Laboratory Information
Name | HA View on WormBase |
---|---|
Allele designation | rt |
Head | Anne Church Hart |
Institution | Brown University |
Address | 60 Olive Street SFH 459 Providence 02912 United States |
Website | http://neuroscience.brown.edu/faculty/profile.php?id=1254250004 |
Gene classes | dos ess grk kcnl nlp oca osm plst pqe sco tkt uso inso tyms gkow erh |
Strains contributed by this laboratory
Strain | Genotype | Species | Description |
---|---|---|---|
HA1019 | osm-11(rt142) X. | C. elegans | Isolated from a deletion library. |
HA1706 | pha-1(e2123) III; rtEx726. | C. elegans | rtEx726 [del-1p::YC2.60 + pha-1(+)] expresses yellow cameleon YC2.60 in a subset of motor neurons. Maintain at 25C to select for the presence of the array. Haspel G, et al. (2010) J. Neurosci. 30:11151-6. |
HA1722 | rtIs29. | C. elegans | rtIs29 [acr-5p::YC2.60 + pha-1(+)] expresses yellow cameleon YC2.60 in all VB and DB motoneurons and some head and tail neurons. Maintain at 25C to select for the presence of the array. Haspel G, et al. (2010) J. Neurosci. 30:11151-6. |
HA1857 | osm-7(tm2256) III. | C. elegans | |
HA2031 | rtIs31 X. | C. elegans | rtIs31 [elt-2p::GFP + Posm-10::HtnQ150]. |
HA2040 | sir-2.4(n5137) I; sir-2.1(ok434) IV; sir-2.2(n5136) X. | C.elegans | Superficially wild-type. Reference: Anderson E, et al.Mech Ageing Dev. 2016 Mar;154:30-42. |
HA2619 | sod-1(tm776) II; rtSi1 IV. | C.elegans | 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. |
HA2823 | smn-1(rt248) I/hT2 [bli-4(e937) let-?(q782) qIs48] (I;III); nuIs175 X. | C.elegans | nuIs175 [myo-2p::RFP + unc-129p::RFP::snb-1] X. smn-1 heterozygotes are WT with pharyngeal GFP signal, and segregate WT GFP, arrested hT2 aneuploids, and non-GFP rt248 homozygotes (larval arrest). Homozygous hT2 [bli-4 let-? qIs48] inviable. Pick WT GFP and check for correct segregation of progeny to maintain. NOTE: myo-2p::RFP is not visible in this strain. rt248 is a 8 bp deletion in smn-1. [rt248: TTTTGATTAGC--------ATCCCAAAC] [wild-type: TTTTGATTAGCTCCGTATCATCCCAAAC] Reference: Dimitriadi M, et al. Proc Natl Acad Sci U S A. 2016 Jul 26;113(30):E4377-86. O'Hern PJ, et al. Elife. 2017 May 2;6. pii: e20752. |
HA2825 | smn-1(ok355) I/hT2 [bli-4(e937) let-?(q782) qIs48] (I;III); rtSi10 IV; nuIs175 X. | C.elegans | rtSi10 [smn-1p::smn-1 + Cbr-unc-119(+)] IV. nuIs175 [myo-2p::RFP + unc-129p::RFP::snb-1] X. rtSi10 transgene partially rescues smn-1(ok355): smn-1 homozygotes normally arrest as larvae, but somatic defects, including late larval lethality, are ameliorated by rtSi10. Sterility in smn-1(ok355) homozygotes is not rescued by rtSi10. Heterozygotes are WT with pharyngeal GFP signal, and segregate WT GFP, arrested hT2 aneuploids, and non-GFP ok355 homozygotes (sterile due to partial rescue by rtSi10). Homozygous hT2[bli-4 let-? qIs48] inviable. Note: qIs48 has been observed to recombine off hT2, typically leaving behind a functional homozygous viable hT2 with Bli-4 phenotype. Pick WT GFP and check for correct segregation of progeny to maintain. Reference: O'Hern PJ, et al. eLife 2017;6:e20752 doi: 10.7554/eLife.20752 |
