Overview

These C57BL/6-plt mice harbor the spontaneous plt (or "paucity of lymph node T cells") deletion of the Ccl19 and Ccl21a loci on chromosome 4. Lack of expression of these two CCR7 receptor ligands in the secondary lymphoid organs results in abnormal leukocyte migration and impaired immune response. These mutant mice may be useful in studying leukocyte migration into lymphatic tissues, elucidating differences between T cell and B cell trafficking, and the role of stromal cells in bringing naive T cells and dendritic cells together for the initiation of immune responses.

Donating Investigator

Hideki Nakano, NIEHS/NIH

Genetic overview

Genetic Background	Generation

plt

Allele Type	Gene Symbol	Gene Name
Spontaneous	plt	paucity of lymph node T cells

View Genetics

Research Applications

Research Tools
Immunology, Inflammation and Autoimmunity Research
Developmental Biology Research
Internal/Organ Research
Cardiovascular Research
Hematological Research
Cancer Research

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Base Price

Starting at:

$2,854.50 Domestic price Cryo Recovery

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Details

Detailed Description

Homozygous C57BL/6-plt mice are viable and fertile, harboring the spontaneous plt (or "paucity of lymph node T cells") deletion of both the Ccl19 and Ccl21a loci on chromosome 4. Lack of expression of these two CCR7 ligands in the secondary lymphoid organs results in abnormal leukocyte migration and impaired immune response. Specifically, homozygous mice have disrupted trafficking/homing of T cells and dendritic cells to lymphoid tissues. No reported abnormalities in B cell distribution/cellularity are reported for homozygous mice. Transient migration of antigen-stimulated B cells in lymphoid organs (which facilitates B cell/helper T cell interactions) is also impaired in homozygous mice. Homozygous mice exhibit mature single-positive thymocyte arrest in the thymic cortex that results in defective formation of the medullary region of the thymus. Thymic export of T cells in these mice is compromised during the neonatal period but not in adulthood. While CCL21 expression is absent in lymphoid organs because of the Ccl21a deletion, CCL21 expression in non-lymphoid organs is observed because the upstream Cc121b locus remains intact. These C57BL/6-plt mice may be useful in studying leukocyte migration into lymphatic tissues, elucidating differences between T cell and B cell trafficking, and the role of stromal cells in bringing naive T cells and dendritic cells together for the initiation of immune responses.

The donating investigator provided these C57BL/6-plt mice, as well as plt mice congenic on a BALB/c genetic background (BALB/c-plt ; Stock No. 012873). The donating investigator reports dendritic cell migration is severely impaired in both homozygous strains. In addition, they report T cell homing to lymph nodes is severely impaired in BALB/c-plt homozygotes, but mildly impaired in C57BL/6-plt homozygotes. BALB/c-plt homozygous mice have been shown to allow enhanced survival of MHC-mismatched islet allografts (this phenotype is not characterized for C57BL/6-plt mice)[July 2010]).

Development

In 1997, Dr. Hideki Nakano (while at the Laboratory Animal Research Center, University of Tokyo, Japan) reported that their colony of DDD/1 inbred mice exhibited greatly diminished T cell numbers in lymph nodes. This spontaneous deletion, designated plt (or "paucity of lymph node T cells"), behaves as a single autosomal recessive allele and deletes a portion of chromosome 4 including both the Ccl19 (Epstein-Barr virus-induced molecule-1 ligand chemokine [ELC], ELC-atg, or Scya19) and Ccl21a (6CKine-ser, 6CKBAC2, secondary lymphoid organ chemokine [SLC], SLC-Ser) loci. Some plt-mutant mice were backcrossed to C57BL/6NCrl for eleven generations to generate the C57BL6-plt congenic strain. Dr. Hideki Nakano (while at NIEHS/NIH, Research Triangle Park. North Carolina USA) sent homozygous C57BL6-plt females and males to The Jackson Laboratory Repository in 2010. Upon arrival, C57BL6-plt mice were bred together to maintain the colony. During backcrossing, the Y chromosome may not have been fixed to the C57BL/6NCrl genetic background.

