ced-5 encodes the C. elegans ortholog of mammalian DOCK1 (DOCK180), a non-conventional GEF that activates Rac GTPases. In the signaling branch of the engulfment pathway, CED-5 acts in a complex with CED-2 and CED-12 to drive CED-10/Rac activation and the actin reorganization required for corpse internalization.
DOCK proteins are central regulators of cell migration, immune-cell function, and cancer metastasis in mammals. CD BioSciences designs and delivers custom ced-5 alleles — knockout, GEF-domain point mutants, and fluorescent knockins — for DOCK-Rac biology and metastasis research.
| Gene symbol | ced-5 (Dock180 homolog, engulfment GEF) |
|---|---|
| Protein product | CED-5 — Dock180-family Rac GEF |
| Mammalian homolog | DOCK1 / DOCK2 / DOCK5 (DOCK180 family) |
| Biological role | GEF for the CED-10 / Rac GTPase; core of the CED-2 / CED-5 / CED-12 signaling complex that drives actin dynamics for engulfment. |
| Loss-of-function phenotype | Persistent cell corpses; engulfment-defective; cell-migration defects in some contexts. |
| Why edit it | DOCK1 family in immunity, cell migration, and cancer metastasis; phagocytic-cup formation. |
| Recommended background | N2 (wild type); can be combined with ced-1, ced-2, ced-10, or ced-12 mutants. |
| Representative allele | Standard knockout (ok / tm / gk series); n1812 is a canonical reference allele. |
ced-5 at a glance: blocks engulfment of apoptotic corpses; persistent-cell-corpse phenotype easy to score. Editing ced-5 alone is a powerful way to dissect CED-5 function in vivo, with conserved relevance to human DOCK1 biology.
gRNA-guided Cas9 cutting with NHEJ repair to introduce frameshift indels, generating premature stop codons and null / strong-loss-of-function ced-5 alleles.
Homology-directed repair (HDR) inserts GFP / HA / FLAG or other tags at the ced-5 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-5.
Build tissue-specific or inducible configurations and reporter lines for spatiotemporal analysis of CED-5 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-5 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-5 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.
Yes. We routinely engineer DHR2-domain point mutations that abolish Rac-GEF activity while leaving the protein expressed and able to scaffold. This is a powerful tool to dissect GEF-dependent versus -independent functions of CED-5 / DOCK1.
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. Gadea G., Blangy A. Dock-family exchange factors in cell migration and disease. Small GTPases, 2014, 5(2): e972800.
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