of DHA reverses the pancreatic phenotype
      • pancreatic acinar cell zymogen granule accumulation (MGI Ref ID J:58571)
        • zymogen granule accumulation at the apical pole of the acinar cells
    • decreased corpora lutea number (MGI Ref ID J:145380)
      • female homozygotes show an average of 1.5 +/- 2.0 corpora lutea per ovary vs 9.3 +/- 1.4 in wild-type females, even though other follicle stages are present
    • small ovary (MGI Ref ID J:145380)
      • at 7 weeks of age, female homozygotes display smaller ovaries than wild-type females
      • decreased ovary weight (MGI Ref ID J:145380)
        • at 6-8 and 14-16 weeks of age, the average weight of mutant ovaries is reduced by 50% and 36%, respectively, relative to that of wild-type ovaries
        • however, mutant ovarian weight is restored to wild-type values after superovulation
  • reproductive system phenotype
    • abnormal cervix morphology (MGI Ref ID J:145380)
      • only 1 of 15 female homozygotes showed cervical mucus accumulation with no other physical signs of obstruction in the uterus
    • abnormal sperm physiology (MGI Ref ID J:145380)
      • sperm transport within the mutant female reproductive system is significantly impaired: the average number of sperm found in mutant oviducts is only ~10% that of wild-type
      • however, no differences in capacitation of oviductal sperm from mutant and wild-type females are observed
    • absent estrous cycle (MGI Ref ID J:145380)
      • unlike wild-type females, 41.7% of 14-16-wk-old mutant females never enter estrus but are constantly in diestrus
    • decreased corpora lutea number (MGI Ref ID J:145380)
      • female homozygotes show an average of 1.5 +/- 2.0 corpora lutea per ovary vs 9.3 +/- 1.4 in wild-type females, even though other follicle stages are present
    • decreased litter size (MGI Ref ID J:145380)
      • female homozygotes show a significant decrease in average number of pups per litter relative to wild-type females (3.55 +/- 1.92 vs 6.56 +/- 2.36, respectively)
    • decreased ovulation rate (MGI Ref ID J:145380)
      • female homozygotes display reduced oocyte ovulation rates relative to wild-type females
      • however, normal ovulation rates are observed after superovulation with exogenous hormone (PMSG + hCG) injections
    • delayed sexual maturation (MGI Ref ID J:145380)
      • female homozygotes display a delayed onset of puberty relative to wild-type controls
    • impaired fertilization (MGI Ref ID J:145380)
      • at 48 hrs after hCG treatment, 100% of mutant oocytes remain unfertilized, whereas the majority of embryos from superovulated wild-type females are at the 2- to 4-cell stages
      • however, no significant differences in in vitro fertilization rates are observed, suggesting that decreased in vivo fertilization is more likely due to inadequate fluid control in the reproductive tract, resulting in decreased sperm number in the oviduct
    • prolonged estrous cycle (MGI Ref ID J:145380)
      • at 14-16 weeks of age, female homozygotes that display at least one estrous cycle show half as many cycles as wild-type females, resulting in a 2-fold increase in average cycle length
    • reduced female fertility (MGI Ref ID J:145380)
      • female homozygotes exhibit reduced fertility with significantly fewer numbers of litters and smaller litter sizes relative to wild-type females
      • 20% of female homozygotes are unable to give birth over a 5-month mating period
      • following induction of superovulation, only 1 of 10 mutant females that displayed vaginal plugs gave birth, but that female did give birth to 20 pups
    • small ovary (MGI Ref ID J:145380)
      • at 7 weeks of age, female homozygotes display smaller ovaries than wild-type females
      • decreased ovary weight (MGI Ref ID J:145380)
        • at 6-8 and 14-16 weeks of age, the average weight of mutant ovaries is reduced by 50% and 36%, respectively, relative to that of wild-type ovaries
        • however, mutant ovarian weight is restored to wild-type values after superovulation
    • small uterus (MGI Ref ID J:145380)
      • at 7 weeks of age, female homozygotes display smaller uteri than wild-type females
      • however, no physical signs of obstruction are observed in the uterus
      • decreased uterus weight (MGI Ref ID J:145380)
        • at 6-8 and 14-16 weeks of age, the average weight of mutant uteri is reduced by 56% and 36%, respectively, relative to that of wild-type uteri
