Strain Detail Sheet

Strain Name    :

B6;129S5-Slc26a5tm1Jnz/Mmnc

Stock Number :

010570-UNC

Gene Information

Gene Details [Including genotyping protocols]

(provided by MGI)
Allele Symbol: Slc26a5tm1Jnz
Name: targeted mutation 1, Jian Zuo
Alteration at locus: Knockout
Gene Symbol: Slc26a5
Name: solute carrier family 26, member 5
Chromosome: 5
Alteration at locus: Knockout

Genetic Alterations:
Replacement of exons 3-7 with Neo.

Genotype Determination:

ES Cell Line: AB2.2 derived from 129/SvEv

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

Phenotype

Homozygous phenotype: Hearing loss: 40-60 dB threshold elevation using auditory brainstem response (ABR).

Heterozygousphenotype: Appears to have 6 dB threshold elevation.


Mammalian Phenotype Terms:(provided by MGI)      Extend all MPTs
      assigned by genotype
Slc26a5tm1Jnz/Slc26a5+
        involves: 129S7/SvEvBrd * C57BL/6J
  • hearing/vestibular/ear phenotype
    • abnormal cochlear outer hair cell morphology (MGI Ref ID J:79029)
      • at 7-9 weeks, F2 heterozygotes exhibit intermediate OHC lengths in all cochlear turns relative to wild-type and homozygous mutant mice
      • however, hair bundle morphology on all three rows of OHCs appears unaffected
      • cochlear outer hair cell degeneration (MGI Ref ID J:79029)
        • at 7-9 weeks, F2 heterozygotes show scattered loss of cochlear OHCs in the basal 25% of the cochlear spiral
        • however, no OHC loss is noted at P7
    • abnormal distortion product otoacoustic emission (MGI Ref ID J:79029)
      • at 6-8 weeks of age, DPOAE-based thresholds are 3.1-6.4 dB higher than those in control mice, excluding the highest test frequencies, where OHC loss complicates interpretation
    • abnormal distortion product otoacoustic emission (MGI Ref ID J:118929)
      • DPOAEs are reduced in F2 but not in F3-F5 heterozygotes
    • cochlear inner hair cell degeneration (MGI Ref ID J:79029)
      • at 7-9 weeks, F2 heterozygotes show scattered loss of cochlear IHCs in the basal 25% of the cochlear spiral
      • however, no IHC loss is noted at P7
    • decreased brainstem auditory evoked potential (MGI Ref IDs J:79029, J:91680)
      • at 6-8 weeks of age, ABR thresholds for responses originating from cochlear regions with all hair cells present (frequencies 22.6 kHz) are elevated by 1-8 dB (MGI Ref ID J:79029)
      • at P21, heterozygotes exhibit a significant increase in high-frequency ABR auditory thresholds (~3.5 dB) relative to wild-type littermates (MGI Ref ID J:91680)
    • decreased cochlear outer hair cell electromotility (MGI Ref ID J:79029)
      • in response to voltage steps (-120-60 mV in 20-mV steps) in whole-cell, voltage clamp recordings, OHCs isolated from F2 generation heterozygotes show a 54% reduction in in vitro electromotility relative to wild-type OHCs
    • impaired hearing (MGI Ref IDs J:118929, J:79029)
      • at 6-8 weeks, F2 generation heterozygotes show a 6 dB loss of cochlear sensitivity, i.e. a ~2-fold increase in cochlear thresholds relative to wild-type mice, due to a 54% reduction in OHC electromotility (MGI Ref ID J:79029)
      • in stark contrast to F2 heterozygotes, F3-F5 heterozygotes display normal CAP thresholds, CAP tuning curves and CM input-output functions, with no significant differences in non-linear capacitance or OHC electromotility relative to wild-type mice (MGI Ref ID J:118929)
      • consistent with normal hearing data in F3-F5 heterozygotes, immunocytochemical and western blot analyses show that wild-type-like prestin protein expression is attained in adolescent heterozygotes prior to P33 (MGI Ref ID J:118929)
  • nervous system phenotype
    • abnormal cochlear outer hair cell morphology (MGI Ref ID J:79029)
      • at 7-9 weeks, F2 heterozygotes exhibit intermediate OHC lengths in all cochlear turns relative to wild-type and homozygous mutant mice