HA2845 | fust-1(rt255) II. | C.elegans | Superficially wild-type. This is the appropriate control strain for FUS disease models HA2846 and HA2847. This control strain contains presumably silent edits inserted by CRISPR editing while creating the FUS disease models in HA2846 and HA2847, and was back-crossed to remove the pha-1 allele used in strain construction. Reference: Baskoylu S, et al. bioRxiv 799932; doi: https://doi.org/10.1101/799932 |
HA2846 | fust-1(rt256[R446S]) II. | C.elegans | fust-1(rt256[R446S]) was created by CRISPR editing of arginine codon in C. elegans fust-1 to create FUS disease model for human mutation R524S. This strain also contains additional silent edits (also present in control strain HA2845), and was back-crossed to remove the pha-1 allele used in strain construction. Under normal culture conditions HA2846 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 |
HA2847 | fust-1(rt257[P447L]) II. | C.elegans | fust-1(rt257[P447L]) was created by CRISPR editing of proline codon in C. elegans fust-1 to create FUS disease model for human mutation P525L. This strain also contains additional silent edits (also present in control strain HA2845), and was back-crossed to remove the pha-1 allele used in strain construction. Under normal culture conditions HA2847 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 |
HA2986 | sod-1(rt448[sod-1WT C]) II. | C. elegans | 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. | C. elegans | 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.] |
HA3 | nuIs11. | C. elegans | nuIs11 [osm-10::GFP + lin-15(+)]. Array contains pool28; KP#57-59 (osm-10::GFP insert at Nrul site) and pJM24 [lin-15(+) rescues n765 at 20C]. GFP expressed in ASH, ASI, PHA and PHB after 3-fold. nuIs11 may be inserted on LG I. |
HA300 | lin-15B&lin-15A(n765) X; rtEx223. | C. elegans | rtEx223 [nlp-6p::GFP + lin-15(+)]. Maintain at 20C or warmer. Pick GFP+ non-Muv to maintain. Reference: Nathoo AN, et al. Proc Natl Acad Sci U S A. 2001 Nov 20;98(24):14000-5. |
HA307 | lin-15B&lin-15A(n765) X; rtEx224. | C. elegans | rtEx224 [F18E9.2::GFP + lin-15(+)]. Maintain by picking non-Muv. Maintain at 20C. |
HA328 | lin-15B&lin-15A(n765) X; rtEx233. | C. elegans | rtEx233 [nlp-11p::GFP + lin-15(+)]. Raise at 20C or higher and pick non-Muv to maintain array. |
HA329 | lin-15B&lin-15A(n765) X; rtEx234. | C. elegans | rtEx234 [nlp-13p::GFP + lin-15(+)]. Raise at 20C or higher and pick non-Muv or GFP+ to maintain array. |
HA3299 | sod-1(rt451[sod-1(G85R C)]) II. | C. elegans | 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.] |
HA341 | lin-15B&lin-15A(n765) X; rtEx235. | C. elegans | rtEx235 [nlp-3p::GFP + lin-15(+)]. Maintain at 20C or warmer. Pick GFP+ non-Muv to maintain. Reference: Nathoo AN, et al. Proc Natl Acad Sci U S A. 2001 Nov 20;98(24):14000-5. |
HA353 | lin-15B&lin-15A(n765) X; rtEx247. | C. elegans | rtEx247 [nlp-14p::GFP + lin-15(+)]. Raise at 20C or higher and pick non-Muv to maintain array. |
HA357 | lin-15B&lin-15A(n765) X; rtEx251. | C. elegans | rtEx251 [nlp-15p::GFP + lin-15(+)]. Raise at 20C or higher and pick non-Muv to maintain array. |
HA367 | lin-15B&lin-15A(n765) X; rtEx256. | C. elegans | rtEx256 [nlp-18p::GFP + lin-15(+)]. Raise at 20C or higher and pick non-Muv to maintain array. |