        • however, mutant uterus weight is restored to wild-type values after superovulation
    • thin uterus (MGI Ref ID J:145380)
      • mutant uteri are thinner than wild-type
Cftrtm1Unc/Cftrtm1Unc
        involves: 129P2/OlaHsd
  • mortality/aging
    • partial postnatal lethality (MGI Ref ID J:2079)
      • many die during the first 5 days of postnatal development
    • premature death (MGI Ref ID J:2079)
      • surviving mutants die by 40 days of age, with most dying during the week after weaning
  • growth/size phenotype
    • decreased body size (MGI Ref ID J:2079)
      • remain 10-50% smaller throughout life
    • distended abdomen (MGI Ref ID J:2079)
      • distended abdomen precedes death
  • digestive/alimentary phenotype
    • abnormal intestine morphology (MGI Ref ID J:2079)
      • distension of the proximal segments of the intestine is seen in mutants with severe intestinal obstruction
      • observe dark fecal matter in the intestine and peritoneal cavity and perforation of the intestine
      • abnormal colon morphology (MGI Ref ID J:2079)
        • narrowing of the colon is seen in mutants with severe intestinal obstruction
      • abnormal crypts of Lieberkuhn morphology (MGI Ref ID J:2079)
        • severity of damage in the crypts follows a proximal to distal gradient, with mildest changes in the duodenum and most extreme changes in the ileum and colon
        • dilation of crypts and formation of concretions and cast-like structures that extend the entire length of the crypts and villi, with crypts and villi almost completely destroyed in some cases
        • distended crypts contain increased amounts of mucus and are even present in ileum and colon of mutants without intestinal obstructions
      • abnormal duodenum morphology (MGI Ref ID J:2079)
        • most of the Brunner's gland is destroyed and the lumens of remaining ducts are distended
      • coiled cecum (MGI Ref ID J:2079)
        • cecum is coiled and worm-like in appearance and the lumen is narrowed and partially or completely impacted with hard, sticky fecal pellets
    • abnormal submandibular gland morphology (MGI Ref ID J:2079)
      • submaxillary glands show varying degrees of disruption of the serous acini, however observe no dilation of ducts or presence of inspissated material in ducts
    • intestinal obstruction (MGI Ref ID J:2079)
      • some mutants develop severe intestinal obstruction and meconium ileus consisting of a mixture of mucus and fecal material
      • ileum is the common site of obstruction in mice dying just after weaning while the large intestine is in mice dying more than a few days after weaning
    • peritoneal inflammation (MGI Ref ID J:2079)
      • develop peritonitis
  • endocrine/exocrine gland phenotype
    • abnormal gland morphology (MGI Ref ID J:2079)
      • presence of inspissated secretions in various glands
      • abnormal crypts of Lieberkuhn morphology (MGI Ref ID J:2079)
        • severity of damage in the crypts follows a proximal to distal gradient, with mildest changes in the duodenum and most extreme changes in the ileum and colon
        • dilation of crypts and formation of concretions and cast-like structures that extend the entire length of the crypts and villi, with crypts and villi almost completely destroyed in some cases
        • distended crypts contain increased amounts of mucus and are even present in ileum and colon of mutants without intestinal obstructions
      • abnormal gallbladder morphology (MGI Ref ID J:2079)
        • gallbladders are distended or ruptured, however no lesions are observed in the liver
        • mutants with intestinal obstructions exhibit almost complete destruction of the gallbladder wall with some polymorphonuclear cells presen
        • dilated gallbladder (MGI Ref ID J:2079)
      • abnormal pancreas morphology (MGI Ref ID J:2079)
        • dramatic alterations are not observed in the pancreas, however it is often smaller and paler and 2 of 5 mutants exhibit one or two lobes that contain some enlarged acini and contain eosinophilic material
        • small pancreas (MGI Ref ID J:2079)
          • often smaller
      • abnormal submandibular gland morphology (MGI Ref ID J:2079)
        • submaxillary glands show varying degrees of disruption of the serous acini, however observe no dilation of ducts or presence of inspissated material in ducts
  • immune system phenotype