      • however, hair bundle morphology on all three rows of OHCs appears unaffected
      • cochlear outer hair cell degeneration (MGI Ref ID J:79029)
        • at 7-9 weeks, F2 heterozygotes show scattered loss of cochlear OHCs in the basal 25% of the cochlear spiral
        • however, no OHC loss is noted at P7
    • cochlear inner hair cell degeneration (MGI Ref ID J:79029)
      • at 7-9 weeks, F2 heterozygotes show scattered loss of cochlear IHCs in the basal 25% of the cochlear spiral
      • however, no IHC loss is noted at P7
    • decreased cochlear outer hair cell electromotility (MGI Ref ID J:79029)
      • in response to voltage steps (-120-60 mV in 20-mV steps) in whole-cell, voltage clamp recordings, OHCs isolated fr om F2 generation heterozygotes show a 54% reduction in in vitro electromotility relative to wild-type OHCs
  • growth/size phenotype
    • decreased body weight (MGI Ref ID J:79029)
      • at 1 month, F2 heterozygotes are viable and behaviorally normal but display a ~5% reduction in body weight relative to wild-type littermates
Slc26a5tm1Jnz/Slc26a5tm1Jnz
        involves: 129S7/SvEvBrd * C57BL/6J
  • hearing/vestibular/ear phenotype
    • abnormal Claudius cell morphology (MGI Ref ID J:91680)
      • at P21-P35, some apoptosis occurs in Claudius cells, esp. in the basal-middle cochlear turn
    • abnormal distortion product otoacoustic emission (MGI Ref IDs J:124148, J:79029)
      • at 6-8 weeks of age, the increased DPOAE threshold shifts (45 - 55 dB) were similar to those seen with ABR (MGI Ref ID J:79029)
      • at 1-2 months of age, DPOAEs are only measurable in ~50% of homozygotes, with the strongest responses noted for f2 = 22.6 and 8.0 kHz, i.e. frequencies close to the regions of maximum sensitivity in these mutants (MGI Ref ID J:124148)
      • homozygotes in which DPOAEs are measurable correspond to cases with the lowest CAP thresholds (MGI Ref ID J:124148)
      • when present, DPOAE amplitudes are clearly lower than those in either wild-type or heterozygous mice, with a horizontal shift of ~50 dB, i.e. matching the observed CAP threshold shift (""loss of cochlear amplifier gain"") (MGI Ref ID J:124148)
      • persistence of attenuated high-level DPOAEs indicates that OHC somatic motility is not required for their production (MGI Ref ID J:124148)
      • absent distortion product otoacoustic emissions (MGI Ref ID J:124148)
        • distortion products in both CM and otoacoustic emissions disappear rapidly after death, suggesting that these DPOAEs are produced by "active" processes in OHC stereocilia
    • absent cochlear microphonics (MGI Ref ID J :79029)
      • homozygotes display decay of the cochlear microphonic at the cessation of the tone burst, as expected for a passive system
      • no disruption of mechano-electrical transduction is noted in cochlear OHCs
    • absent cochlear outer hair cell electromotility (MGI Ref ID J:79029)
      • in response to voltage steps (-120-60 mV in 20-mV steps) in whole-cell, voltage clamp recordings, isolated homozygous mutant cochlear OHCs show absence of in vitro electromotility at all points tested
    • cochlear hair cell degeneration (MGI Ref ID J:91680)
      • only sporadic cochlear hair cell loss is noted at P21
      • a striking increase in hair cell loss is observed between P28 and P42
      • at all stages, % of hair cell decreases gradually from the basal turn to the middle turn of the cochlea
      • apoptosis of hair cells begins at P28, as confirmed by TUNEL assays
      • loss of cochlear IHCs lags behind that of OHCs
      • no significant cochlear hair cell loss occurs prior to P28
      • cochlear inner hair cell degeneration (MGI Ref IDs J:79029, J:91680)
        • at 7-9 weeks, homozygotes show a nearly complete loss of cochlear IHCs in the basal 25% of the cochlear spiral (MGI Ref ID J:79029)