HA3703 | tdp-1(tgx58) I. | C. elegans | Null allele. CRISPR-engineered deletion of the tdp-1 locus precisely eliminates all known tdp-1 exons and introns. Reference: Lins J, et al. Generation of a C. elegans tdp-1 null allele and humanized TARDBP containing human disease-variants. MicroPubl Biol. 2023 Jun 6;2023:10.17912/micropub.biology.000693. doi: 10.17912/micropub.biology.000693. PMID: 37351305. |
HA371 | lin-15B&lin-15A(n765) X; rtEx260. | C. elegans | rtEx260 [nlp-19p::GFP + lin-15(+)]. Raise at 20C or higher and pick non-Muv to maintain array. |
HA444 | lin-15B&lin-15A(n765) X; rtEx330. | C. elegans | rtEx330 [nlp-21p::GFP + lin-15(+)]. Raise at 20C or higher and pick non-Muv to maintain array. |
HA446 | lin-15B&lin-15A(n765) X; rtEx332. | C. elegans | rtEx332 [nlp-20p::GFP + lin-15(+)]. Pick non-Muv or GFP+ to maintain. |
HA449 | lin-15B&lin-15A(n765) X; rtEx335. | C. elegans | rtEx335 [nlp-10p::GFP + lin-15(+)]. Maintain at 20C or warmer. Pick GFP+ non-Muv to maintain. Reference: Nathoo AN, et al. Proc Natl Acad Sci U S A. 2001 Nov 20;98(24):14000-5. |
HA450 | lin-15B&lin-15A(n765) X; rtEx336. | C. elegans | rtEx336 [nlp-12p::GFP + lin-15(+)]. Raise at 20C or higher and pick non-Muv to maintain array. |
HA659 | rtIs11 V. | C. elegans | rtIs11 [osm-10p::GFP + osm-10p::HtnQ150 + dpy-20(+)]. HtnQ150 causes ASH degeneration 30% at 8 days. |
HA661 | rtIs18 I. | C. elegans | rtIs18 [elt-2p::GFP + osm-10p::HtnQ150]. |
HA759 | pqe-1(rt13) III; rtIs11 V. | C. elegans | rtIs11 [osm-10p::GFP + osm-10p::HtnQ150 + dpy-20(+)]. osm-10 promoter drives expression of both GFP and Htn-Q150 strongly in ASH and more weakly in other neurons of the head and tail. pqe-1(rt13) accelerates Htn-Q150 induced toxicity resulting in ASH neuron cell death predominantly during larval stages. Hence, many adult animals will lack overt GFP expression in ASH neurons. rtEx377 in the original HA759 was selected against leaving only rtIs11 in the strain available at the CGC. |
HA865 | grk-2(rt97) III. | C. elegans | Grossly normal but defective for chemosensory response, including detection of octanol, diacetyl, and isoamyl alcohol. |
HA98 | lin-15B&lin-15A(n765) X; rtEx66. | C. elegans | rtEx66 [nlp-2p::GFP + lin-15(+)]. Maintain at 20C or warmer. Pick GFP+ non-Muv to maintain. Reference: Nathoo AN, et al. Proc Natl Acad Sci U S A. 2001 Nov 20;98(24):14000-5. |
IE53215 | ttTi53215 V. | C. elegans | Homozygous. |
KP696 | eos-2(nu268) III. | C. elegans | Weak Osm as homozygote. Non-allelic non-complementor of osm-10(n1602). |
KP715 | eos-1(nu288) IV. | C. elegans | Weak Osm as homozygote. Non-allelic non-complementor of osm-10(n1602). |
KP987 | lin-15B&lin-15A(n765) nuIs1 X. | C. elegans | nuIs1 [glr-1p::GFP + glr-1(+) + lin-15(+)] X. GFP expression in 17 classes of neurons after 3-fold (see WBPaper00002309). This strain is WT at glr-1. |
YS4 | cbp-1(bm2) dpy-18(e364)/qC1 [dpy-19(e1259) glp-1(q339)] III. | C. elegans | Heterozygotes are WT and segregate WT, Dpy Steriles and dead eggs. cbp-1 is embyronic lethal. ys4 is an N-terminal deletion in cbp-1. NOTE: THIS STRAIN WAS FORMERLY IDENTIFIED AS HA990 cbp-1(ys4) dpy-18(e364)/qC1 dpy-19(e1259) glp-1(q339) III. The strain name and allele were corrected per Anne Hart, 2010. |
Alleles contributed by this laboratory
Allele | Type | DNA Change | Protein Change |
---|---|---|---|
rt142 | Allele | deletion | |
rt13 | Allele | substitution | nonsense |
rt97 | Allele | substitution |