Strain Information
| Name | HA3299 View On Wormbase |
|---|---|
| Species | C. elegans |
| Genotype | sod-1(rt451[sod-1(G85RC)]) II. |
| Description | Superficially wild-type at 25C. Can be maintained 15-25C, and latent defects observed after oxidative stress. rt451 was created by CRISPR editing of the cognate glycine codon in C. elegans sod-1 to create a disease model for human mutation SOD1 G85R. This strain contains additional silent edits in sod-1, and was back-crossed to remove the edited pha-1 allele used in strain construction. The appropriate control is HA2986. Reference: Baskoylu S, et al. PLOS Genetics(https://journals.plos.org/plosgenetics/article?id=10.1371/j ournal.pgen.1007682). NOTE: A micropublication (PMID: 33474528) incorrectly described sod-1 alleles in the text. This strain contains rt451, which is sod-1[G85RC], while rt449 is sod-1[G93AC] and rt448 is the wild-type control for both. |
| Mutagen | Crispr/Cas9 |
| Outcrossed | x4 |
| Made by | Saba Baskoylu |
| Laboratory | HA |
| Reference | Single copy/knock-in models of ALS SOD1 in C. elegans suggest loss and gain of function have different contributions to cholinergic and glutamatergic neurodegeneration. PLoS Genet. 2018;14(10):e1007682. Published 2018 Oct 8. doi:10.1371/journal.pgen.1007682 |
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