        • homozygotes show no remarkable cochlear IHC loss prior to P35; however, 29.3% of IHC are lost in the basal-most cochlear turn by P42 (MGI Ref ID J:91680)
        • no IHC loss is noted at P7 (MGI Ref ID J:79029)
      • cochlear outer hair cell degeneration (MGI Ref IDs J:79029, J:91680)
        • at 7-9 weeks, homozygotes a nearly complete loss of cochlear OHCs in the basal 25% of the cochlear spiral (MGI Ref ID J:79029)
        • in a basal-most 7% cochlear region, 1.6% of OHCs are lost at P21, 10.6% of OHCs are lost at P28, and 94% of OHCs are lost at P42 (MGI Ref ID J:91680)
        • at P28, the innermost row of OHCs shows significantly more loss relative to the middle and outermost OHC rows in the basal-middle cochlear turns (MGI Ref ID J:91680)
        • by P42, 47.1% of OHCs are lost in the basal-most cochlear turn (MGI Ref ID J:91680)
        • the number of apoptotic OHCs is maximal at P28 and P35, consistent with OHC loss (MGI Ref ID J:91680)
        • at P42, more apoptotic cells are detected in the basal turn than in the middle and apical turns of the cochlea (MGI Ref ID J:91680)
        • no OHC loss is noted at P7 (MGI Ref ID J:79029)
    • decreased brainstem auditory evoked potential (MGI Ref IDs J:79029, J:91680)
      • at 6-8 weeks of age, ABR thresholds were 45 - 65 dB higher than those in wild-type mice, a decrease in sensitivity of two to three orders of magnitude (MGI Ref ID J:79029)
      • as early as P14, homozygotes exhibit a significant increase in ABR auditory thresholds (~25 dB) relative to wild-type littermates (MGI Ref ID J:91680)
      • at P21, high-frequency ABR auditory thresholds are elevated by ~50 dB (MGI Ref ID J:91680)
    • decreased cochlear microphonics (MGI Ref IDs J:105502, J:124148)
      • at 30-58 days of age, homozygotes exhibit a significant reduction in cochlear microphonic (CM) at 16 kHz relative to wild-type or heterozygous mice (MGI Ref ID J:105502)
      • in homozygotes, CM remains ~12 dB below that in wild-type mice even at the highest levels (MGI Ref ID J:105502)
      • OHC forward transduction appears normal, as homozygotes have wild-type-like nonlinear responses including harmonic and intermodulation distortion, CM pseudotransducer functions, both summating potential polarities, as well as normal uptake of the dye AM1-43 via transducer channels (MGI Ref ID J:105502)
      • at 1-2 months of age, distortion product cochlear microphonics (DPCM) amplitudes are significantly depressed, esp. at low stimulus levels (MGI Ref ID J:124148)
      • homozygotes exhibiting measurable DPOAEs have larger DPCM than those for which DPOAEs are below the noise floor (MGI Ref ID J:124148)
      • in addition, the horizontal shift in DPCM growth functions is smaller than the loss of gain measured via CAP or via DPOAEs (MGI Ref ID J:124148)
      • DPCM at 2 f1-f2 is ~20 dB down from the primaries, at high SPLs, in both mutant and wildtype mice, and no differences in CM Lissajous patterns are observed (MGI Ref ID J:124148)
    • decreased cochlear nerve compound action potential (MGI Ref IDs J:105502, J:124148)
      • at 30-58 days of age, homozygotes display CAP thresholds shifts in a frequency-dependent manner, with a gain change of ~45 dB at 5 kHz and of ~60 dB at 33 kHz (MGI Ref ID J:105502)
      • CAP input-output functions indicate that the low-level segment is absent, and response magnitudes are reduced for the high-level segment, especially at 12 and 32 kHz (MGI Ref ID J:105502)
      • CAP input-output functions at 6 kHz show near-normal magnitudes at high levels where minimal amplification is expected (MGI Ref ID J:105502)
      • simultaneous masking curves for CAPs produced in response to a 12 kHz probe tone indicate absence of frequency selectivity (i.e. no tuning) in homozygotes (MGI Ref ID J:105502)
      • at 1-2 months of age, homozygotes of the F3-F5 generation display significant increases in CAP thresholds relative to wild-type mice, ranging from ~35 dB at 3.2 kHz to ~55 dB at 16 kHz (MGI Ref ID J:124148)
