Overview

This strain combines the semidominant transgene insertion, Krd with the wild type allele of Pde6b. Mice heterozygous for Krd have a high incidence of kidney defects including aplastic, hypoplastic, and cystic kidneys. Retinal defects include abnormal electroretinograms and a reduction of cell numbers that is most extreme in the inner cell and ganglion layers. Homozygosity results in early embryonic lethality.

Genetic overview

Genetic Background	Generation
	+F21 (2020-04-23 00:00:00)

Krd

Allele Type
Transgenic

Pde6b⁺

Allele Type	Gene Symbol	Gene Name
Not Applicable	Pde6b	phosphodiesterase 6B, cGMP, rod receptor, beta polypeptide

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Research Applications

Sensorineural Research
Mouse/Human Gene Homologs
Internal/Organ Research

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Base Price

Starting at:

$205.71 Domestic price for female

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Details

Important Note

This strain carries a Chromosome 19 deletion that includes: Abcc2, Fgf8, Nkx2-3, Pax2, Scd1, Tlx1, Wnt8b, and Hps1^ep. This congenic is homozygous for the wildtype Pde6b⁺ allele.

Detailed Description

This strain combines the semidominant transgene insertion, Krd with the wild type allele of Pde6b. Mice heterozygous for Krd have a high incidence of kidney defects including aplastic, hypoplastic, and cystic kidneys. Retinal defects include abnormal electroretinograms and a reduction of cell numbers that is most extreme in the inner cell and ganglion layers. Homozygosity results in early embryonic lethality.

Development

(C57BL/6J x C3H)F1 eggs were microinjected with an amylase/rat elastase/chloramphenicol acetyltransferase construct and the founders were bred to C57BL/6J, then to YBR (Johnson et al., 1993). This strain came to The Jackson Laboratory from Dr. Miriam Meisler at the University of Michigan in 1995 as STOCK Tg8052/C3H at N2 to C3H. At The Jackson Laboratory it was bred to C3HeB/FeJ, then one generation to BALB/cByJ. The Krd/+ F1 offspring were then mated with C3.BliA-Pde6b⁺ (001912) at each generation to produce the congenic C3.BLiA-Pde6b⁺ -Krd/+ (002802) that we currently offer. The X and Y chromosomes from C3.BliA-Pde6b⁺ (001912) were captured and fixed in 002802 within the first 3 backcross generations. Since 1995 the Krd/+ breeders were selected primarily by expression of the retinal degeneration phenotype. This strain has passed through only approximately 2 generations per year.

Expression Data

Expressed Gene	Pde6b, phosphodiesterase 6B, cGMP, rod receptor, beta polypeptide, mouse, laboratory
Site of Expression	Retina.

Control Suggestions

Wild-type from the colony
001912 C3A.BLiA-Pde6b⁺/J

Additional Information

Considerations for Choosing Controls

Genetics

Krd

Allele Symbol: Krd

Allele Name	kidney and retinal defects
Allele Type	Transgenic
Allele Synonym(s)	Tg8052
Gene Symbol and Name	Krd, kidney and retinal defects
Gene Synonym(s)
Strain of Origin	Not Specified
Chromosome	19
Molecular Note	The phenotype of this mouse has been attributed to a 7 cM transgene induced deletion, Del(19)TgN8052Mm, which includes the Pax2 and Pkd2l1. The transgene inserted into a LINE element in the distal region of Chromosome 19. The Scd1 and pale ear Hps1 genes are also deleted in Del(19)TgN8052Mm mice, along with several D19Mit markers.

Pde6b⁺

Allele Symbol: Pde6b⁺

Allele Name	wild type
Allele Type	Not Applicable
Allele Synonym(s)
Gene Symbol and Name	Pde6b, phosphodiesterase 6B, cGMP, rod receptor, beta polypeptide
Gene Synonym(s)
Expressed Gene	Pde6b, phosphodiesterase 6B, cGMP, rod receptor, beta polypeptide, mouse, laboratory
Site of Expression	Retina.
Strain of Origin	Not Applicable
Chromosome	5

Disease/Phenotype

Disease Terms

Research Areas By Phenotype

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

Genotype: Krd related

Sensorineural Research
- Eye Defects
Internal/Organ Research
- Kidney Defects

Genotype: Pde6b⁺ related

Mouse/Human Gene Homologs
- retinitis pigmentosa, wildtype
Sensorineural Research
- Retinal Degeneration
  - wild-type

Mammalian Phenotype Terms by Genotype

The following phenotype information is associated with a similar, but not exact match to this JAX^® Mice strain

Genotype: Krd/Krd⁺
involves: C3H/He * C57BL/6 * YBR/Ki

growth/size/body region phenotype

slow postnatal weight gain
- normal weight is eventually reached
- the growth of these mice is retarded for the first 2 months of birth being about 80% of littermate controls

vision/eye phenotype

abnormal eye electrophysiology
- both a- and b- waves are abnormal in mice in affected mice
- the electroretinograms of eight mice varied from three in low normal range to three that are extremely abnormal

abnormal retinal layer morphology
- retinas of some mice are noticeably thinner than controls, with extreme hypocellularity occurring in different positions in the retina

disorganized retinal layers
- all mice contain malformations of the retina
- rs
- these malformations differed between animals but include zones of narrowing, an excess of somota in a single nuclear layer, photoreceptor nuclei lying ectopically within the photoreceptor layer, and rosettes of photoreceptors enclosed between retinal layers

