C. elegans Mutation Packages

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C. elegans Point Mutation Service

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Our Point Mutation service uses CRISPR/Cas9, which is the best gene editing method for creating small, precise edits to introduce a small number of nucleotide changes at a target site. With this service you can:

  • study a disease-causing mutation
  • humanize a critical amino acid
  • explore the binding site of an enzyme
  • introduce phosphomimetics
  • mutate isoform start sites or make any specific mutation of interest.

Our CRISPR/Cas9 editing is typically very efficient. Among the F1 candidates with the Co-CRISPR edit, our average percentage of animals with the target edit was 65.7%. Edit percentages as high as 95% were observed.

We can generate Point mutations quickly. For these projects, our average time from injection to sequence confirmation of two independent homozygous lines was 15.3 days. Our quickest project only took 10 days!

96 point mutations in 1 gene. All 96 mutations were created in the STXBP1 gene (which is associated with epilepsy in humans) via CRISPR. The worm homolog of STXBP1, unc-18, causes uncoordination and near-complete lack of pharyngeal pumping when knocked out. The functionality is restored by replacing the worm gene with the coding sequence for human STXBP1.

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Service Details (price reflects academic pricing)

Service PackagePriceEst. Delivery Time
Full Build $4,075 - $4,3606 - 8 Weeks
Candidate Lines $2,554 - $2,839 3 - 4 Weeks
Custom Injection Mix $995 - $1,295
1 - 2 Weeks

Point Mutation Publications

  • Single Amino Acid Changes in the Ryanodine Receptor in the Human Population Have Effects In Vivo on Caenorhabditis elegans Neuro-Muscular Function

    Brittany Graham, Marie-Anne Shaw and Ian A. Hope. Front. Genet., 26 February 2020

  • Repurposing the aldose reductase inhibitor and diabetic neuropathy drug epalrestat for the congenital disorder of glycosylation PMM2-CDG

    Sangeetha Iyer, Feba S. Sam, Nina DiPrimio, Graeme Preston, Jan Verheijen, Kausalya Murthy, Zachary Parton, Hillary Tsang, Jessica Lao, Eva Morava2 and Ethan O. Perlstein. Disease Models & Mechanisms (2019) 12.

  • Repurposing the aldose reductase inhibitor and diabetic neuropathy drug epalrestat for the congenital disorder of glycosylation PMM2-CDG

    Iyer S, Murthy K, Parton Z, Tsang H, Sam FS. bioRxiv. 2019 May 3; 1-29

  • Regulation of the sperm-to-oocyte transition in Caenorhabditis briggsae hermaphrodites by the Cbr-met-2 and Cbr-fem-3 genes

    Berenson AL, Baird SE. Mol Reprod Dev. 2018 Jun;85(6):532-542.

  • NALCN channelopathies: Distinguishing gain-of-function and loss-of-function mutations

    Bend, EG; Si, Y; Stevenson, DA; Bayrak-Toydemir, P; Newcomb, TM; Jorgensen, EM; Swoboda, KJ. Neurology. 2016 Sep 13;87(11):1131-9.

  • An RNAi-based suppressor screen identifies interactors of the Myt1 ortholog of Caenorhabditis elegans

    Allen, AK; Nesmith, JE; Golden, A. G3 (Bethesda). 2014 Oct 8;4(12):2329-43.

  • LEM-3 is a midbody-tethered DNA nuclease that resolves chromatin bridges during cytokinesis

    HONG, Y; Sonneville, R; Wang, B; Scheidt, V; Meier, B; Woglar, A; Demetriou, S; Labib, K; Jantsch, V; Gartner, A. Nat Commun. 2018 Feb 20;9(1):728.

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