CRISPR/cas9 endonuclease mediated genome editing of the sterile alpha and HEAT/Armadillo motif containing 1 (Sarm1) gene was used to introduce 62 bp deletion in exon 1. This mutation results in a frameshift and a 38 amino acid product. No potential off-target sites are present. Sarm1, also known as MyD88-5, is highly conserved across phyla and is expressed predominantly in neurons. It is a member of the TIR domain-containing family of adaptor molecules for Toll-like receptors, and promotes neurodegeneration. These Sarm1AGS3 mice have no macrophage defects in response to lipopolysaccharide (LPS) or TNF&alpha;, and are protected from axonal degeneration. They are more susceptible to West Nile virus infection (WNV) infection than wildtype mice, yet show similar susceptibility when infected with lethal La Crosse virus (LACV) and lethal Vesicular Stomatitis virus (VSV) infection. Sarm1AD mice (Stock No. <a href="https://www.jax.org/strain/018069"">018069</a>) are a similar strain produced on a B6.129X1 congenic background. These mice are also protected from axonal degeneration. They exhibit defects in the production of chemokines in response to LPS or TNF&alpha; and are protected from lethal VSV infection and have similar susceptibility to LACV and WNV infection as wildtype mice. These differences may be attributed to sequence variation between B6 and 129 in the closely linked XIAP associated factor 1 (Xaf1) gene.

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Sarm1AGS3 mice carry a CRISPR/Cas9 generated 62 bp insertion in exon 1, making this strain useful when studying the role of Sarm1 in axonal degeneration and chemokine expression during viral infection. Mice are more susceptible to West Nile virus infection (WNV) infection than wildtype mice, yet show similar susceptibility when infected with lethal La Crosse virus (LACV) and lethal Vesicular Stomatitis virus (VSV) infection.

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