The donating investigator reports that C57BL6-plt mice should have retained the plt haplotype at the Chemokine Locus on Mouse Chromosome 4 (Cklc4^plt). Thus the genomic organization of Cklc4 would be the same as DDD/1-plt mice: Ccl21b intact and functional (Ccl21a deleted), Scya19-ps1 (Ccl19-ps1) intact (Scya19 [Ccl19] deleted), Scya27a (Ccl27a) intact and functional, and Il11ra1 intact and functional. The Jackson Laboratory will verify these mice harbor the plt deletion, but will not extensively verify the genetic composition of the other loci described for the Cklc4^plt haplotype. The Cklc4^plt haplotype will need to be verified by the investigator using the mice if necessary.

Control Suggestions

Approximate Controls

005304 C57BL/6NJ

Additional Information

Considerations for Choosing Controls

Selected References

Gunn MD; Kyuwa S; Tam C; Kakiuchi T; Matsuzawa A; Williams LT ; Nakano H. 1999. Mice lacking expression of secondary lymphoid organ chemokine have defects in lymphocyte homing and dendritic cell localization [see comments] J Exp Med 189(3):451-60PubMed: 9927507 MGI: J:52567
Junt T; Nakano H; Dumrese T; Kakiuchi T; Odermatt B; Zinkernagel RM; Hengartner H; Ludewig B. 2002. Antiviral immune responses in the absence of organized lymphoid T cell zones in plt/plt mice. J Immunol 168(12):6032-40PubMed: 12055211 MGI: J:76943
Luther SA; Tang HL; Hyman PL; Farr AG; Cyster JG. 2000. Coexpression of the chemokines ELC and SLC by T zone stromal cells and deletion of the ELC gene in the plt/plt mouse Proc Natl Acad Sci U S A 97(23):12694-9PubMed: 11070085 MGI: J:65808
Nakano H; Gunn MD. 2001. Gene duplications at the chemokine locus on mouse chromosome 4: multiple strain-specific haplotypes and the deletion of secondary lymphoid-organ chemokine and EBI-1 ligand chemokine genes in the plt mutation J Immunol 166(1):361-9PubMed: 11123313 MGI: J:66381
Nakano H; Mori S; Yonekawa H; Nariuchi H; Matsuzawa A; Kakiuchi T. 1998. A novel mutant gene involved in T-lymphocyte-specific homing into peripheral lymphoid organs on mouse chromosome 4. Blood 91(8):2886-95PubMed: 9531599 MGI: J:47460
Nakano H; Tamura T; Yoshimoto T; Yagita H; Miyasaka M; Butcher EC; Nariuchi H; Kakiuchi T; Matsuzawa A. 1997. Genetic defect in T lymphocyte-specific homing into peripheral lymph nodes. Eur J Immunol 27(1):215-21PubMed: 9022021 MGI: J:47819
Ueno T; Saito F; Gray DH; Kuse S; Hieshima K; Nakano H; Kakiuchi T; Lipp M; Boyd RL; Takahama Y. 2004. CCR7 signals are essential for cortex-medulla migration of developing thymocytes. J Exp Med 200(4):493-505PubMed: 15302902 MGI: J:93960
Vassileva G; Soto H; Zlotnik A; Nakano H; Kakiuchi T; Hedrick JA; Lira SA. 1999. The reduced expression of 6Ckine in the plt mouse results from the deletion of one of two 6Ckine genes. J Exp Med 190(8):1183-8PubMed: 10523616 MGI: J:58157
Wang L; Han R; Lee I; Hancock AS; Xiong G; Gunn MD; Hancock WW. 2005. Permanent survival of fully MHC-mismatched islet allografts by targeting a single chemokine receptor pathway. J Immunol 175(10):6311-8PubMed: 16272282 MGI: J:119345

View All References

Genetics

plt

Allele Symbol: plt

Allele Name	paucity of lymph node T-cells
Allele Type	Spontaneous
Allele Synonym(s)
Gene Symbol and Name	plt, paucity of lymph node T cells
Gene Synonym(s)
Strain of Origin	DDD/1
Chromosome	4
Molecular Note	This mutation is a deletion region on chromosome 4 which includes the Ccl19 and Ccl21a genes (see also revised nomenclature for the Ccl21 family of genes).
Mutations Made By	Hideki Nakano, NIEHS/NIH

Disease/Phenotype

Disease Terms

Models with phenotypic similarity to human diseases where etiology is unknown or involving genes where ortholog is unknown.