    • abnormal thymus involution (MGI Ref ID J:2079)
      • mutants present with thymic involution after development of intestinal obstruction
    • peritoneal inflammation (MGI Ref ID J:2079)
      • develop peritonitis
    • spleen hyperplasia (MGI Ref ID J:2079)
      • hypocellularity of the spleen is seen after the development of intestinal obstruction
  • liver/biliary system phenotype
    • abnormal gallbladder morphology (MGI Ref ID J:2079)
      • gallbladders are distended or ruptured, however no lesions are observed in the liver
      • mutants with intestinal obstructions exhibit almost complete destruction of the gallbladder wall with some polymorphonuclear cells presen
      • dilated gallbladder (MGI Ref ID J:2079)
  • respiratory system phenotype
    • abnormal nasal mucosa morphology (MGI Ref ID J:2079)
      • glands in the nasal mucosa exhibit dilation of ducts but no acinar hyperplasia
    • abnormal paranasal sinus morphology (MGI Ref ID J:2079)
    • abnormal trachea morphology (MGI Ref ID J:2079)
      • observe squamous metaplasia in the trachea of the oldest surviving mice
      • glands in the proximal trachea exhibit dilation of the ducts
    • increased respiratory mucosa goblet cell number (MGI Ref ID J:2079)
      • increased numbers of goblet cells in the respiratory tract
  • behavior/neurological phenotype
    • abnormal gait (MGI Ref ID J:2079)
      • awkward gait precedes death
  • hematopoietic system phenotype
    • abnormal thymus involution (MGI Ref ID J:2079)
      • mutants present with thymic involution after development of intestinal obstruction
    • spleen hyperplasia (MGI Ref ID J:2079)
      • hypocellularity of the spleen is seen after the development of intestinal obstruction
  • reproductive system phenotype
    • female infertility (MGI Ref ID J:2079)
      • a successful mating of one female that survived to maturity did not result in pregnancy, possibly indicating infertility, however males exhibit no abnormalities of reproductive organs
  • craniofacial phenotype
    • abnormal nasal mucosa morphology (MGI Ref ID J:2079)
      • glands in the nasal mucosa exhibit dilation of ducts but no acinar hyperplasia
    • abnormal paranasal sinus morphology (MGI Ref ID J:2079)
Cftrtm1Unc/Cftrtm1Unc
        involves: 129P2/OlaHsd * C57BL/6 * FVB/N
  • mortality/aging
    • partial postnatal lethality (MGI Ref ID J:21934)
      • only 5% of mice survive until weaning due to complications from intestinal obstruction
  • digestive/alimentary phenotype
    • abnormal crypts of Lieberkuhn morphology (MGI Ref ID J:21934)
      • crypts are dilated with mucus
    • abnormal intestinal goblet cells (MGI Ref ID J:21934)
      • goblet cell hyperplasia occurs throughout the intestinal tract from ileum to the colon
    • coiled cecum (MGI Ref ID J:21934)
      • the cecum has a coiled "worm-like" structure
  • endocrine/exocrine gland phenotype
    • abnormal crypts of Lieberkuhn morphology (MGI Ref ID J:21934)
      • crypts are dilated with mucus
  • homeostasis/metabolism phenotype
    • abnormal ion homeostasis (MGI Ref ID J:21934)
      • cyclic-AMP stimulated transport of Cl- ions does not occur in the intestinal epithelium
Cftrtm1Unc/Cftrtm1Unc
    ;     involves: 129P2/OlaHsd * C57BL/6J
  • mortality/aging
    • partial postnatal lethality (MGI Ref ID J:44904)
      • reduced relative to homozygotes on a congenic C57BL/6J background
      • at P20 survival is 15.5% of all live births
  • respiratory system phenotype
    • respiratory system phenotype (MGI Ref ID J:44904)
      • at 6 months of age bronchiolar and alveolar surfaces appear similar to wild-type as does the amount of acidic mucopolysacharides in material lining the airways and the proportion of non-ciliated cells in the broncheolar epithlium, unlike in homozygotes on a congenic C57BL/6J background
      • lung compliance corrected for body weight is similar to wild-type
      • abnormal respiratory system physiology (MGI Ref ID J:44904)
        • elevated negative basal nasal potential difference and absence of response to imposition of a luminally directed Cl- gradient
        • abnormal vital capacity (MGI Ref ID J:44904)
          • forced vital capacity per kg body weight is reduced compared to wild-type mice
  • growth/size phenotype
    • postnatal growth retardation (MGI Ref ID J:44904)
      • less severe than in homozygous mice on a congenic C57BL/6J background