      • however, homozygotes with the highest CAP thresholds show no measurable ear canal distortions, even at the highest SPLs (MGI Ref ID J:124148)
    • degeneration of organ of Corti supporting cells (MGI Ref ID J:91680)
      • by P42, homozygotes show complete loss of supporting cells in the basal-middle turns
      • apoptosis is noted in inner phalangeal cells and Deiters cells as well as in inner sulcus cells
    • impaired hearing (MGI Ref ID J:79029)
      • at 6-8 weeks, homozygotes exhibit a frequency-dependent reduction in cochlear sensitivity, ranging from ~40 dB at 5.6 kHz to >60 dB at 22.6 kHz, due to a loss of OHC electromotility
      • deafness (MGI Ref ID J:91680)
        • P21 homozygotes exhibit significant hearing loss (25 to 50 dB SPL) prior to any substantial cochlear hair cell loss
    • organ of Corti degeneration (MGI Ref ID J:91680)
      • at P14 and P21, the organ of Corti appears intact in the basal-middle cochlear turns, whereas OHC los s is noted at P28
      • at P35, collapse of the organ of Corti and loss of three rows of OHCs are noted in the basal-middle turns; few remaining supporting cells are observed
      • by P42, complete collapse of the organ of Corti and loss of hair cells and supporting cells are observed in the basal-middle turns
    • short cochlear outer hair cells (MGI Ref IDs J:79029, J:91680)
      • at 7-9 weeks, homozygotes exhibit a decrement in OHC lengths in all cochlear turns while hair bundle morphology on all three rows of OHCs is normal (MGI Ref ID J:79029)
      • at P21 (when OHC loss is minimal but ABR thresholds are elevated), mutant OHCs display reduced cell length (MGI Ref ID J:91680)
      • however, no ultrastructural abnormalities in sterocilla, lateral wall, tight junction or synapses are noted at P21 (MGI Ref ID J:91680)
  • nervous system phenotype
    • absent cochlear microphonics (MGI Ref ID J:79029)
      • homozygotes display decay of the cochlear microphonic at the cessation of the tone burst, as expected for a passive system
      • no disruption of mechano-electrical transduction is noted in cochlear OHCs
    • absent cochlear outer hair cell electromotility (MGI Ref ID J:79029)
      • in response to voltage steps (-120-60 mV in 20-mV steps) in whole-cell, voltage clamp recordings, isolated homozygous mutant cochlear OHCs show absence of in vitro electromotility at all points tested
    • cochlear ganglion degeneration (MGI Ref ID J:91680)
      • in the basal cochlear turn, spiral ganglion undergoes apoptosis later than OHCs and IHCs
    • cochlear hair cell degeneration (MGI Ref ID J:91680)
      • only sporadic cochlear hair cell loss is noted at P21
      • a striking increase in hair cell loss is observed between P28 and P42
      • at all stages, % of hair cell decreases gradually from the basal turn to the middle turn of the cochlea
      • apoptosis of hair cells begins at P28, as confirmed by TUNEL assays
      • loss of cochlear IHCs lags behind that of OHCs
      • no significant cochlear hair cell loss occurs prior to P28
      • cochlear inner hair cell degeneration (MGI Ref IDs J:79029, J:91680)
        • at 7-9 weeks, homozygotes show a nearly complete loss of cochlear IHCs in the basal 25% of the cochlear spiral (MGI Ref ID J:79029)
        • homozygotes show no remarkable cochlear IHC loss prior to P35; however, 29.3% of IHC are lost in the basal-most cochlear turn by P42 (MGI Ref ID J:91680)
        • no IHC loss is noted at P7 (MGI Ref ID J:79029)
      • cochlear outer hair cell degeneration (MGI Ref IDs J:79029, J:91680)
        • at 7-9 weeks, homozygotes a nearly complete loss of cochlear OHCs in the basal 25% of the cochlear spiral (MGI Ref ID J:79029)
        • in a basal-most 7% cochlear region, 1.6% of OHCs are lost at P21, 10.6% of OHCs are lost at P28, and 94% of OHCs are lost at P42 (MGI Ref ID J:91680)
