Strain Information
| Name | HA2987 View On Wormbase |
|---|---|
| Species | C. elegans |
| Genotype | sod-1(rt449[G93AC]) II; vsIs48. |
| Description | vsIs48 [unc-17::GFP]. Superficially wild-type at 25C. Can be maintained 15-25C, and latent defects observed after oxidative stress. GFP expressed in all cholinergic neurons. rt449 was created by CRISPR editing of the cognate glycine codon in C. elegans sod-1 to create a disease model for human mutation SOD1 G93A. 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 rt449, which is sod-1[G93AC], while rt451 is sod-1[G85RC] and rt448 is the wild-type control for both. |
| Mutagen | |
| Outcrossed | x4 |
| Made by | Saba Baskoylu |
| Laboratory | HA |
| Reference | doi: 10.1371/journal.pgen.1007682 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 Baskoylu SN et.al |
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