Overview

Also Known As:SP-D null

These SP-D knock-out mice exhibit progressive accumulation of lung surfactant lipids and proteins and are mildly obese. They are suitable for use in applications related to lung surfactant homeostasis, innate immunity and pulmonary inflammatory response.

Donating Investigator

Anne Marie Gillespie, University of California San Francisco

Genetic overview

Genetic Background	Generation

Sftpd^tm1Haw

Allele Type	Gene Symbol	Gene Name
Targeted (Null/Knockout)	Sftpd	surfactant associated protein D

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Research Applications

Diabetes and Obesity Research
Research Tools
Neurobiology Research
Developmental Biology Research
Internal/Organ Research
Metabolism Research

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Base Price

Starting at:

$2,854.50 Domestic price Cryo Recovery

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Details

Detailed Description

The Sftpd gene encodes for the C-type lectin glycoprotein surfactant protein D, which is secreted by pulmonary alveolar type II cells and nonciliated airway cells. The protein binds and coats bacteria and viruses to promote phagocytosis. These mice carry a knock-out mutation of the Sftpd gene in which exon 2, including the translation start site, has been replaced by a PGK-NEO cassette. Mice that are homozygous for the targeted mutation are viable and fertile. No gene product (mRNA or protein) is detected by Northern or Western blot analysis of lung tissue from homozygotes. Knock-mice mice exhibit progressive accumulation of surfactant lipids, surfactant protein A, and surfactant protein B in the alveolar space. By 8 weeks of age, the alveolar phospholipid pool was 8-fold higher than wildtype controls and a 10-fold increase in the number of alveolar macrophages is observed. Homozygotes are mildly obese and exhibit hyperphagia, elevated energy consumption, redistribution of fat deposits and insulin resistance. Knock-out mice have a 2 fold increase in basal levels of systemic gram negative bacterial endotoxin when compared to controls. During backcrossing, the Y chromosome may not have been fixed to the C57BL/6 genetic background.

Development

A targeting vector containing a PGK-NEO cassette was used to disrupt exon 2. The construct was electroporated into C57BL/6J x (Rb(11.16)2H x Rb(16.17)32Lub)F1 derived CB1-4 embryonic stem (ES) cells. Correctly targeted ES cells were injected into CD-1 blastocysts.
The resulting chimeric male animals were crossed to albino CD-1 female mice, and then backcrossed to C57BL/6 for at least 10 generations.
Upon arrival at The Jackson Laboratory, the mice were crossed to C57BL/6J (Stock No. 000664) at least once to establish the colony.

Control Suggestions

000664 C57BL/6J

Additional Information

Considerations for Choosing Controls

Selected References

Botas C; Poulain F; Akiyama J; Brown C; Allen L; Goerke J; Clements J; Carlson E; Gillespie AM; Epstein C; Hawgood S. 1998. Altered surfactant homeostasis and alveolar type II cell morphology in mice lacking surfactant protein D. Proc Natl Acad Sci U S A 95(20):11869-74PubMed: 9751757 MGI: J:50147

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Genetics

Sftpd^tm1Haw

Allele Symbol: Sftpd^tm1Haw

Allele Name	targeted mutation 1, Samuel Hawgood
Allele Type	Targeted (Null/Knockout)
Allele Synonym(s)	Sftpd^-; SP-D-; Spd-
Gene Symbol and Name	Sftpd, surfactant associated protein D
Gene Synonym(s)
Strain of Origin	C57BL/6J x (Rb(11.16)2H x Rb(16.17)32Lub)F1
Chromosome	14
Molecular Note	Replacement of exon 2 with a neomycin cassette.

Disease/Phenotype

Disease Terms

Research Areas By Phenotype

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

Diabetes and Obesity Research
- Insulin Resistance
Research Tools
- Diabetes and Obesity Research
- Metabolism Research
Neurobiology Research
- Behavioral and Learning Defects
Developmental Biology Research
- Internal/Organ Defects
  - lung
Internal/Organ Research
- Lung Defects
Metabolism Research

Mammalian Phenotype Terms by Genotype

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

Genotype: Sftpd^tm1Haw/Sftpd^tm1Haw
involves: C57BL/6J * CD-1

hematopoietic system phenotype

abnormal alveolar macrophage morphology
- at 8 and 24 weeks, homozygotes exhibit a 4- and 10-fold increase in BAL alveolar macrophage number, respectively
- by 8 weeks, homozygotes exhibit a significant increase in alveolar macrophage size, with many macrophages being both multinucleated and foamy in appearance

abnormal macrophage physiology
- consistent with emphysema-like changes, homozygotes exhibit a significant increase in macrophage activation, as shown by increased MMP-12 expression in alveolar macrophages (>300-fold) and in whole lung tissue (>30-fold)

mammalian phenotype

mortality/aging
- Normal - homozygotes are viable, fertile, overtly normal and apparently free of viral infections up to 7 months of age

respiratory system phenotype

abnormal alveolar macrophage morphology
- at 8 and 24 weeks, homozygotes exhibit a 4- and 10-fold increase in BAL alveolar macrophage number, respectively
- by 8 weeks, homozygotes exhibit a significant increase in alveolar macrophage size, with many macrophages being both multinucleated and foamy in appearance