        • at P28, the innermost row of OHCs shows significantly more loss relative to the middle and outermost OHC rows in the basal-middle cochlear turns (MGI Ref ID J:91680)
        • by P42, 47.1% of OHCs are lost in the basal-most cochlear turn (MGI Ref ID J:91680)
        • the number of apoptotic OHCs is maximal at P28 and P35, consistent with OHC loss (MGI Ref ID J:91680)
        • at P42, more apoptotic cells are detected in the basal turn than in the middle and apical turns of the cochlea (MGI Ref ID J:91680)
        • no OHC loss is noted at P7 (MGI Ref ID J:79029)
    • decreased cochlear microphonics (MGI Ref IDs J:105502, J:124148)
      • at 30-58 days of age, homozygotes exhibit a significant reduction in cochlear microphonic (CM) at 16 kHz relative to wild-type or heterozygous mice (MGI Ref ID J:105502)
      • in homozygotes, CM remains ~12 dB below that in wild-type mice even at the highest levels (MGI Ref ID J:105502)
      • OHC forward transduction appears normal, as homozygotes have wild -type-like nonlinear responses including harmonic and intermodulation distortion, CM pseudotransducer functions, both summating potential polarities, as well as normal uptake of the dye AM1-43 via transducer channels (MGI Ref ID J:105502)
      • at 1-2 months of age, distortion product cochlear microphonics (DPCM) amplitudes are significantly depressed, esp. at low stimulus levels (MGI Ref ID J:124148)
      • homozygotes exhibiting measurable DPOAEs have larger DPCM than those for which DPOAEs are below the noise floor (MGI Ref ID J:124148)
      • in addition, the horizontal shift in DPCM growth functions is smaller than the loss of gain measured via CAP or via DPOAEs (MGI Ref ID J:124148)
      • DPCM at 2 f1-f2 is ~20 dB down from the primaries, at high SPLs, in both mutant and wildtype mice, and no differences in CM Lissajous patterns are observed (MGI Ref ID J:124148)
    • decreased cochlear nerve compound action potential (MGI Ref IDs J:105502, J:124148)
      • at 30-58 days of age, homozygotes display CAP thresholds shifts in a frequency-dependent manner, with a gain change of ~45 dB at 5 kHz and of ~60 dB at 33 kHz (MGI Ref ID J:105502)
      • CAP input-output functions indicate that the low-level segment is absent, and response magnitudes are reduced for the high-level segment, especially at 12 and 32 kHz (MGI Ref ID J:105502)
      • CAP input-output functions at 6 kHz show near-normal magnitudes at high levels where minimal amplification is expected (MGI Ref ID J:105502)
      • simultaneous masking curves for CAPs produced in response to a 12 kHz probe tone indicate absence of frequency selectivity (i.e. no tuning) in homozygotes (MGI Ref ID J:105502)
      • at 1-2 months of age, homozygotes of the F3-F5 generation display significant increases in CAP thresholds relative to wild-type mice, ranging from ~35 dB at 3.2 kHz to ~55 dB at 16 kHz (MGI Ref ID J:124148)
      • however, homozygotes with the highest CAP thresholds show no measurable ear canal distortions, even at the highest SPLs (MGI Ref ID J:124148)
    • short cochlear outer hair cells (MGI Ref IDs J:79029, J:91680)
      • at 7-9 weeks, homozygotes exhibit a decrement in OHC lengths in all cochlear turns while hair bundle morphology on all three rows of OHCs is normal (MGI Ref ID J:79029)
      • at P21 (when OHC loss is minimal but ABR thresholds are elevated), mutant OHCs display reduced cell length (MGI Ref ID J:91680)
      • however, no ultrastructural abnormalities in sterocilla, lateral wall, tight junction or synapses are noted at P21 (MGI Ref ID J:91680)
  • growth/size phenotype
    • decreased body weight (MGI Ref ID J:79029)
      • at 1 month, homozygotes are viable and behaviorally normal but display a ~15% reduction in body weight relative to wild-type littermates


