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.
Francoise Poirier, CNRS-Université Paris Diderot
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.
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 Lgals3tm1Poi allele.
|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)||AGE-R3; CBP30; CBP35; GAL3; GALBP; GALIG; L-34; L31; LGALS2; MAC2; Mac-2; gal-3; gal3; galectin-3|
|Strain of Origin||STOCK 129/Sv and C57BL/6J and SJL|
|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
The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided,
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