C. elegans ced-9 Functional Gene Editing Service

Service Overview Precision editing of CED-9 in a premier genetic model for cell death research

ced-9 encodes the C. elegans ortholog of mammalian BCL2 and is the central brake on programmed cell death. By sequestering the adaptor CED-4 at the outer mitochondrial membrane, CED-9 prevents inappropriate caspase activation. The pro-apoptotic BH3-only protein EGL-1 relieves this brake during normal development.

Because ced-9 is a functional homolog of BCL2, manipulating it in C. elegans directly models cancer-relevant Bcl-2 family biology. CD BioSciences designs and delivers custom ced-9 alleles — including clean knockouts (typically balanced), knockins, and point mutations that disrupt CED-9/EGL-1 or CED-9/CED-4 interfaces.

About the Target Gene: ced-9 Key biological and practical facts to inform your edit design

Gene symbol	ced-9 (Anti-apoptotic factor (Bcl-2 homolog))
Protein product	CED-9 — Bcl-2-like anti-apoptotic factor
Mammalian homolog	BCL2 / BCL-xL / MCL1 (Bcl-2 family)
Biological role	Anti-apoptotic guardian; sequesters CED-4 at the mitochondrial membrane to prevent CED-3 activation. Antagonized by EGL-1.
Loss-of-function phenotype	Maternal-effect lethality: ced-9(null) mothers produce embryos with massive ectopic cell death. Gain-of-function alleles (e.g. n1950) are viable and apoptosis-defective.
Why edit it	Bcl-2 family / cancer biology; BH3-mimetic drug screening (venetoclax, navitoclax); chemoresistance; mitochondrial apoptosis regulation.
Recommended background	N2; ced-9 loss-of-function alleles are typically maintained balanced or via gain-of-function reference alleles (e.g. n1950).
Representative allele	n1950 (canonical gain-of-function reference); standard knockout alleles available on request.

Fig. 1 Conserved apoptosis pathway in C. elegans. The highlighted (amber) node marks the editing target.

ced-9 at a glance: blocks essentially all programmed somatic cell deaths; a clean Bcl-2-like apoptosis-deficient model. Editing ced-9 alone is a powerful way to dissect CED-9 function in vivo, with conserved relevance to human BCL2 biology.

Our ced-9 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-9 alleles.

Knockin & Tagging

Homology-directed repair (HDR) inserts GFP / HA / FLAG or other tags at the ced-9 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-9.

Conditional & Reporter Alleles

Build tissue-specific or inducible configurations and reporter lines for spatiotemporal analysis of CED-9 function.

Workflow of Our ced-9 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-9 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-9 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-9 model adds value

Bcl-2 family anti-apoptotic mechanism in cancer.
BH3-mimetic drug screening (venetoclax, navitoclax, etc.).
CED-9 / CED-4 protein-protein interaction studies.
CED-9 / EGL-1 BH3-domain interface and mutagenesis.
Mitochondrial outer-membrane permeabilization (MOMP) regulation.
Lymphoma, leukemia, and chemoresistance modeling.
Evolutionary conservation of Bcl-2 family function.

Deliverables What you receive with every project

Genetically verified ced-9 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-9 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-9?

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-9 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.

Why is ced-9 knockout hard to maintain as a homozygote?

ced-9 loss-of-function causes maternal-effect lethality because oocytes arrive pre-loaded with CED-9 protein that decays, leading to ectopic death in progeny. We typically deliver ced-9 knockouts balanced over a deficiency or as engineered gain-of-function alleles, or as point mutations that specifically disrupt the EGL-1 interface.

Start Your ced-9 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.

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. Youle R. J., Strasser A. The BCL-2 protein family: opposing activities that mediate cell death. Nat Rev Mol Cell Biol, 2008, 9(1): 47-59.

For research use only.