thin retinal inner nuclear layer
- the nuclear layers are thinner with fewer somata present than in controls

thin retinal outer nuclear layer
- the nuclear layers are thinner with fewer somata present than in controls

mortality/aging

postnatal lethality
- Background Sensitivity - lethality in the backcrosses to C57BL/6 occurs in the late fetal or early postnatal stage with at least some of the mice dying from kidney aplasia
- Background Sensitivity - percentages of transgenic offspring are closer to expected rates when founder mice are crossed with C3H/HeJ mice with 46% being transgenic in the 2^nd backcross and 42% being transgenic in the 3^rd backcross
- Background Sensitivity - the expected 50% transgenic offspring are observed at weaning when the founder mice are crossed with C57BL/6
- Background Sensitivity - the percentage of transgenic offspring fall in subsequent backcrosses to C57BL/6 with 35% being transgenic in the 2^nd backcross, 19% being transgenic in the 3^rd backcross, and 11% being transgenic in the 4^th

renal/urinary system phenotype

abnormal kidney corticomedullary boundary morphology
- immature mesenchymal tissue is more prominent at the corticomedullary junction

abnormal nephrogenic zone morphology
- the nephrogenic zone is attenuated and disorganized

absent kidney
- kidneys were absent in one stillborn pup that occurred among 24 observed births

decreased kidney weight
- kidneys with no obvious defects weigh significantly less with a mean of 4.8 mg/g bodyweight compared to 6.2 mg/g for kidneys from littermate controls

decreased nephron number
- the number of mature nephrons is smaller

delayed kidney development
- immature mesenchymal tissue is more prominent at the corticomedullary junction
- kidneys from these mice demonstrate considerable immaturity compared with wild-type mice
- the nephrogenic zone is attenuated and disorganized
- the thickness of the cortical tissue is decreased due in part to less numbers of glomeruli and a smaller profile of proximal convoluted tubules
- these immature features are still present at a lesser degree in mice 4 days old but disappear by adulthood

dilated ureter
- is commonly observed

kidney cortex hypoplasia
- the thickness of the cortical tissue is decreased due in part to less numbers of glomeruli and a smaller profile of proximal convoluted tubules

kidney cysts
- unilateral kidney cysts are common in these mice

single kidney
- only one kidney is present in 13% of mice

Genotype: Krd/Krd
involves: C3H/He * C57BL/6 * YBR/Ki

mortality/aging

embryonic lethality at implantation, complete penetrance
- no homozygote embryos are present at E10.5 and the lack of resorbed embryos suggests that lethality occurs before implantation

References

Additional References

Johnson TM; Rosenberg MP; Meisler MH. 1993. An insulin-responsive element in the pancreatic enhancer of the amylase gene. J Biol Chem 268(1):464-8PubMed: 7678001 MGI: J:30983
Keller SA; Jones JM; Boyle A; Barrow LL; Killen PD; Green DG; Kapousta NV; Hitchcock PF; Swank RT; Meisler MH. 1994. Kidney and retinal defects (Krd), a transgene-induced mutation with a deletion of mouse chromosome 19 that includes the Pax2 locus. Genomics 23(2):309-20PubMed: 7835879 MGI: J:20807

Additional - Krd related

Additional - Pde6b⁺ related

Technical Support

CONTACT TECHNICAL SUPPORT

Genotyping Protocols
- Genotyping resources and troubleshooting
Mating System
- Heterozygote x +/+ sibling
- +/+ sibling x Heterozygote
- Maintained homozygous for the wildtype Pde6b⁺ allele and segregating heterozygous for Krd
Appearance
- agouti
  Related Genotype: A/A Krd/+
  
  agouti, unaffected
  Related Genotype: A/A +/+
Citation
When using the C3.Cg-Pde6b⁺ Krd/J mouse strain in a publication, please cite the originating article(s) and include JAX stock #002802 in your Materials and Methods section.

Animal Health Reports

Facility Barrier Level Descriptions

MGL277 (Low)

Pricing & Availability

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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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Genetic overview

Research Applications

Base Price

Important Note

Detailed Description

Development

Expression Data

Control Suggestions

Additional Information

Krd

Allele Symbol: Krd

Pde6b+

Allele Symbol: Pde6b+

Disease Terms

Research Areas By Phenotype

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

Genotype: Krd related

Genotype: Pde6b+ related

Mammalian Phenotype Terms by Genotype

Genotype: Krd/Krd+involves: C3H/He * C57BL/6 * YBR/Ki

growth/size/body region phenotype

vision/eye phenotype

mortality/aging

renal/urinary system phenotype

Genotype: Krd/Krdinvolves: C3H/He * C57BL/6 * YBR/Ki

mortality/aging

References

Additional References

Additional - Krd related

Additional - Pde6b+ related

Genotyping Protocols

Mating System

Appearance

Citation

Animal Health Reports

Live Mouse

Cryorecovery - Pricing

Payment Terms and Conditions

The Jackson Laboratory's Genotype Promise

Terms Of Use

Licensing Information

JAX® Mice, Products & Services Conditions of Use

No Warranty

Credit for PRODUCTS or SERVICES

Animal Care and Use for SERVICES

No Liability

Pde6b⁺

Allele Symbol: Pde6b⁺

Genotype: Pde6b⁺ related

Genotype: Krd/Krd⁺
involves: C3H/He * C57BL/6 * YBR/Ki

Genotype: Krd/Krd
involves: C3H/He * C57BL/6 * YBR/Ki

Additional - Pde6b⁺ related