A curated, pathway-organized overview of the functional genes we routinely edit in Caenorhabditis elegans — the premier in vivo model in which 60–80% of human genes have a conserved counterpart. Each gene below links to a dedicated CRISPR/Cas9 editing service page with pathway diagrams, human ortholog context, editing strategies, and applications.
C. elegans is the organism in which programmed cell death was genetically defined. Loss of a single ced gene blocks the deaths of 131 identifiable somatic cells, and every core component has a conserved mammalian counterpart — making these knockouts the most direct in vivo models for caspase biology, Bcl-2 regulation, and apoptotic-cell clearance.
The executioner caspase; cleaves cellular substrates to implement death. The flagship apoptosis knockout model.
View editing service →Apaf-1-like apoptosome adaptor that activates CED-3; the caspase-activation hub of the pathway.
View editing service →Bcl-2 homolog that sequesters CED-4 at mitochondria; the anti-apoptotic brake of the cascade.
View editing service →BH3-only pro-apoptotic trigger that antagonizes CED-9; the decision point that initiates death.
View editing service →Apoptosis-related mitochondrial factor acting in the death-execution branch downstream of the core cascade.
View editing service →Pro-apoptotic factor redundant with egl-1-class function; required for DNA-damage-induced germline apoptosis.
View editing service →Phosphatidylserine (eat-me signal) receptor that recognizes apoptotic corpses for engulfment.
View editing service →Adaptor that transduces the CED-1 recognition signal toward the cytoskeletal engulfment machinery.
View editing service →ABC transporter required for eat-me-signal presentation on dying cells and for corpse clearance.
View editing service →CrkII-like signaling adaptor of the engulfment branch controlling cytoskeletal rearrangement.
View editing service →Dock180-like guanine-nucleotide exchange factor that activates CED-10/Rac during engulfment.
View editing service →ELMO scaffold that partners with CED-5/DOCK to form the bipartite Rac guanine-exchange complex.
View editing service →Rac GTPase where both engulfment branches converge to drive actin-mediated corpse internalization.
View editing service →Reduced insulin/IGF-1 signaling can double C. elegans lifespan while the animal stays active and fertile. Every node is conserved in mammals, from the insulin receptor to the FOXO transcription factor, making these knockouts the standard entry point for longevity, metabolic-disease, and FOXO-biology research.
The insulin/IGF-1 receptor; reduced signaling (e.g. e1370) roughly doubles adult lifespan.
View editing service →PI3K catalytic subunit downstream of DAF-2; loss extends lifespan by ~40%.
View editing service →PTEN lipid phosphatase opposing AGE-1/PI3K; the tumor-suppressor brake on IIS.
View editing service →Master kinase activating both AKT and SGK branches downstream of PI3K.
View editing service →AKT kinase that phosphorylates and inhibits DAF-16/FOXO; redundant with akt-2.
View editing service →Second AKT isoform acting redundantly with akt-1 in FOXO regulation; double knockouts maximize output.
View editing service →Serum/glucocorticoid-regulated kinase acting in parallel to AKT on DAF-16.
View editing service →The master FOXO transcription factor and principal output of IIS; required for daf-2 longevity.
View editing service →Mild mitochondrial impairment extends lifespan while severe electron leak shortens it, and dietary restriction acts through dedicated transcriptional programs — discoveries made in exactly these mutants. This set covers both directions of the dose–response and the two major nutrient pathways of aging.
Coenzyme Q (ubiquinone) biosynthesis hydroxylase; founding ‘clock’ gene of aging (qm30).
View editing service →Complex III Rieske iron-sulfur protein; partial loss (qm150) markedly extends lifespan.
View editing service →Complex I subunit; a modest mitochondrial superoxide signal (qm200) triggers increased longevity.
View editing service →Complex II subunit C; electron leak and excess superoxide shorten lifespan — the classic pro-aging mutant.
View editing service →Nicotinic acetylcholine receptor subunit; slow pumping makes the standard genetic model of dietary restriction.
View editing service →FoxA transcription factor required for the longevity response to dietary restriction (zu225).
View editing service →Notch receptor maintaining germline stem cells; removing the germline extends lifespan.