Sjogren's syndrome

Research Areas By Phenotype

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

Research Tools
- Immunology, Inflammation and Autoimmunity Research
  - genes regulating susceptibility to infectious disease and endotoxin
  - T cell deficiency
  - specific T cell deficiency
  - T cell deficiency, xenograft/transplant host
- Cancer Research
  - T cell deficiency
  - specific T cell deficiency
  - xenograft/transplant host
- Toxicology Research
  - xenograft/transplant host
Immunology, Inflammation and Autoimmunity Research
- Immunodeficiency
  - specific T cell deficiency
  - T cell deficiency
  - multiple immune defects
- CD Antigens, Antigen Receptors, and Histocompatibility Markers
  - genes regulating susceptibility to infectious disease and endotoxin
- Lymphoid Tissue Defects
  - Lymphocyte Homing
  - selective lymph node development defects
- Growth Factors/Receptors/Cytokines
- Graft vs. Host Disease
Developmental Biology Research
- Internal/Organ Defects
  - Lymphoid Tissue Defects
- Lymphoid Tissue Defects
Internal/Organ Research
- Lymphoid Tissue Defects
  - T cell deficiency
Cardiovascular Research
- Vascular Defects
  - defective leukocyte function
Hematological Research
- Immunological Defects
Cancer Research
- Toxicology
  - xenograft/transplant host

Mammalian Phenotype Terms by Genotype

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

Genotype: plt/plt
C.DDD-plt

hematopoietic system phenotype

decreased single-positive T cell number
- the amount of CD4+ or CD8+ T cells are decreased in lymph nodes compared to in wild-type mice
- Normal - however, remaining single positive cells undergo normal activation and proliferation alloresponses

abnormal T cell activation
- mice exhibit impaired T cell activation following receipt of islet allografts compared to wild-type mice
- Normal - however, T cell alloresponses are normal

immune system phenotype

increased length of allograft survival
- Normal - however, cardiac allografts are rejected at the same tempo as in wild-type mice
- unlike in wild-type mice, cardiac allograft survival time is doubled after the spleen is removed
- islet allografts function for over 120 days compared to in wild-type mice in which rejection occurs at 14 days

decreased single-positive T cell number
- Normal - however, remaining single positive cells undergo normal activation and proliferation alloresponses
- the amount of CD4+ or CD8+ T cells are decreased in lymph nodes compared to in wild-type mice

abnormal T cell activation
- mice exhibit impaired T cell activation following receipt of islet allografts compared to wild-type mice
- Normal - however, T cell alloresponses are normal

Genotype: plt/plt
involves: DDD/1

cellular phenotype

abnormal leukocyte migration
- Normal - however, neutrophil and macrophage recruitment stimulated by thioglycolate is normal
- T cell migration into peripheral lymph nodes, Peyer's patches and the spleen is defective
- T cell migration into lymph nodes is defective

immune system phenotype

abnormal peripheral lymph node morphology
- the amount of T cells in the subcortical area is extremely low

decreased single-positive T cell number
- the number of either CD4+ or CD8+ T cells is decreased compared to in CBA, B6, C3H and BALB/c mice

increased memory T cell number
- the number of T cells in the peripheral lymph nodes and Peyer's patches with memory phenotype is increased compared to in wild-type mice

abnormal spleen white pulp morphology
- unlike in wild-type spleens, few T cells are found within the white pulp

lymph node hypoplasia
- the number of lymph node cells is reduced by 10 and 6 times in males and females, respectively, than in CBA and B6 mice
- T cell cellularity within the peripheral lymph nodes is decreased

abnormal immune system physiology

abnormal leukocyte migration
- T cell migration into lymph nodes is defective
- Normal - however, neutrophil and macrophage recruitment stimulated by thioglycolate is normal
- T cell migration into peripheral lymph nodes, Peyer's patches and the spleen is defective