abnormal lung morphology
- starting at 3 weeks, homozygotes display progressive accumulation of surfactant lipids in the alveolar space, foamy macrophages, and peribronchial cellular infiltrate, with no histological evidence of lung inflammation or injury at any age

abnormal pulmonary alveolus epithelium morphology
- homozygotes display reduced alveolar epithelial surface area relative to wild-type mice

abnormal pulmonary alveolus morphology
- homozygotes exhibit progressive accumulation of surfactant lipids and apoproteins in the alveolar space
- notably, abnormal surfactant homeostasis is not associated with detectable alterations in surfactant surface activity, postnatal respiratory function, or survival

abnormal surfactant physiology
- homozygotes develop abnormal surfactant phospholipid homeostasis, as shown by progressive accumulation of pulmonary surfactant lipids and altered phospholipid structures

abnormal surfactant secretion
- at 8 weeks, homozygotes exhibit a 2.4- and 6-fold increase in BAL SP-A and SP-B protein levels, respectively

emphysema
- mutant lungs show emphysematous changes including reduced alveolar surface area, thicker alveolar septae, and fewer but larger alveoli relative to wild-type lungs

enlarged alveolar lamellar bodies

increased type II pneumocyte number
- hyperplasia and hypertrophy of type II cells is associated with an increased intracellular surfactant pool due to an increased number of lamellar bodies per cell
- mutant alveolar type II cells appear to be more numerous and occasionally contain giant lamellar bodies that are rarely found in wild-type cells
- starting at 3 weeks, homozygotes exhibit progressive hyperplasia of type II pneumocytes with massive enlargement of intracellular lamellar bodies evident at >8 weeks

overexpanded pulmonary alveoli
- homozygotes exhibit fewer but enlarged distal air spaces and accumulation of intra-alveolar surfactant material, organized as lamellar body-like forms, tubular myelin, and unilamellar vesicles

thick pulmonary interalveolar septum

homeostasis/metabolism phenotype

abnormal cholesterol homeostasis
- at 8 weeks, homozygotes exhibit a 6-fold increase in the cholesterol content of cell-free BAL relative to wild-type mice

immune system phenotype

abnormal alveolar macrophage morphology
- at 8 and 24 weeks, homozygotes exhibit a 4- and 10-fold increase in BAL alveolar macrophage number, respectively
- by 8 weeks, homozygotes exhibit a significant increase in alveolar macrophage size, with many macrophages being both multinucleated and foamy in appearance

abnormal macrophage physiology
- consistent with emphysema-like changes, homozygotes exhibit a significant increase in macrophage activation, as shown by increased MMP-12 expression in alveolar macrophages (>300-fold) and in whole lung tissue (>30-fold)

References

Botas C; Poulain F; Akiyama J; Brown C; Allen L; Goerke J; Clements J; Carlson E; Gillespie AM; Epstein C; Hawgood S. 1998. Altered surfactant homeostasis and alveolar type II cell morphology in mice lacking surfactant protein D. Proc Natl Acad Sci U S A 95(20):11869-74PubMed: 9751757 MGI: J:50147

Additional - Sftpd^tm1Haw related

Technical Support

CONTACT TECHNICAL SUPPORT

Genotyping Protocols
- Standard PCR:Sftpd-Alternate 1
- Genotyping resources and troubleshooting
Breeding Considerations

When maintaining a live colony, these mice can be bred as homozygotes.
- Additional Breeding and Husbandry Support
Citation
When using the SP-D null mouse strain in a publication, please cite the originating article(s) and include JAX stock #027302 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 Sftpd<tm1Haw>

Payment Terms and Conditions

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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

Additional Use Restrictions Apply

Use of MICE by companies or for-profit entities requires a license prior to shipping.

Licensing Information

Phone: 207-288-6470

Email: TechTran@jax.org

JAX® Mice, Products & Services Conditions of Use

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Also Known As:SP-D null

Donating Investigator

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Control Suggestions

Additional Information

Selected References

Sftpdtm1Haw

Allele Symbol: Sftpdtm1Haw

Disease Terms

Research Areas By Phenotype

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

Mammalian Phenotype Terms by Genotype

Genotype: Sftpdtm1Haw/Sftpdtm1Hawinvolves: C57BL/6J * CD-1

hematopoietic system phenotype

mammalian phenotype

respiratory system phenotype

homeostasis/metabolism phenotype

immune system phenotype

References

Additional - Sftpdtm1Haw 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

Payment Terms and Conditions

The Jackson Laboratory's Genotype Promise

Terms Of Use

Additional Use Restrictions Apply

Licensing Information

JAX® Mice, Products & Services Conditions of Use

No Warranty

Credit for PRODUCTS or SERVICES

Animal Care and Use for SERVICES

No Liability

Sftpd^tm1Haw

Allele Symbol: Sftpd^tm1Haw

Genotype: Sftpd^tm1Haw/Sftpd^tm1Haw
involves: C57BL/6J * CD-1

Additional - Sftpd^tm1Haw related