Service Overview Precision editing of CED-4 in a premier genetic model for cell death research

ced-4 encodes the central adaptor of the C. elegans apoptosis pathway. Analogous to mammalian APAF1, CED-4 nucleates a caspase-activation platform (the apoptosome) that drives CED-3 maturation and downstream substrate cleavage. As such, ced-4 is the linchpin between the regulatory triad (EGL-1 / CED-9) and the executioner CED-3.

CD BioSciences provides an optimized, full-stack CRISPR/Cas9 platform for C. elegans. We design and deliver custom ced-4 alleles — including targeted knockouts, fluorescent or epitope tag knockins, and site-specific point mutations — with complete genotype verification and a transparent reporting package.

About the Target Gene: ced-4 Key biological and practical facts to inform your edit design

Gene symbolced-4 (Apoptosis activator (Apaf-1 homolog))
Protein productCED-4 — Apaf-1-like apoptosis adaptor
Mammalian homologAPAF1 (mammalian Apaf-1)
Biological roleAdaptor that scaffolds CED-3 caspase activation; core component of the C. elegans apoptosome-like complex.
Loss-of-function phenotypeLoss of ced-4 blocks essentially all programmed somatic cell deaths; animals viable with extra cells.
Why edit itFoundational model for apoptosome assembly, intrinsic (mitochondrial) apoptosis, and cancer drug resistance linked to apoptosome defects.
Recommended backgroundN2 (wild type); can be crossed into reporter or co-CRISPR selection backgrounds.
Representative alleleStandard knockout (ok / tm / gk series); reference alleles widely available.
CED-4 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 blocks essentially all programmed somatic cell deaths; a clean Apaf-1-like apoptosis-deficient model.
Fig. 1 Conserved apoptosis pathway in C. elegans. The highlighted (amber) node marks the editing target.

ced-4 at a glance: blocks essentially all programmed somatic cell deaths; a clean Apaf-1-like apoptosis-deficient model. Editing ced-4 alone is a powerful way to dissect CED-4 function in vivo, with conserved relevance to human APAF1 biology.

Our ced-4 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-4 alleles.

Knockin & Tagging

Homology-directed repair (HDR) inserts GFP / HA / FLAG or other tags at the ced-4 locus for endogenous expression and subcellular localization studies.

Point Mutation

Introduce specific amino-acid substitutions to dissect functional domains and separate catalytic from scaffolding roles of CED-4.

Conditional & Reporter Alleles

Build tissue-specific or inducible configurations and reporter lines for spatiotemporal analysis of CED-4 function.

Workflow of Our ced-4 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-4 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-4 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-4 model adds value

  • Apoptosome assembly mechanism (CED-4 / CED-3 scaffold).
  • Mammalian intrinsic (mitochondrial) apoptosis via APAF1.
  • Cancer drug resistance linked to apoptosome defects.
  • Caspase-9 activation platform and cytochrome c dependency.
  • MOMP-driven apoptosis in development and disease.
  • CED-9 / CED-4 mitochondrial tethering and release studies.
  • Epistasis with egl-1, ced-9, and ced-3 to dissect the linear cascade.

Deliverables What you receive with every project

  • Genetically verified ced-4 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-4 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 characteristic phenotype assays.

Can you add a GFP or epitope tag to endogenous ced-4?

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-4 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.

Is ced-4 essential for animal viability?

No. ced-4 loss-of-function animals are viable and fertile, but they retain the 131 cells that normally die during development. This mirrors Apaf-1 knockout in mammals, making ced-4 an exceptionally clean genetic null.

Start Your ced-4 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

References
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.
2. Riedl S. J., Shi Y. Molecular mechanisms of caspase regulation during apoptosis. Nat Rev Mol Cell Biol, 2004, 5(11): 897-907.

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