abnormal lymph node T cell domain morphology
- T cells are hardly observed in T cell zones but are observed in B cell zones
- low density of T cells in subcortical area

abnormal leukocyte cell number

abnormal spleen red pulp morphology
- unlike in wild-type spleens, T cells are found within the red pulp

decreased T cell number
- the total number of T cells in lymph nodes is smaller than in BALB/c mice

increased T cell number
- the number of T cells in the blood and spleen is increased compared to in wild-type mice

small Peyer's patches
- most Peyer's patches are smaller than in wild-type mice

abnormal immune system organ morphology

hematopoietic system phenotype

abnormal leukocyte migration
- Normal - however, neutrophil and macrophage recruitment stimulated by thioglycolate is normal
- T cell migration into peripheral lymph nodes, Peyer's patches and the spleen is defective
- T cell migration into lymph nodes is defective

increased memory T cell number
- the number of T cells in the peripheral lymph nodes and Peyer's patches with memory phenotype is increased compared to in wild-type mice

abnormal spleen white pulp morphology
- unlike in wild-type spleens, few T cells are found within the white pulp

abnormal leukocyte cell number

abnormal spleen red pulp morphology
- unlike in wild-type spleens, T cells are found within the red pulp

decreased single-positive T cell number
- the number of either CD4+ or CD8+ T cells is decreased compared to in CBA, B6, C3H and BALB/c mice

decreased T cell number
- the total number of T cells in lymph nodes is smaller than in BALB/c mice

increased T cell number
- the number of T cells in the blood and spleen is increased compared to in wild-type mice

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

Genotype: plt/plt
B6.DDD-plt

cellular phenotype

abnormal leukocyte migration
- single positive T cells are retained in the cortex of the thymus
- single positive T cells fail to localize to the medulla of the thymus in newborns

immune system phenotype

abnormal thymus cortex morphology
- single positive thymocytes are retained by the cortex rather than migrating to the medulla

abnormal leukocyte migration
- single positive T cells are retained in the cortex of the thymus
- single positive T cells fail to localize to the medulla of the thymus in newborns

small thymus medulla
- medullary volume is about 50% that found in controls
- reduced in size in the adult thymus

mammalian phenotype

immune system phenotype
- Normal - no single positive T cell abnormalities other than the migration defect from cortex to medulla of the thymus

endocrine/exocrine gland phenotype

abnormal thymus cortex morphology
- single positive thymocytes are retained by the cortex rather than migrating to the medulla

small thymus medulla
- medullary volume is about 50% that found in controls
- reduced in size in the adult thymus

hematopoietic system phenotype

abnormal thymus cortex morphology
- single positive thymocytes are retained by the cortex rather than migrating to the medulla

abnormal leukocyte migration
- single positive T cells are retained in the cortex of the thymus
- single positive T cells fail to localize to the medulla of the thymus in newborns

small thymus medulla
- medullary volume is about 50% that found in controls
- reduced in size in the adult thymus

Genotype: plt/plt
either: B6.DDD-plt or C.DDD-plt

cellular phenotype

abnormal leukocyte migration
- FTY720-treated mice exhibit an accumulation of mature thymocytes in the cortex rather than medulla of the thymus as in similarly treated wild-type mice

endocrine/exocrine gland phenotype

lacrimal gland inflammation
- lacrimal glands exhibit periductal lymphocyte infiltration unlike in wild-type mice
- mice exhibit dacryoadenitis unlike wild-type mice

abnormal gland morphology
- as early as 5 weeks of age, mice exhibit lesions in exocrine glands unlike wild-type mice

abnormal parotid gland morphology
- mice exhibit parotid gland tissue damage associated with inflammation unlike wild-type mice

parotid gland inflammation
- parotid glands exhibit periductal lymphocyte infiltration unlike in wild-type mice

abnormal submandibular gland morphology
- mice exhibit submandibular gland tissue damage associated with inflammation unlike wild-type mice

salivary gland inflammation
- mice exhibit sialadenitis unlike wild-type mice

abnormal lacrimal gland morphology
- lacrimal glands exhibit periductal lymphocyte infiltration causing destruction of acinar cells unlike in wild-type mice

