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B6.Cg-Lpcat1rd11/Boc
Stock No: 006947
  • Congenic
  • Spontaneous Mutation
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Overview

This spontaneous mutation is valuable for the study of photoreceptor and retinal degeneration, particularly the role of specific fatty acids in this process, as well as other biological processes involving fatty acid regulation by Lpcat1.

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Genetic overview

Genetic Background Generation
N5F22
(2020-04-23 00:00:00)

Lpcat1rd11

Allele Type Gene Symbol Gene Name
Spontaneous Lpcat1 lysophosphatidylcholine acyltransferase 1
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Research Applications

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Base Price

Starting at:

$277.98 Domestic price for female
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Details

Detailed Description

In Lpcat1rd11 homozygotes photoreceptors develop normally, but degenerate quickly after 21 days of age, with less than half the normal number of rows of photoreceptor nuclei remaining by 31 days of age, and even fewer at 47 days of age. By 36 days of age retinal vessels are attenuated and by 113 days of age there is clear retinal degeneration. Dark-adapted electroretinography shows a reduced rod photoreceptor a-wave at 3 weeks of age, which is flattened by 4 weeks of age. Cone photoreceptor response is normal at 3 weeks of age but substantially reduced at 4 and 5 weeks of age. Lipid extracts from retina analyzed by HPLC and mass spectrometry show that the ratio of dipalmitoylphosphatidylcholine (DPPC) to the peak lipid class is decreased from 84% in C57BL/6J to 38% in Lpcat1rd11 homozygotes. Distinctly lower levels of platelet activating factor C16 and lyso-platelet activating factor C16 were found in retinas of homozygotes compared with C57BL/6J. Administration of DPPC in the chow did not prevent retinal degeneration. The Lpcat1rd11 allele seems slightly more severe than the Lpcat1rd11-2J allele.

Selected References

  • Friedman JS; Chang B; Krauth DS; Lopez I; Waseem NH; Hurd RE; Feathers KL; Branham KE; Shaw M; Thomas GE; Brooks MJ; Liu C; Bakeri HA; Campos MM; Maubaret C; Webster AR; Rodriguez IR; Thompson DA; Bhattacharya SS; Koenekoop RK; Heckenlively JR; Swaroop A. 2010. Loss of lysophosphatidylcholine acyltransferase 1 leads to photoreceptor degeneration in rd11 mice. Proc Natl Acad Sci U S A 107(35):15523-8PubMed: 20713727MGI: J:163743
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Genetics

Lpcat1rd11

Allele Symbol: Lpcat1rd11

Allele Name retinal degeneration 11
Allele Type Spontaneous
Allele Synonym(s)
Gene Symbol and Name Lpcat1, lysophosphatidylcholine acyltransferase 1
Gene Synonym(s)
Strain of Origin B6.D2/22Ei
Chromosome 13
General Note Phenotypic Similarity to Human Syndrome: Retinal Degeneration J:229509 .
Molecular Note This spontaneous insertion of a single G residue in exon 3 causes a frame shift predicted to encode an abnormal protein sequence after amino acid 140 and a stop codon after residue 178. RT-PCR of retinal RNA shows a 3 fold decrease in expression level and western blotting fails to detect protein product.

Disease/Phenotype

Disease Terms

Research Areas By Phenotype

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

Mammalian Phenotype Terms by Genotype

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

Genotype: Lpcat1rd11/Lpcat1rd11
B6.Cg-Lpcat1/Boc

cardiovascular system phenotype

  • abnormal retinal vasculature morphology
    • fundus examination reveals attenuated retinal vessels by 36 days of age
    • (MGI Ref ID J:163743)

homeostasis/metabolism phenotype

  • abnormal phospholipid level
    • decreased retinal dipalmitoylphospatidylcholine, platelet activating factor C16 and lyso-platelet activating factor C16
    • (MGI Ref ID J:163743)

