ced-1 encodes a transmembrane receptor on engulfing cells that recognizes phosphatidylserine-like eat-me signals on apoptotic corpses. As the C. elegans ortholog of mammalian MEGF10 / MEGF11, CED-1 is the gateway to corpse clearance in the recognition branch of the engulfment pathway.
Because corpse clearance is a conserved process relevant to development, immunity, and neurodegeneration, manipulating ced-1 provides a clean, in vivo model. CD BioSciences delivers custom ced-1 alleles — knockout, fluorescent tag knockin, and CED-6-binding interface mutants — with full verification.
| Gene symbol | ced-1 (Engulfment receptor (MEGF10 homolog)) |
|---|---|
| Protein product | CED-1 — phagocytic engulfment receptor |
| Mammalian homolog | MEGF10 / MEGF11 (mammalian engulfment receptors) |
| Biological role | Phagocytic receptor on engulfing cells; recognizes phosphatidylserine-like eat-me signals on apoptotic corpses and triggers their internalization. |
| Loss-of-function phenotype | Persistent cell corpses; engulfment-defective — apoptotic cells are made but not cleared. |
| Why edit it | MEGF10-related disease modeling; phagocytic receptor biology; tissue homeostasis and nervous-system pruning. |
| Recommended background | N2 (wild type); can be combined with ced-5/ced-10 or apoptosis-deficient backgrounds. |
| Representative allele | Standard knockout (ok / tm / gk series); e1751 is a canonical reference allele. |
ced-1 at a glance: blocks engulfment of apoptotic corpses; persistent-cell-corpse phenotype easy to score by DIC microscopy. Editing ced-1 alone is a powerful way to dissect CED-1 function in vivo, with conserved relevance to human MEGF10 biology.
gRNA-guided Cas9 cutting with NHEJ repair to introduce frameshift indels, generating premature stop codons and null / strong-loss-of-function ced-1 alleles.
Homology-directed repair (HDR) inserts GFP / HA / FLAG or other tags at the ced-1 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-1.
Build tissue-specific or inducible configurations and reporter lines for spatiotemporal analysis of CED-1 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-1 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-1 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.
Persistent cell corpses are scored by DIC microscopy in the head of L1-L2 larvae using the standard 4-cell region. The assay is sensitive, quantitative, and widely used.
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. Zhou Z., Yu X. Phagosome maturation during the removal of apoptotic cells. Cell Biol Int, 2006, 30(10): 789-792.
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