submandibular gland inflammation
- submandibular glands exhibit periductal lymphocyte infiltration unlike in wild-type mice

hematopoietic system phenotype

abnormal leukocyte migration
- FTY720-treated mice exhibit an accumulation of mature thymocytes in the cortex rather than medulla of the thymus as in similarly treated wild-type mice

homeostasis/metabolism phenotype

abnormal physiological response to xenobiotic
- FTY720-treated mice exhibit an accumulation of mature thymocytes in the cortex rather than medulla of the thymus as in similarly treated wild-type mice

immune system phenotype

parotid gland inflammation
- parotid glands exhibit periductal lymphocyte infiltration unlike in wild-type mice

increased susceptibility to autoimmune disorder
- mice exhibit autoimmune exocrinopathy unlike wild-type mice

abnormal leukocyte migration
- FTY720-treated mice exhibit an accumulation of mature thymocytes in the cortex rather than medulla of the thymus as in similarly treated wild-type mice

submandibular gland inflammation
- submandibular glands exhibit periductal lymphocyte infiltration unlike in wild-type mice

lacrimal gland inflammation
- lacrimal glands exhibit periductal lymphocyte infiltration unlike in wild-type mice
- mice exhibit dacryoadenitis unlike wild-type mice

increased inflammatory response

salivary gland inflammation
- mice exhibit sialadenitis unlike wild-type mice

vision/eye phenotype

abnormal lacrimal gland morphology
- lacrimal glands exhibit periductal lymphocyte infiltration causing destruction of acinar cells unlike in wild-type mice

lacrimal gland inflammation
- mice exhibit dacryoadenitis unlike wild-type mice
- lacrimal glands exhibit periductal lymphocyte infiltration unlike in wild-type mice

digestive/alimentary phenotype

salivary gland inflammation
- mice exhibit sialadenitis unlike wild-type mice

abnormal parotid gland morphology
- mice exhibit parotid gland tissue damage associated with inflammation unlike wild-type mice

abnormal submandibular gland morphology
- mice exhibit submandibular gland tissue damage associated with inflammation unlike wild-type mice

parotid gland inflammation
- parotid glands exhibit periductal lymphocyte infiltration unlike in wild-type mice

submandibular gland inflammation
- submandibular glands exhibit periductal lymphocyte infiltration unlike in wild-type mice

References

Gunn MD; Kyuwa S; Tam C; Kakiuchi T; Matsuzawa A; Williams LT ; Nakano H. 1999. Mice lacking expression of secondary lymphoid organ chemokine have defects in lymphocyte homing and dendritic cell localization [see comments] J Exp Med 189(3):451-60PubMed: 9927507 MGI: J:52567
Junt T; Nakano H; Dumrese T; Kakiuchi T; Odermatt B; Zinkernagel RM; Hengartner H; Ludewig B. 2002. Antiviral immune responses in the absence of organized lymphoid T cell zones in plt/plt mice. J Immunol 168(12):6032-40PubMed: 12055211 MGI: J:76943
Luther SA; Tang HL; Hyman PL; Farr AG; Cyster JG. 2000. Coexpression of the chemokines ELC and SLC by T zone stromal cells and deletion of the ELC gene in the plt/plt mouse Proc Natl Acad Sci U S A 97(23):12694-9PubMed: 11070085 MGI: J:65808
Nakano H; Gunn MD. 2001. Gene duplications at the chemokine locus on mouse chromosome 4: multiple strain-specific haplotypes and the deletion of secondary lymphoid-organ chemokine and EBI-1 ligand chemokine genes in the plt mutation J Immunol 166(1):361-9PubMed: 11123313 MGI: J:66381
Nakano H; Mori S; Yonekawa H; Nariuchi H; Matsuzawa A; Kakiuchi T. 1998. A novel mutant gene involved in T-lymphocyte-specific homing into peripheral lymphoid organs on mouse chromosome 4. Blood 91(8):2886-95PubMed: 9531599 MGI: J:47460
Nakano H; Tamura T; Yoshimoto T; Yagita H; Miyasaka M; Butcher EC; Nariuchi H; Kakiuchi T; Matsuzawa A. 1997. Genetic defect in T lymphocyte-specific homing into peripheral lymph nodes. Eur J Immunol 27(1):215-21PubMed: 9022021 MGI: J:47819
Ueno T; Saito F; Gray DH; Kuse S; Hieshima K; Nakano H; Kakiuchi T; Lipp M; Boyd RL; Takahama Y. 2004. CCR7 signals are essential for cortex-medulla migration of developing thymocytes. J Exp Med 200(4):493-505PubMed: 15302902 MGI: J:93960
Vassileva G; Soto H; Zlotnik A; Nakano H; Kakiuchi T; Hedrick JA; Lira SA. 1999. The reduced expression of 6Ckine in the plt mouse results from the deletion of one of two 6Ckine genes. J Exp Med 190(8):1183-8PubMed: 10523616 MGI: J:58157
Wang L; Han R; Lee I; Hancock AS; Xiong G; Gunn MD; Hancock WW. 2005. Permanent survival of fully MHC-mismatched islet allografts by targeting a single chemokine receptor pathway. J Immunol 175(10):6311-8PubMed: 16272282 MGI: J:119345