vision/eye phenotype

  • retinal degeneration
    • histologically evident at 3 weeks of age and at 4 weeks of age there are white retinal vessels
    • (MGI Ref ID J:163976)
    • treatment with gene replacement therapy (fast-acting tyrosine-capsid mutant AAV8) rescues retinal degeneration
    • (MGI Ref ID J:229509)
    • retinal degeneration by 113 days of age
    • (MGI Ref ID J:163976)
  • retinal photoreceptor degeneration
    • although histologically normal at 3 weeks of age, there is rapid photoreceptor degeneration thereafter such that by 31 days of age the number of rows of photoreceptor nuclei is diminished from 10-12 to 4-5 and at 47 days of age only one row of nuclei remain
    • (MGI Ref ID J:163743)
    • in
    • (MGI Ref ID J:163743)
    • transmission electron microscopy of retinas at 21 days of age shows that photoreceptor nuclei are less ordered than in C57BL/6J controls
    • (MGI Ref ID J:163743)
  • absent photoreceptor outer segment
      (MGI Ref ID J:229509)
  • decreased b-wave amplitude
    • scotopic and photopic b-wave amplitudes are nearly absent
    • (MGI Ref ID J:229509)
  • abnormal eye electrophysiology
    • electroretinograms are nondetectable at 2 months of age
    • (MGI Ref ID J:163976)
    • electroretinograms show a reduced dark-adapted alpha wave which flattens out at 4 weeks of age, and a light-adapted response that is normal at 3 weeks of age but significantly reduced by 4 and 5 weeks of age
    • (MGI Ref ID J:163743)
  • decreased total retina thickness
      (MGI Ref ID J:229509)
  • retinal cone cell degeneration
      (MGI Ref ID J:163743)
  • abnormal rod electrophysiology
      (MGI Ref ID J:163743)
  • abnormal ocular fundus morphology
      (MGI Ref ID J:163743)
  • abnormal retinal vasculature morphology
    • fundus examination reveals attenuated retinal vessels by 36 days of age
    • (MGI Ref ID J:163743)
  • retinal rod cell degeneration
      (MGI Ref ID J:163743)
  • thin retinal outer plexiform layer
      (MGI Ref ID J:229509)
  • abnormal cone electrophysiology
      (MGI Ref ID J:163743)
  • abnormal electroretinogram waveform feature
    • both scotopic and photopic ERG responses are nearly absent
    • (MGI Ref ID J:229509)
  • abnormal vision
    • mice show increased latency time to escape to the platform under room light conditions and under very dim light conditions in the water maze visually-guided behavioral test
    • (MGI Ref ID J:229509)
  • thin retinal outer nuclear layer
    • outer nuclear layer is nearly absent, with only one incomplete layer of nuclei in the outer nuclear layer
    • (MGI Ref ID J:229509)

nervous system phenotype

  • absent photoreceptor outer segment
      (MGI Ref ID J:229509)
  • retinal photoreceptor degeneration
    • transmission electron microscopy of retinas at 21 days of age shows that photoreceptor nuclei are less ordered than in C57BL/6J controls
    • (MGI Ref ID J:163743)
    • although histologically normal at 3 weeks of age, there is rapid photoreceptor degeneration thereafter such that by 31 days of age the number of rows of photoreceptor nuclei is diminished from 10-12 to 4-5 and at 47 days of age only one row of nuclei remain
    • (MGI Ref ID J:163743)
    • in
    • (MGI Ref ID J:163743)
  • retinal cone cell degeneration
      (MGI Ref ID J:163743)
  • retinal rod cell degeneration
      (MGI Ref ID J:163743)

References

  • Friedman JS; Chang B; Krauth DS; Lopez I; Waseem NH; Hurd RE; Feathers KL; Branham KE; Shaw M; Thomas GE; Brooks MJ; Liu C; Bakeri HA; Campos MM; Maubaret C; Webster AR; Rodriguez IR; Thompson DA; Bhattacharya SS; Koenekoop RK; Heckenlively JR; Swaroop A. 2010. Loss of lysophosphatidylcholine acyltransferase 1 leads to photoreceptor degeneration in rd11 mice. Proc Natl Acad Sci U S A 107(35):15523-8PubMed: 20713727MGI: J:163743

Additional References

  • Chang B; Hawes NL; Hurd RE; Wang J; Howell D; Davisson MT; Roderick TH; Nusinowitz S; Heckenlively JR. 2005. Mouse models of ocular diseases. Vis Neurosci 22(5):587-93PubMed: 16332269MGI: J:156373
  • Hawes NL; Chang B; Hurd RE; Nusinowitz JR; Heckenlively JR; Davisson MT. 2002. A new mouse model of retinal degeneration (rd11) Invest Ophthalmol Vis Sci 43(13):3669MGI: J:163976

Additional - Lpcat1rd11 related

Technical Support

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  • Citation

    When using the B6.Cg-Lpcat1rd11/Boc mouse strain in a publication, please cite the originating article(s) and include JAX stock #006947 in your Materials and Methods section.

Animal Health Reports

Facility Barrier Level Descriptions

MGL277 (Low)

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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. We do not guarantee breeding performance and therefore suggest that investigators order more than one breeding pair to avoid delays in their research.

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