ced-12 encodes the C. elegans ortholog of mammalian ELMO1. In the signaling branch of the engulfment pathway, CED-12 forms a complex with CED-2 and CED-5 (DOCK180) that activates the CED-10 / Rac GTPase to drive actin dynamics. CED-12 also binds CED-1, providing cross-talk between the two engulfment branches.
ELMO-DOCK complexes are central to cell migration and cancer metastasis. CD BioSciences designs and delivers custom ced-12 alleles — knockout, ELMO-domain point mutants, and fluorescent knockins — for DOCK-ELMO biology and cell-migration research.
| Gene symbol | ced-12 (ELMO homolog (engulfment scaffold)) |
|---|---|
| Protein product | CED-12 — ELMO-family scaffold |
| Mammalian homolog | ELMO1 / ELMO2 / ELMO3 (mammalian ELMO family) |
| Biological role | Scaffold of the CED-2 / CED-5 / CED-12 signaling complex; cooperates with DOCK180 (CED-5) to activate Rac (CED-10); also binds CED-1 to bridge the two engulfment branches. |
| Loss-of-function phenotype | Persistent cell corpses; engulfment-defective. |
| Why edit it | ELMO1 in cell migration, cancer metastasis, and DOCK-ELMO complex biology; phagocytic-cup formation. |
| Recommended background | N2 (wild type); can be combined with ced-1, ced-2, ced-5, or ced-10 mutants. |
| Representative allele | Standard knockout (ok / tm / gk series); reference alleles available on request. |
ced-12 at a glance: blocks engulfment of apoptotic corpses; persistent-cell-corpse phenotype easy to score. Editing ced-12 alone is a powerful way to dissect CED-12 function in vivo, with conserved relevance to human ELMO1 biology.
gRNA-guided Cas9 cutting with NHEJ repair to introduce frameshift indels, generating premature stop codons and null / strong-loss-of-function ced-12 alleles.
Homology-directed repair (HDR) inserts GFP / HA / FLAG or other tags at the ced-12 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-12.
Build tissue-specific or inducible configurations and reporter lines for spatiotemporal analysis of CED-12 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-12 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-12 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 PH domain mediates membrane recruitment, the ELMO domain binds CED-5 / DOCK180, and the BH domain contributes to CED-10 / Rac activation and CED-1 cross-talk. Disrupting each in turn provides a clean functional dissection.
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. Patel M., Margaron Y., Fradet-Turcotte A., Bhat M. ELMO and RGS proteins: emerging targets in cancer cell migration and metastasis. Cell Signal, 2020, 75: 109753.
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