| FX776 |
sod-1(tm776) II. |
Homozygous viable. 612 bp deletion. 17154/17155 - 17766/17767. Attribution: This strain was generated by the National Bioresource Project at the Tokyo Women's Medical University School of Medicine, which is part of the International C. elegans Gene Knockout Consortium, which should be acknowledged in any publications resulting from its use. Paper_evidence WBPaper00041807 |
| GA187 |
sod-1(tm776) II. |
Superficially wild-type. |
| HA2619 |
sod-1(tm776) II; rtSi1 IV. |
rtSi1 [sod-1p::sod-1(WT) + Cbr-unc-119(+)] (inserted into cxTi10882) IV. Superficially wild-type. HA2619 serves as a control strain for HA2464. Reference: Baskoylu SN, et al. PLoS Genet. 2018;14(10):e1007682. |
| HA2986 |
sod-1(rt448[sod-1WT C]) II. |
Superficially wild-type at 25C. Can be maintained 15-25C. rt448 is wild-type control strain for HA3299 containing all the silent codon changes needed for CRISPR/Cas9 genome editing. Reference: Baskoylu SN, et al. PLoS Genet. 2018;14(10):e1007682. NOTE: A micropublication on these strains (PMID: 33474528) incorrectly described sod-1(rt448) as the G85R mutant version and sod-1(rt449) as the control. Additionally, the strains list in the paper also incorrectly describes rt449 as sod-1 [G85RC]. The correct descriptions are that rt448 is the wild-type control, rt449 is the sod-1 [G93AC] mutant version, and rt451 is the sod-1 [G85RC] mutant version.] |
| HA2987 |
sod-1(rt449[G93A C]) II. |
sod-1(rt449[G93A C]) was created by CRISPR editing of the cognate glycine codon in C. elegans sod-1 to create a disease model for human mutation G93A. This strain also contains additional silent edits, and was back-crossed to remove the pha-1 allele used in strain construction. Under normal culture conditions HA2987 animals are superficially wild-type; after stress latent defects are observed. Reference: Baskoylu S, et al. bioRxiv 799932; doi: https://doi.org/10.1101/799932 [NOTE: A micropublication on these strains (PMID: 33474528) incorrectly described sod-1(rt448) as the G85R mutant version and sod-1(rt449) as the control. Additionally, the strains list in the paper also incorrectly describes rt449 as sod-1 [G85RC]. The correct descriptions are that rt448 is the wild-type control, rt449 is the sod-1 [G93AC] mutant version, and rt451 is the sod-1 [G85RC] mutant version.] |
| HA3299 |
sod-1(rt451[sod-1(G85R C)]) II. |
Superficially wild-type with increased sensitivity to paraquat in multiple assays. Can be maintained 15-25C. rt451 is CRISPR/Cas9 engineered G85R missense mutation in endogenous sod-1 locus mimicking human ALS SOD1 model. Reference: Baskoylu SN, et al. PLoS Genet. 2018;14(10):e1007682. NOTE: A micropublication on these strains (PMID: 33474528) incorrectly described sod-1(rt448) as the G85R mutant version and sod-1(rt449) as the control. Additionally, the strains list in the paper also incorrectly describes rt449 as sod-1 [G85RC]. The correct descriptions are that rt448 is the wild-type control, rt449 is the sod-1 [G93AC] mutant version, and rt451 is the sod-1 [G85RC] mutant version.] |
| MQ1766 |
sod-2(ok1030) I; sod-5 (tm1146) sod-1(tm783) II; sod-4(gk101) III; sod-3(tm760) X. |
Normal lifespan. Increased sensitivity to oxidative stress, osmotic stress, cold stress, and heat stress. Slow development, slow physiological rates (thrashing, defecation), and reduced fertility. van Raamsdonk J & Hekimi S. Proc Natl Acad Sci U S A. 2012 Apr 10;109(15):5785-90. |