ced-10 encodes the C. elegans ortholog of mammalian Rac1 (RAC1/2/3). As the convergence point of both branches of the engulfment pathway, CED-10 integrates signals from the recognition branch (CED-1/-6/-7) and the signaling branch (CED-2/-5/-12) to drive actin polymerization around the apoptotic corpse.
Because Rac GTPases are central to cell migration, immune-cell function, and cancer metastasis in mammals, manipulating ced-10 directly informs these fields. CD BioSciences delivers knockout, GTPase-domain point mutants (constitutively active / dominant negative), and fluorescent knockins for Rac biology.
| Gene symbol | ced-10 (Rac1 homolog GTPase (engulfment)) |
|---|---|
| Protein product | CED-10 — Rac-family GTPase |
| Mammalian homolog | RAC1 / RAC2 / RAC3 (Rho-family GTPases) |
| Biological role | Rho-family GTPase that drives actin polymerization and cytoskeletal remodeling for corpse engulfment; the convergence point of both the recognition (CED-1/-6/-7) and signaling (CED-2/-5/-12) branches. |
| Loss-of-function phenotype | Persistent cell corpses; engulfment-defective; cell-migration defects. |
| Why edit it | Rac1 in cancer invasion, immunity, and NADPH oxidase regulation; actin dynamics in phagocytosis. |
| Recommended background | N2 (wild type); can be combined with ced-1, ced-2, ced-5, or ced-12 mutants. |
| Representative allele | Standard knockout (ok / tm / gk series); n1993 is a canonical reference allele. |
ced-10 at a glance: blocks engulfment of apoptotic corpses; persistent-cell-corpse phenotype easy to score. Editing ced-10 alone is a powerful way to dissect CED-10 function in vivo, with conserved relevance to human RAC1 biology.
gRNA-guided Cas9 cutting with NHEJ repair to introduce frameshift indels, generating premature stop codons and null / strong-loss-of-function ced-10 alleles.
Homology-directed repair (HDR) inserts GFP / HA / FLAG or other tags at the ced-10 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-10.
Build tissue-specific or inducible configurations and reporter lines for spatiotemporal analysis of CED-10 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-10 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-10 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. G12V (constitutively active) and T17N (dominant negative) are well-established in the C. elegans Rac literature. We can also build switch-I or switch-II point mutants to dissect GTP / GDP binding, Mg2+ coordination, and effector interactions.
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. Bosco E. E., Mulloy J. C., Zheng Y. Rac1 GTPase: a “Rac” of all trades. Cell Mol Life Sci, 2009, 66(23): 3701-3719.
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