ced-11 is an apoptosis-related gene in C. elegans linked to mitochondrial function. While it is less characterized than the canonical CED-3 / CED-4 / CED-9 / EGL-1 axis, it represents an emerging node in the cell-death network and an opportunity for first-of-its-kind genetic dissection.
Because ced-11 is not well covered by legacy alleles, CRISPR-based custom editing is the route of choice. CD BioSciences delivers clean knockouts, fluorescent tag knockins, and promoter / enhancer deletions to characterize the locus in apoptosis and mitochondrial contexts.
| Gene symbol | ced-11 (Apoptosis-related mitochondrial factor) |
|---|---|
| Protein product | CED-11 — apoptosis-related mitochondrial factor |
| Mammalian homolog | No clear mammalian ortholog (under characterization). |
| Biological role | Implicated in apoptosis and mitochondrial function in C. elegans; less characterized than the core ced-3/ced-4/ced-9 axis. |
| Loss-of-function phenotype | Limited published characterization; emerging phenotype data suggest mild apoptosis-related defects. |
| Why edit it | An emerging apoptosis / mitochondrial factor; a first-of-its-kind model for a less-studied node in the cell-death network. |
| Recommended background | N2 (wild type); suitable for CRISPR-based knockout and tagging studies. |
| Representative allele | Standard knockout (ok / tm / gk series) on request. |
ced-11 at a glance: an emerging apoptosis-related factor; clean CRISPR knockout enables first-of-its-kind loss-of-function analysis. Editing ced-11 alone is a powerful way to dissect CED-11 function in vivo, with conserved relevance to human No clear mammalian ortholog biology.
gRNA-guided Cas9 cutting with NHEJ repair to introduce frameshift indels, generating premature stop codons and null / strong-loss-of-function ced-11 alleles.
Homology-directed repair (HDR) inserts GFP / HA / FLAG or other tags at the ced-11 locus for endogenous expression and subcellular localization studies.
Introduce specific amino-acid substitutions to dissect functional domains and separate catalytic from scaffolding roles of CED-11.
Build tissue-specific or inducible configurations and reporter lines for spatiotemporal analysis of CED-11 function.
Define target (knockout / knockin / point mutation), select gRNA(s) and HDR template, confirm against the latest genome build.
Design, validate, and synthesize high-specificity guide RNAs targeting the ced-11 locus.
Build Cas9 / gRNA delivery construct and, for knockin, the homology-arm repair template.
Perform gonadal microinjection of N2 animals with CRISPR components and co-CRISPR selection markers.
PCR, Sanger / sequencing, and phenotype confirmation to isolate edited animals and verify alleles.
Provide homozygous / balanced ced-11 strains plus a full genotype and methods report.
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.
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.
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.
Public data suggest ced-11 contributes to apoptosis-related phenotypes, but redundancy with the core axis has not been fully mapped. Knockout + epistasis with ced-3, ced-4, and ced-9 is the standard first-line approach.
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 UsReferences
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. Conradt B., Xue D. Programmed cell death. WormBook, 2005, ed. The C. elegans Research Community, WormBook, doi/10.1895/wormbook.1.32.1.
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