View editing service →The 28 pages above are our fully documented anchor entries. The remaining catalog below is equally addressable through the same CRISPR/Cas9 pipeline — contact us with a gene or a pathway and we will build the dedicated service package and documentation for it.
| Functional Category | Genes | Representative Genes | Representative Mammalian Orthologs / Relevance |
|---|---|---|---|
| Antioxidant & Oxidative Stress | 11 | sod-1, sod-2, sod-3, ctl-1, ctl-2, skn-1 | SOD1/2/3, catalase, Nrf2 — oxidative defense and stress signaling |
| Epigenetic & Translational Control | 5 | sir-2.1, utx-1, ife-2, let-363 | SIRT1, UTX/KDM6A, eIF4E, mTOR — chromatin and translation in aging |
| Dauer Formation | 13 | daf-7, daf-12, daf-11, daf-21 | TGF-β ligands, VDR-like nuclear receptor, Hsp90 — diapause and neuroendocrine control |
| Development — Ras/MAPK | 11 | let-23, let-60, lin-45, lin-3 | EGFR, KRAS, RAF, EGF — receptor tyrosine kinase signaling and vulval patterning |
| Development — Notch Pathway | 7 | lag-1, lag-2, sel-8, apx-1 | NOTCH, RBPJκ, DSL ligands — lateral signaling and cell-fate decisions |
| Development — Cell Polarity | 9 | par-1–par-6, mex-1, mex-3 | PAR kinases, atypical PKC — asymmetric division and stemness |
| Locomotion & Cytoskeleton | 15 | unc-54, unc-22, myo-3, hlh-1 | myosin heavy chain, twitchin, MyoD-like bHLH — muscle and motor behavior |
| Cilia & Intraflagellar Transport | 18 | bbs-1, bbs-2, bbs-7, che-3, osm-5, osm-6 | BBS proteins, IFT dyneins, IFT57/88 — ciliopathies such as Bardet–Biedl syndrome |
| Sensory & Chemoreception | 13 | odr-3, odr-10, tax-2, tax-4, che-1 | olfactory GPCRs, cyclic-nucleotide-gated channels — chemosensation and sensory neuroscience |
| Neurotransmission | 8 | unc-25, unc-47, eat-4, glr-1, snb-1 | GAD65/67, vGAT, vGLUT, AMPA receptor, synaptobrevin — synaptic transmission |
| Germline & Sex Determination | 12 | fog-1, fog-3, gld-1, mog-1 | CPEB-class RNA regulators, DDX5 helicase — germline stem-cell and sperm/oocyte fate |
| Mechanosensation | 11 | mec-2, mec-4, mec-7, mec-10 | stomatin, DEG/ENaC channels, β-tubulin — touch transduction and channelopathies |
| Stress & Heat-Shock Response | 5 | hsf-1, hsp-16.1, hsp-16.2, hsp-70 | HSF1, HSPB/alpha-crystallin, HSPA — proteostasis and thermotolerance |
| DNA Damage & Radiation Response | 6 | cep-1, mrt-2, hus-1, clk-2 | p53, ATM/ATR checkpoint axis — genome stability and DNA-damage checkpoints |
| Morphology Markers | 6 | dpy series, lon-1, rol-6 | collagens and TGF-β-linked size control — visible markers for strain construction |
Every entry above is editable through the same validated pipeline: knockout, knockin & tagging, point mutation, and conditional / reporter configurations, delivered with full genotype verification.
If your target gene or pathway is not yet documented with a dedicated page, we still build it: the categories above are drawn from our working knockout catalog, and custom targets outside it are routine. Send us the gene name (WormBase ID welcome), the intended allele type, and your experimental question — our scientists will return a design, timeline, and quote.
Gene name or WormBase ID plus the desired edit (KO / knockin / point mutation / conditional).
gRNA selection, HDR template design, and viability assessment by our C. elegans team.
A tailored plan with milestones, validation criteria, and delivery format.
CRISPR/Cas9 microinjection with co-CRISPR selection under traceable conditions.
Sequencing and phenotype confirmation before any strain ships.
Verified strains plus a full genotype and methods report.
Yes. The catalog below covers 178 genes we have curated in depth, but our CRISPR/Cas9 platform addresses essentially any of the roughly 20,000 protein-coding genes in the C. elegans genome. Contact us with the target and intended edit.
Yes — for example akt-1 akt-2 double knockouts, or crosses of edited alleles into reporter and longevity-assay backgrounds. Epistasis strain construction is a routine extension of the service.
It depends on the gene: null or strong alleles suit genes like ced-3, while long-lived mitochondrial and IIS phenotypes are often best reproduced with partial loss-of-function or canonical reference alleles (e1370, qm150, qm200, ad1116). Each gene page includes a recommended-allele note for exactly this reason.
Pick a gene from the portfolio above, or send us any target from the catalog and beyond. CD BioSciences delivers convenient, efficient, and cost-effective C. elegans model customization with full genotype verification.
Contact UsThis resource page links to 28 dedicated gene editing service pages and summarizes a further 150 catalog genes across 15 functional categories.
For research use only.
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