Overview

Also Known As:galactin3^-

Homozygotes carrying the lectin, galactose binding, soluble 3 (Lgals3) knock-out have an impaired acute inflammation response, chondrocyte differentiation during long bone development and myofibroblast activation. This mutant mouse strain may be useful in studies of bone development, endochondral ossification, inflammatory response, and liver fibrosis.

Donating Investigator

Francoise Poirier, CNRS-Université Paris Diderot

Genetic overview

Genetic Background	Generation
	N5+N3F7 (2020-03-19 00:00:00)

Lgals3^tm1Poi

Allele Type	Gene Symbol	Gene Name
Targeted (Null/Knockout)	Lgals3	lectin, galactose binding, soluble 3

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Research Applications

Immunology, Inflammation and Autoimmunity Research
Developmental Biology Research

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Base Price

Starting at:

$236.78 Domestic price for female 4-week

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Details

Detailed Description

Homozygous mutant mice are viable, fertile, normal in size and do not display any gross physical or behavoiral abnormalities. No gene product (mRNA or protein) is detected by in situ hybridization of tibia bones sections from embryonic day 16.4 mice or by immunohistological staining of fetal skin. Homozygotes have an impaired acute inflammation response. Initial inflammatory infiltrate cell recruitment is normal, but four days after intraperitoneal injection of thioglycollate, mutant mice have a four-fold lower number of recruited granulocytes. Mutant mice have impaired chondrocyte differentiation during long bone development. Fewer hypertrophic chondrocytes but more empty lacunae and condensed chondrocytes are found in the chondrovascular junction. Chondrocytes, cartilage matrix and lacunae are morphologically abnormal. Carbon tetrachloride-induced liver fibrosis results in reduced collagen deposition when compared to wildtype controls. Mutant mice also display defective myofibroblast activation. This mutant mouse strain may be useful in studies of bone development, endochondral ossification, inflammatory response, and liver fibrosis.

This strain was transferred from the Consortium for Functional Glycomics strain collection.

It has been the experience of The Jackson Laboratory that these mice experience a transient period of hairloss between the ages of 2-6 weeks, with full hair growth returning by six weeks of age. Analysis of skin sections reveals a pathology similar to what is seen in C57BL/6 alopecia and movement of these alleles onto the C57BL/6J background may have exacerbated this phenotype.

Development

A targeting vector containing neomycin resistance and herpes simplex virus thymidine kinase genes was used to disrupt 3.7kb of sequence that includes exons 2, 3 and 4. The construct was electroporated into WW6 embryonic stem (ES) cells (derived from 129/Sv, C57BL/6, SJL mixed background mice). Correctly targeted ES cells were injected into outbred MF-1 blastocysts. The resulting chimeric male animals were crossed to 129 female mice. Heterozygotes were crossed to generate homozygotes. The mice were then bred to mice homozygous for a targeted mutation of Lgals1, and he double mutant strain was backcrossed to C57BL/6 for 5 generations. Upon arrival at The Jackson Laboratory, the Lgals1mutation was removed by selective breeding; therefore this strain carries only the Lgals3^tm1Poi allele.

Control Suggestions

000664 C57BL/6J

Additional Information

Considerations for Choosing Controls

Selected References

Colnot C; Fowlis D; Ripoche MA; Bouchaert I; Poirier F. 1998. Embryonic implantation in galectin 1/galectin 3 double mutant mice. Dev Dyn 211(4):306-13PubMed: 9566950 MGI: J:47227

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Genetics

Lgals3^tm1Poi

Allele Symbol: Lgals3^tm1Poi

Allele Name	targeted mutation 1, Francoise Poirier
Allele Type	Targeted (Null/Knockout)
Allele Synonym(s)	GaL3^-; galectin 3^-
Gene Symbol and Name	Lgals3, lectin, galactose binding, soluble 3
Gene Synonym(s)
Strain of Origin	STOCK 129/Sv and C57BL/6J and SJL
Chromosome	14
Molecular Note	3.7kb of sequence, encompassing exons 2 through 4, was replaced via the insertion of a neomycin selection cassette. Immunostaining of fetal skin showed an absence of protein in homozygous mutant embryos.
Mutations Made By	Richard Cummings, University of Oklahoma

Disease/Phenotype

Disease Terms

Research Areas By Phenotype

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

Immunology, Inflammation and Autoimmunity Research
- Inflammation
Developmental Biology Research
- Skeletal Defects