The following phenotype information may relate to one or more alleles on a genetic background differing from this MMRRC strain.
Slc26a5tm1Jnz/Slc26a5tm1Jnz
        involves: 129S7/SvEvBrd
  • hearing/vestibular/ear phenotype
    • abnormal cochlear outer hair cell morphology (MGI Ref ID J:145297)
      • outer hair cell stiffness is lost
    • abnormal otoacoustic response (MGI Ref ID J:160851)
      • electrically evoked otoacoustic emissions amplitudes are nearly completely lost unlike in wild-type mice
    • increased cochlear nerve compound action potential (MGI Ref ID J:145297)
      • threshold is increased and tuning is absent
  • nervous system phenotype
    • abnormal cochlear outer hair cell morphology (MGI Ref ID J:145297)
      • outer hair cell stiffness is lost
    • increased cochlear nerve compound action potential (MGI Ref ID J:145297)
      • threshold is increased and tuning is absent

Strain of Origin: 129/SvEv (AB2.2)

Strain genetic background: 129/C57B6L/J mixed

Strain Development: Sib-mating for 6 generations since the roginal description (Liberman et al., Nature 2002).

Suggested Control Mice:

  • Wildtype littermates

Research Applications

  • Cell Biology
  • Developmental Biology
  • Models for Human Disease
  • Neurobiology
  • Sensorineural

Strain Origin

Donor: Jian Zuo, Ph.D., St. Jude Children's Research Hospital

Primary Reference:

  • Liberman MC, Gao J, He DZ, Wu X, Jia S, Zuo J. Prestin is required for electromotility of the outer hair cell and for the cochlear amplifier. Nature. 2002 Sep 19;419(6904):300-4. Epub 2002 Aug 28. PMID: 12239568 (Medline PMID: 12239568)
  • Wu X, Gao J, Guo Y, Zuo J. Hearing threshold elevation precedes hair-cell loss in prestin knockout mice. Brain Res Mol Brain Res. 2004 Jul 5;126(1):30-7. PMID: 15207913 (Medline PMID: 15207913 )
  • Cheatham MA, Huynh KH, Gao J, Zuo J, Dallos P. Cochlear function in Prestin knockout mice. J Physiol. 2004 Nov 1;560(Pt 3):821-30. Epub 2004 Aug 19. PMID: 15319415 (Medline PMID: 15319415)

Colony and Husbandry Information

Special Considerations

None

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
010570-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.

This site requires JavaScript. Tested for Firefox 3.5+, Microsoft Internet Explorer 7+, Google Chrome.

Generated: 04/24/2014