Service Overview Precision editing of the central apoptosis caspase in a premier genetic model

ced-3 encodes a cysteine protease (caspase) that acts as the central executioner of programmed cell death (apoptosis) in C. elegans. As the founding member of the apoptosis pathway first defined in this organism, ced-3 loss-of-function mutants are viable yet block the vast majority of somatic cell deaths, making them an indispensable tool for studying cell death mechanisms, corpse clearance, and synthetic lethal interactions.

CD BioSciences has established a mature, optimized genome-editing platform for C. elegans. Leveraging CRISPR/Cas9 and the broadly used co-CRISPR selection markers, we design and deliver custom ced-3 alleles — including targeted knockouts, fluorescent or epitope tag knockins, and site-specific point mutations — with full genotype verification and a clear reporting package.

About the Target Gene: ced-3 Key biological and practical facts to inform your edit design

Gene symbolced-3 (cell death abnormal-3)
Protein productCED-3 — executioner/inflammatory-type cysteine protease (caspase)
Mammalian homologCASP3 / CASP7 / CASP9 (apoptotic caspases)
Biological roleCentral executioner of somatic apoptosis; activated downstream of EGL-1 → CED-9 → CED-4
Loss-of-function phenotypeBlocks ~109 of 131 programmed somatic cell deaths; animals viable with persistent extra cells
Why edit itFoundational model for apoptosis, cell-death regulation, corpse engulfment, and human caspase-related disease
Recommended backgroundN2 (wild type); can be crossed into co-CRISPR selection or fluorescent reporter backgrounds
CED-3 in the C. elegans Apoptosis Cascade activates inhibits induces inhibits inhibits activates executes Apoptotic stimulus egl-1 BH3-only · pro ced-9 Bcl-2 · anti ced-4 Apaf-1-like ced-3 ★ Executioner Cell death substrate cleavage Loss of ced-3 blocks ~109/131 somatic deaths yet remains viable → a clean apoptosis-deficient model.
Fig. 1 Conserved apoptosis pathway in C. elegans. ced-3 sits at the execution node; loss-of-function alleles phenocopy the cell-death-defective state.

A summary of the conserved apoptosis pathway in C. elegans: egl-1 (BH3-only) antagonizes ced-9 (anti-apoptotic), releasing ced-4 (Apaf-1-like) to activate ced-3, which cleaves cellular substrates to execute death. Editing ced-3 alone is typically sufficient to phenocopy the cell-death-defective state.

Our ced-3 Editing Strategies Choose the allele that matches your experimental question

Gene Knockout

gRNA-guided Cas9 cutting with NHEJ repair to introduce frameshift indels, generating premature stop codons and null/strong-loss-of-function ced-3 alleles.

Knockin & Tagging

Homology-directed repair (HDR) inserts GFP/HA/FLAG or other tags at the ced-3 locus for endogenous expression and subcellular localization studies.

Point Mutation

Introduce specific amino-acid substitutions (e.g., catalytic-site mutations) to separate catalytic from scaffolding functions of CED-3.

Conditional & Reporter Alleles

Build tissue-specific or inducible configurations and caspase-activity reporters for spatiotemporal analysis of apoptosis.

Workflow of Our ced-3 Editing Service From sequence to validated strain in a streamlined pipeline

Strategy Design

Define target (knockout / knockin / point mutation), select gRNA(s) and HDR template, confirm against the latest genome build.

gRNA Synthesis

Design, validate, and synthesize high-specificity guide RNAs targeting the ced-3 locus.

Vector & Template Construction

Build Cas9/gRNA delivery construct and, for knockin, the homology-arm repair template.

Microinjection

Perform gonadal microinjection of N2 animals with CRISPR components and co-CRISPR selection markers.

Screening & Verification

PCR, Sanger/sequencing, and phenotype confirmation to isolate edited animals and verify alleles.

Delivery & Report

Provide homozygous/balanced ced-3 strains plus a full genotype and methods report.

Key Features Why researchers choose CD BioSciences for C. elegans editing

  • High-efficiency, optimized CRISPR/Cas9 platform for C. elegans.
  • Whole-process technical traceability and transparent timelines.
  • Flexible editing: knockout, knockin, tagging, and point mutation.
  • Full genotype verification before strain delivery.
  • One-stop model development integrated with our C. elegans portfolio.
  • Competitive pricing and short turnaround.
  • Direct access to scientists and prompt inquiry response.
  • Reliable, convenient global shipping of frozen stocks.

Applications Where a custom ced-3 model adds value

  • Mechanistic studies of programmed cell death and apoptosis execution.
  • Regulation of caspase activation by EGL-1 / CED-9 / CED-4.
  • Cell-corpses engulfment and clearance assays (with ced-1, ced-2, ced-5, ced-10).
  • Synthetic-lethal and genetic-interaction screens involving death pathways.
  • Developmental lineage analysis of surviving "extra" cells.
  • Human caspase (CASP3/7/9) disease modeling via conserved apoptosis nodes.
  • Small-molecule and drug screens targeting apoptotic machinery.
  • Stress-induced germline apoptosis (e.g., DNA-damage response via CEP-1/p53).

Deliverables What you receive with every project

  • Genetically verified ced-3 edited strain(s) (homozygous or balanced).
  • Detailed genotyping report (editing strategy, allele sequence, verification data).
  • Methods summary and rearing/storage recommendations.
  • Optional: crosses into reporter or co-CRISPR selection backgrounds.
  • Optional: phenotype confirmation and imaging support.

Frequently Asked Questions

What type of ced-3 allele will I get from a knockout project?

Standard knockout projects deliver a frameshift indel allele predicted to produce a premature stop and a loss-of-function phenotype. We confirm the edit by sequencing and, where relevant, by the characteristic cell-death-defective phenotype.

Can you add a GFP or epitope tag to endogenous ced-3?

Yes. Using HDR with a designed repair template, we can insert GFP, HA, or FLAG tags at the C- or N-terminus while preserving endogenous promoter and regulation.

How long does a typical ced-3 editing project take?

Timelines vary with editing type and validation needs, but our optimized pipeline and co-CRISPR selection typically shorten turnaround versus conventional approaches. Contact us with your design for a project-specific estimate.

Do you provide strains in backgrounds other than N2?

We primarily edit the N2 background but can outcross edited alleles into fluorescent reporter or other requested backgrounds upon request.

Start Your ced-3 Editing Project

CD BioSciences is committed to convenient, efficient, and cost-effective C. elegans model customization. Tell us your target design — knockout, knockin, tagging, or point mutation — and our scientists will respond with a tailored plan and quote.

Contact Us

Reference
1. Kim H. M., Colaiácovo M. P. CRISPR-Cas9-guided genome engineering in C. elegans. Current Protocols in Molecular Biology, 2016, 115(1): 31.7.1–31.7.18.

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