Mammalian Phenotype Terms by Genotype

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

Genotype: Lgals3^tm1Poi/Lgals3^tm1Poi
involves: 129 * C57BL/6J * SJL

mammalian phenotype

integument phenotype
- Normal - mice exhibit normal skin structure

mortality/aging
- Normal - mice exhibit a normal lifespan

reproductive system phenotype
- Normal - mice exhibit normal reproduction

Genotype: Lgals3^tm1Poi/Lgals3^tm1Poi
involves: 129/Sv * C57BL/6 * SJL

cellular phenotype

impaired macrophage chemotaxis
- when stimulated by IL-4 and IL-13

impaired macrophage phagocytosis
- Normal - however, phagocytosis of S. pneumonia is normal
- phagocytosis of apoptotic neutrophils by bone marrow-derived macrophages is impaired

homeostasis/metabolism phenotype

decreased susceptibility to injury
- Normal - however, macrophage recruitment and cytokine production induced by UUO is normal
- mice exhibit less renal fibrosis following unilateral ureter obstruction (UUO) compared to wild-type mice

immune system phenotype

abnormal macrophage physiology
- Normal - however, macrophage activation by IFN-gamma and LPS is normal
- macrophage activation by IL-4 and IL-13 stimulation Is impaired

impaired macrophage chemotaxis
- when stimulated by IL-4 and IL-13

impaired macrophage phagocytosis
- Normal - however, phagocytosis of S. pneumonia is normal
- phagocytosis of apoptotic neutrophils by bone marrow-derived macrophages is impaired

impaired neutrophil recruitment
- 15 hours after infection with S. pneumoniae
- Normal - however, myeloperoxidase activity is similar to in wild-type mice 15 hours after infection with S. pneumoniae

increased interleukin-6 secretion
- 15 hours after infection with S. pneumoniae, IL-6 concentration in bronchoalveolar lavage is increased compared to in wild-type mice

increased susceptibility to bacterial infection
- after 15 hours, mice infected with S. pneumoniae exhibit a 450-fold increase in bacterial load compared to wild-type mice and blood cultures indicate 100 % bacteremia compared to 30% in wild-type mice
- after 15 hours, mice infected with S. pneumoniae exhibit increased cell infiltrate but decreased total cell counts in the lungs and develop severe pneumonia with increased lung injury and septicemia compared to wild-type mice
- mice infected with S. pneumoniae exhibit high mortality after 24 hours

increased tumor necrosis factor secretion
- 15 hours after infection with S. pneumoniae, TNF-alpha concentration in bronchoalveolar lavage is increased compared to in wild-type mice

lung inflammation
- after 15 hours, mice infected with S. pneumoniae exhibit increased cell infiltrate in the lungs and develop severe pneumonia with increased lung injury and septicemia compared to wild-type mice

sepsis
- after 15 hours, mice infected with S. pneumoniae exhibit septicemia unlike wild-type mice

mortality/aging

increased sensitivity to induced morbidity/mortality
- mice infected with S. pneumoniae exhibit high mortality after 24 hours

renal/urinary system phenotype

abnormal kidney physiology
- Normal - however, macrophage recruitment and cytokine production induced by UUO is normal
- mice exhibit less renal fibrosis following unilateral ureter obstruction (UUO) compared to wild-type mice

respiratory system phenotype

lung inflammation
- after 15 hours, mice infected with S. pneumoniae exhibit increased cell infiltrate in the lungs and develop severe pneumonia with increased lung injury and septicemia compared to wild-type mice

skeleton phenotype

abnormal long bone epiphyseal plate morphology
- unlike in wild-type mice, a large zone of empty lacunae is observed between the last row of hypertrophic cells and the vascular invasion front

abnormal long bone hypertrophic chondrocyte zone
- chondrocytes in the zone contain unusually large intracellular glycogen aggregates
- chondrocytes within the hypertrophic zone are larger and more vacuolated than in wild-type mice
- mice exhibit an increased number of nonhypertrophic cells in the late hyprtrophic zone compared to in wild-type mice

decreased width of hypertrophic chondrocyte zone
- the hypertrophic zone is reduced in size and contains 20% fewer hypertrophic cells than in wild type mice

hematopoietic system phenotype

abnormal macrophage physiology
- Normal - however, macrophage activation by IFN-gamma and LPS is normal
- macrophage activation by IL-4 and IL-13 stimulation Is impaired

impaired macrophage chemotaxis
- when stimulated by IL-4 and IL-13

impaired macrophage phagocytosis
- Normal - however, phagocytosis of S. pneumonia is normal
- phagocytosis of apoptotic neutrophils by bone marrow-derived macrophages is impaired

impaired neutrophil recruitment
- 15 hours after infection with S. pneumoniae
- Normal - however, myeloperoxidase activity is similar to in wild-type mice 15 hours after infection with S. pneumoniae

Genotype: Lgals3^tm1Poi/Lgals3^tm1Poi
involves: 129/Sv * C57BL/6 * MF1 * SJL

hematopoietic system phenotype

decreased granulocyte number
- Normal - however, granulocyte apoptosis rates and phagocytosis of apoptotic granulocytes are normal
- while recruitment of granulocytes following treatment with thioglycolate is normal, granulocyte numbers 3 to 4 days after treatment are reduced 4-fold compared to in wild-type mice

immune system phenotype

decreased granulocyte number
- Normal - however, granulocyte apoptosis rates and phagocytosis of apoptotic granulocytes are normal
- while recruitment of granulocytes following treatment with thioglycolate is normal, granulocyte numbers 3 to 4 days after treatment are reduced 4-fold compared to in wild-type mice

