This CRISPR/Cas9 generated mutant of the Tuba4a gene carries a 50 nucleotide deletion in the single coding exon. These mice may be useful in studies related to the cytoskeleton and amyotrophic lateral sclerosis (ALS).
Cathleen Lutz, The Jackson Laboratory
CRISPR/cas9 endonuclease mediated genome editing of the Tuba4a, tubulin, alpha 4A, gene was used to introduce a 50 nucleotide deletion in the single coding exon. Some mutations in the human TUBA4A are associated with amyotrophic lateral sclerosis. The Tuba4a gene encodes one of the major constituents of microtubules. Homozygous mice are viable and fertile. As the mice are characterized, we will modify the strain description and add phenotype data.
Plasmids encoding a signal guide RNA designed to introduce a 50 nucleotide deletion in the single coding exon of the Tuba4a gene and the cas9 nuclease were introduced into the cytoplasm C57BL/6J-derived fertilized eggs with well recognized pronuclei. Embryos were transferred to pseudopregnant females. Correctly targeted pups were identified by sequencing and PCR and further bred to C57BL/6J (Stock No. 000664) for 2 generations to develop the colony.
|Allele Name||endonuclease-mediated mutation 5, Cathy Lutz|
|Allele Type||Endonuclease-mediated (Not Specified)|
|Gene Symbol and Name||Tuba4a, tubulin, alpha 4A|
|Strain of Origin||C57BL/6J|
|Molecular Note||CRISPR/Cas9 genome editing is used to introduce a 50 nucleotide deletion in the single coding exon of the gene.|
When maintaining a live colony, these mice can be bred as homozygotes.
When using the Tuba4a del50 mouse strain in a publication, please cite the originating article(s) and include JAX stock #027047 in your Materials and Methods section.