Homozygous Lgals1 (originally Lect14) knock-out mice exhibit abnormal proportions of axon subpopulations and a larger number of myelinated axons in dorsal root ganglia and abnormal axon targeting to the caudal region of the olfactory bulb in neonates. This strain may be useful in studies relating to development of the nervous system.
Dr. Elizabeth Robertson, University of Oxford
Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical abnormalities. No gene product (mRNA or protein) is detected by in situ hybridization of dorsal root ganglia and facial motorneuron nucleus and Western blot analysis of adult muscle tissue. Neonate mice homozygous for the mutation have abnormal axon targeting to the caudal region of the olfactory bulb. Mutant mice have fewer neural progenitor cells in the subventricular zone of the forebrain, although the number of apoptotic cells are not affected. Homozygotes exhibit hypoalgesia with a diminished nocifensive withdraw response to thermal testing. Immunohistological analysis of dorsal root ganglia from homozygotes reveals abnormal proportions of axon subpopulations and a larger number of myelinated axons. Mutant mice have a longer recovery of motorneuron function after experimental nerve injury. This mutant mouse strain represents a model that may be useful in studies of pain reception, motorneuron regeneration, axonal growth and guidance and development of the nervous system.
This strain was transferred from the collection of the Consortium for Functional Glycomics.
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 1.0kb of sequence that includes exon 2. The construct was electroporated into 129S6/SvEvTac derived CCE embryonic stem (ES) cells. Correctly targeted ES cells were injected into outbred MF-1 blastocysts. The resulting chimeric male animals were crossed to outbred MF-1 female mice. Heterozygotes were crossed to generate homozygotes. The mice were then bred to mice homozygous for a targeted mutation of Lgals3. The double mutant strain was then backcrossed to C57BL/6 for 5 generations. Upon arrival at The Jackson Laboratory, the second allele was removed by selective breeding. These mice carry only the Lgals1tm1Rob allele.
|Allele Name||targeted mutation 1, Elizabeth J Robertson|
|Allele Type||Targeted (Null/Knockout)|
|Allele Synonym(s)||gal-1-; gal1-; Lgals1-|
|Gene Symbol and Name||Lgals1, lectin, galactose binding, soluble 1|
|Strain of Origin||129S/SvEv-Gpi1c|
|Molecular Note||Exon 2, encoding the carbohydrate-binding domain, was replaced with a neomycin selection cassette. Western blot analysis and immunostaining of sections showed an absence of encoded protein in muscle tissue obtained from adult homozygous mutant mice.|
|Mutations Made By|| |
Richard Cummings, University of Oklahoma
When maintaining a live colony, these mice are bred as homozygotes.
When using the B6.Cg-Lgals1tm1Rob/J mouse strain in a publication, please cite the originating article(s) and include JAX stock #006337 in your Materials and Methods section.