Additional - plt related

Technical Support

CONTACT TECHNICAL SUPPORT

Genotyping Protocols
- Standard PCR:plt/Nkno (D4Mit286)
- Standard PCR:plt/Nkno (D4Mit237)
- Genotyping resources and troubleshooting
Breeding Considerations

When maintaining a live colony, homozygous mice may be bred together.
- Additional Breeding and Husbandry Support
Citation
When using the B6N.DDD-plt/NknoJ mouse strain in a publication, please cite the originating article(s) and include JAX stock #012866 in your Materials and Methods section.

Animal Health Reports

Facility Barrier Level Descriptions

Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200

Pricing & Availability

Cryo Recovery

Domestic
International

Live Mouse

Age

Genotype

Price

weeks

Cryorecovery - Pricing

Service/Product	Description	Price
> >	Heterozygous for plt

Related Products and Services

Frozen Mouse Embryo	B6N.DDD-plt/NknoJ Frozen Embryo	$2595.00
Frozen Mouse Embryo	B6N.DDD-plt/NknoJ Frozen Embryo	$2595.00
Frozen Mouse Embryo	B6N.DDD-plt/NknoJ Frozen Embryo	$3373.50
Frozen Mouse Embryo	B6N.DDD-plt/NknoJ Frozen Embryo	$3373.50

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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.

Terms Of Use

General Terms and Conditions

Questions about Terms of Use

Licensing Information

Phone: 207-288-6470

Email: TechTran@jax.org

Donating Investigator

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Control Suggestions

Approximate Controls

Additional Information

Selected References

plt

Allele Symbol: plt

Disease Terms

Models with phenotypic similarity to human diseases where etiology is unknown or involving genes where ortholog is unknown.

Research Areas By Phenotype

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

Mammalian Phenotype Terms by Genotype

Genotype: plt/pltC.DDD-plt

hematopoietic system phenotype

immune system phenotype

Genotype: plt/pltinvolves: DDD/1

cellular phenotype

immune system phenotype

hematopoietic system phenotype

Genotype: plt/pltB6.DDD-plt

cellular phenotype

immune system phenotype

mammalian phenotype

endocrine/exocrine gland phenotype

hematopoietic system phenotype

Genotype: plt/plteither: B6.DDD-plt or C.DDD-plt

cellular phenotype

endocrine/exocrine gland phenotype

hematopoietic system phenotype

homeostasis/metabolism phenotype

immune system phenotype

vision/eye phenotype

digestive/alimentary phenotype

References

Additional - plt related

Genotyping Protocols

Breeding Considerations

Citation

Animal Health Reports

Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200

Live Mouse

Cryorecovery - Pricing

Related Products and Services

Payment Terms and Conditions

The Jackson Laboratory's Genotype Promise

Terms Of Use

Licensing Information

Genotype: plt/plt
C.DDD-plt

Genotype: plt/plt
involves: DDD/1

Genotype: plt/plt
B6.DDD-plt

Genotype: plt/plt
either: B6.DDD-plt or C.DDD-plt