C57BL/6J-Il11^em2Cook/J

Stock number: 034464
Product name: IL11 KO , Il11^-
Research areas: Immunology, Inflammation and Autoimmunity Research, Internal/Organ Research

Description

Il11^- mice carry a CRISPR/Cas9-derived knock-out allele of the mouse Il11 (interleukin 11) gene that incorporates a deletion of exons 2-4.

Detailed description

IL11 (interleukin 11) is a member of the IL6 family of cytokines, which share the gp130 coreceptor. IL11RA and IL6R are expressed on different cell types, IL11RA mostly on stromal and parenchymal cells whereas IL6R is expressed more on immune-type cells. IL11 itself is unregulated in many cell types in response to pro-fibrotic stimulation or injury.

These Il11^- CRISPR/Cas9-derived mutant mice carry a knock-out allele of the mouse Il11 gene that incorporates a deletion of exons 2-4. Homozygotes are born at normal Mendelian ratios, appear healthy, and have normal blood hematological and chemistry profiles.

Homozygous IL11 knockout mice are protected from lung fibrosis and their fibroblasts are resistant to pro-fibrotic stimulation.

Development

Specific single guide RNA (sgRNA) sequences with recognition sites on introns 1 and 4 along with Cas9 were microinjected into fertilized C57BL/6J zygotes with a goal of deleting exons 2-4. This deletion is predicted to cause a shift in the reading frame from the splicing of coding sequences present within exons 1 and 5, resulting in the generation of a mutant peptide (62 amino acid in length) that does not align to that of known proteins. This effectively results in the inactivation of the gene. Resultant mice were further backcrossed to C57BL/6J mice for one generation by the donating laboratory.

Allele

Symbol: Il11^em2Cook
Name: endonuclease-mediated mutation 2, Stuart A Cook
MGI accession ID: MGI:6514818
Generation method: Endonuclease-mediated
Attributes: Null/Knockout
Marker symbol: Il11
Marker name: interleukin 11
Marker synonyms: AGIF; IL-11
Chromosome: 7
Strain of origin: C57BL/6J
Molecular note: CRISPR/cas9 genome editing is used to delete exons 2-4. This deletion is predicted to cause a shift in the reading frame from the splicing of coding sequences present within exons 1 and 5, resulting in the generation of a mutant peptide (62 amino acid in length) that does not align to that of known proteins. This effectively results in the inactivation of the gene.