Genotype: Lgals3^tm1Poi/Lgals3^tm1Poi
involves: 129S/SvEv

behavior/neurological phenotype

abnormal social/conspecific interaction
- social dominance

aggression towards inanimate objects

impaired cued conditioning behavior

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

Genotype: Lgals3^tm1Poi/Lgals3^tm1Poi
B6.Cg-Lgals3/J

adipose tissue phenotype

increased total body fat amount
- 6-7 month old mice exhibit an increase in adiposity

behavior/neurological phenotype

abnormal circadian behavior
- 2-3 and 6-7 month old mice exhibit perturbed behavioral circadian rhythms, with greater day-to-day variability in feeding, drinking, and movement

abnormal stationary movement
- 2-3 and 6-7 month old mice exhibit less total movement compared to wild-type mice, especially during the circadian dark cycle

hypoactivity
- 2-3 and 6-7 month old mice exhibit decreased movement-in-place behaviors due to decreased bout numbers, initiation rates, and durations
- 6-7 month old mice exhibit decreased forward locomotion due to decreased bout numbers, initiation rates, and durations

growth/size/body region phenotype

increased body weight
- 6-7, but not 2-3, month old mice exhibit greater body weights

skeleton phenotype

increased bone mineral density
- 6-7 month old mice exhibit an increase in bone mineral density

References

Colnot C; Fowlis D; Ripoche MA; Bouchaert I; Poirier F. 1998. Embryonic implantation in galectin 1/galectin 3 double mutant mice. Dev Dyn 211(4):306-13PubMed: 9566950 MGI: J:47227

Additional - Lgals3^tm1Poi related

Technical Support

CONTACT TECHNICAL SUPPORT

Genotyping Protocols
- Standard PCR:Lgals3
- Standard PCR:Lgals3
- Genotyping resources and troubleshooting
Dietary Information
- LabDiet® 5K52 formulation (6% fat)
Breeding Considerations

When maintaining a live colony, these mice are bred as homozygotes.
- Additional Breeding and Husbandry Support
Mating System
- Homozygote x Homozygote
Citation
When using the galactin3^- mouse strain in a publication, please cite the originating article(s) and include JAX stock #006338 in your Materials and Methods section.

Animal Health Reports

Facility Barrier Level Descriptions

AX10 (Standard)

Pricing & Availability

Available

Domestic
International

Live Mouse

Age

Genotype

Price

weeks

Cryorecovery - Pricing

Service/Product	Description	Price
	Heterozygous for Lgals3<tm1Poi>

Related Products and Services

Frozen Mouse Embryo	B6.Cg-Lgals3<tm1Poi>/J Frozen Embryo	$2595.00
Frozen Mouse Embryo	B6.Cg-Lgals3<tm1Poi>/J Frozen Embryo	$2595.00
Frozen Mouse Embryo	B6.Cg-Lgals3<tm1Poi>/J Frozen Embryo	$3373.50
Frozen Mouse Embryo	B6.Cg-Lgals3<tm1Poi>/J 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.

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Also Known As:galactin3-

Donating Investigator

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Control Suggestions

Additional Information

Selected References

Lgals3tm1Poi

Allele Symbol: Lgals3tm1Poi

Disease Terms

Research Areas By Phenotype

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

Mammalian Phenotype Terms by Genotype

Genotype: Lgals3tm1Poi/Lgals3tm1Poiinvolves: 129 * C57BL/6J * SJL

mammalian phenotype

Genotype: Lgals3tm1Poi/Lgals3tm1Poiinvolves: 129/Sv * C57BL/6 * SJL

cellular phenotype

homeostasis/metabolism phenotype

immune system phenotype

mortality/aging

renal/urinary system phenotype

respiratory system phenotype

skeleton phenotype

hematopoietic system phenotype

Genotype: Lgals3tm1Poi/Lgals3tm1Poiinvolves: 129/Sv * C57BL/6 * MF1 * SJL

hematopoietic system phenotype

immune system phenotype

Genotype: Lgals3tm1Poi/Lgals3tm1Poiinvolves: 129S/SvEv

behavior/neurological phenotype

Genotype: Lgals3tm1Poi/Lgals3tm1PoiB6.Cg-Lgals3/J

adipose tissue phenotype

behavior/neurological phenotype

growth/size/body region phenotype

skeleton phenotype

References

Additional - Lgals3tm1Poi related

Genotyping Protocols

Dietary Information

Breeding Considerations

Mating System

Citation

Animal Health Reports

Live Mouse

Cryorecovery - Pricing

Related Products and Services

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

Also Known As:galactin3^-

Lgals3^tm1Poi

Allele Symbol: Lgals3^tm1Poi

Genotype: Lgals3^tm1Poi/Lgals3^tm1Poi
involves: 129 * C57BL/6J * SJL

Genotype: Lgals3^tm1Poi/Lgals3^tm1Poi
involves: 129/Sv * C57BL/6 * SJL

Genotype: Lgals3^tm1Poi/Lgals3^tm1Poi
involves: 129/Sv * C57BL/6 * MF1 * SJL

Genotype: Lgals3^tm1Poi/Lgals3^tm1Poi
involves: 129S/SvEv

Genotype: Lgals3^tm1Poi/Lgals3^tm1Poi
B6.Cg-Lgals3/J

Additional - Lgals3^tm1Poi related