ced-6 encodes the C. elegans ortholog of mammalian GULP1, a key adapter that transduces the CED-1 / MEGF10 receptor signal to the actin-regulatory machinery during corpse engulfment. It sits at a critical node in the recognition branch, integrating receptor input to downstream effectors.
Because GULP1 is implicated in atherosclerosis and lipid-handling in mammals, ced-6 provides an in vivo model for CED-6 / GULP1 biology. CD BioSciences delivers knockout, knockin, and PTB-domain point mutants for functional dissection.
| Gene symbol | ced-6 (Engulfment adaptor (GULP1 homolog)) |
|---|---|
| Protein product | CED-6 — engulfment adapter (GULP1 ortholog) |
| Mammalian homolog | GULP1 (mammalian engulfment adapter) |
| Biological role | Adapter in the recognition branch of the engulfment pathway; transduces the CED-1 receptor signal to downstream actin regulators and the engulfment machinery. |
| Loss-of-function phenotype | Persistent cell corpses; engulfment-defective. |
| Why edit it | GULP1 / LRP1 biology; phagocytic signaling; atherosclerosis and lipid handling; cell-corpse recognition. |
| Recommended background | N2 (wild type); can be combined with ced-1, ced-7, or ced-10 mutants. |
| Representative allele | Standard knockout (ok / tm / gk series); n1813 is a canonical reference allele. |
ced-6 at a glance: blocks engulfment of apoptotic corpses; persistent-cell-corpse phenotype easy to score. Editing ced-6 alone is a powerful way to dissect CED-6 function in vivo, with conserved relevance to human GULP1 biology.
gRNA-guided Cas9 cutting with NHEJ repair to introduce frameshift indels, generating premature stop codons and null / strong-loss-of-function ced-6 alleles.
Homology-directed repair (HDR) inserts GFP / HA / FLAG or other tags at the ced-6 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-6.
Build tissue-specific or inducible configurations and reporter lines for spatiotemporal analysis of CED-6 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-6 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-6 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.
The CED-1 intracellular tail binds directly to the CED-6 PTB domain. This is conserved in mammals between MEGF10 and GULP1. Mutating the CED-1 NPXY motif or the CED-6 PTB domain abolishes the interaction, providing a clean functional readout.
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. Penberthy K. K., Ravichandran K. S. Apoptotic cell recognition receptors and scavenger receptors. Immunol Rev, 2016, 269(1): 44-59.
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