Strain of Origin: 129/Ola-BALB/c-DBA/2-C57BL6

Strain genetic background: BALB/cJ

Strain Development: Twelve consecutive crosses to purchased BALB/cJ mice.

Suggested Control Mice:

  • Wildtype littermates

Research Applications

  • Immunology and Inflammation
  • Models for Human Disease

Strain Origin

Donor: Beverly Koller, Ph.D., University of North Carolina, Chapel Hill

Primary Reference:

  • Koller BH, Kim HS, Latour AM, Brigman K, Boucher RC Jr, Scambler P, Wainwright B, Smithies O. Toward an animal model of cystic fibrosis: targeted interruption of exon 10 of the cystic fibrosis transmembrane regulator gene in embryonic stem cells. Proc Natl Acad Sci U S A. 1991 Dec 1;88(23):10730-4. (Medline PMID: 1720548)
  • Snouwaert JN, Brigman KK, Latour AM, Malouf NN, Boucher RC, Smithies O, Koller BH. An animal model for cystic fibrosis made by gene targeting. Science. 1992 Aug 21;257(5073):1083-8. (Medline PMID: 1380723)
  • Snouwaert JN, Brigman KK, Latour AM, Iraj E, Schwab U, Gilmour MI, Koller BH. A murine model of cystic fibrosis. Am J Respir Crit Care Med. 1995 Mar;151(3 Pt 2):S59-64. (Medline PMID: 7533607)

Colony and Husbandry Information

Special Considerations

-/- animals must be given water supplemented with colyte (PEG-3350) in order to survive.

Health Status Report

Mice recovered from a cryo-archive will have health surveillance performed on recipient females. Health reports will be provided prior to shipment. If you require additional health status information, please email mmrrc_health@med.unc.edu.

Order Request Information

Availability Level

Limited quantities of breeder mice (recovered litter) are available from a cryoarchive; recovered litter usually available to ship in 3 to 4 months.

Conditions of Distribution [Including applicable technology transfer agreements]

Distribution of this strain requires submission of the MMRRC Conditions of Use (COU). A link to the COU web form will be provided via email after an order has been placed; the form should be completed then or the email forwarded to your institutional official for completion.

The donor or their institution limits the distribution to non-profit institutions only.

Fees

Additional charges may apply for any special requests. Shipping costs are in addition to the basic distribution/resuscitation fees. Information on shipping costs and any additional charges will be provided by the supplying MMRRC facility.

Click button to Request this one strain. (Use the MMRRC Catalog Search to request more than one strain.)
MMRRC Item # - Description Distribution
Fee/unit (US $)
Units Notes
029585-UNC-RESUSLitter recovered from cryo-archive
$2,022.00
Non-Profit
Litter Recovered litter1; additional fees for any special requests.

1 The distribution fee covers the expense of resuscitating mice from the cryo-archive; you will receive the resulting litter. The litter will contain at minimum one mutant carrier; the actual number of animals and the gender and genotype ratios will vary. (Typically, multiple breeder pairs can be established from the recovered litter.) Prior to shipment, the MMRRC will provide information about the animals recovered. If you anticipate or find that you need to request specific genotypes, genders or quantities of mice in excess of what is likely from a resuscitated litter, you may discuss available options and pricing with the supplying MMRRC facility.

2 An aliquot is one straw or vial with sufficient sperm to recover at least one litter of mice, as per provided protocols, when performed at the MMRRC facility. The MMRRC makes no guarantee concerning the success of these procedures when performed outside the MMRRC facilities.

3 An aliquot contains a sufficient number of embryos (in one or more vials and based on the transfer success rate of the MMRRC facility) to transfer to at least two recipients. The MMRRC makes no guarantee concerning embryo transfer success experienced in the recipient investigator's laboratory. Neither gender nor genotype ratios are guaranteed.

To request material from the MMRRC: Please fill out our on-line request form (accessible from the catalog search results page, or click the Request this Strain button in the fees section above). If you have questions or need assistance completing this form, you may call Customer Service at (800) 910-2291 (in USA or Canada) or (530) 757-5710 (international calls). Before you call, please have with you: the MMRRC item number, quantity needed, Bill-to and Ship-to contact information.



To request material from the MMRRC: Please fill out our on-line request form (accessible from the catalog search results page, or click the Request this Strain button in the fees section). If you have questions or need assistance completing this form, you may call Customer Service at (800) 910-2291 (in USA or Canada) or (530) 757-5710 (international calls). Before you call, please have with you: the MMRRC item number, quantity needed, Bill-to and Ship-to contact information.



The MMRRC is a collaborative effort, funded by grants from DPCPSI of the NIH.

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