C. elegans daf-7 Functional Gene Editing Service

Service Overview Precision editing of DAF-7 in a premier genetic model for dauer formation, developmental plasticity, and aging research

daf-7 encodes the transforming growth factor-β ligand of the Caenorhabditis elegans dauer pathway, related to the mammalian TGF-β and activin ligands. It is produced and secreted by the ASI pair of sensory neurons, and its level tracks the environment directly: high when food is plentiful and crowding is low, suppressed by dauer pheromone and by high temperature.

That positioning makes DAF-7 the decision signal itself rather than a downstream component. It acts through the receptors DAF-1 and DAF-4 to inhibit the DAF-3 / DAF-5 dauer program, so losing it makes the animal arrest regardless of conditions. CD BioSciences delivers custom daf-7 alleles — knockouts, endogenous GFP or epitope tag knockins, promoter-reporter configurations, conditional alleles, and ligand point mutants — with full genotype verification.

About the Target Gene: daf-7 Key biological and practical facts to inform your edit design

Gene symbol	daf-7 (TGF-β family secreted ligand (neuroendocrine signal))
Protein product	DAF-7 — TGF-β family secreted ligand
Mammalian homolog	TGFB1 / TGFB2 (TGF-β and activin branch ligands)
Biological role	The TGF-β ligand that converts environmental information into an organism-wide endocrine decision. DAF-7 is secreted by the ASI sensory neurons when food is available, pheromone is low, and temperature is permissive; its expression level is the integrative readout of those cues, and it is the ligand that licenses reproductive development by switching off the DAF-3 / DAF-5 dauer program through DAF-1 and DAF-4.
Loss-of-function phenotype	Loss of daf-7 produces a dauer-constitutive (Daf-c) phenotype: animals arrest as dauers under favorable conditions because the license to develop reproductively is never issued. Mutants are also long-lived, stress-resistant, and accumulate markedly more fat, and the phenotype is suppressed by daf-3 or daf-5 loss.
Why edit it	TGF-β is a master cytokine in fibrosis, immunity, and cancer, and daf-7 is the canonical model for how a single sensory neuron reads the environment and broadcasts that reading as an endocrine signal to the whole animal. Because daf-7 expression itself is the sensor, a promoter or endogenous reporter gives a live, quantitative readout of environmental assessment.
Recommended background	N2 (wild type). Daf-c alleles including the widely used e1372 are viable; we recommend scoring dauer formation against pheromone or food cues, and a daf-7 reporter configuration when you want to watch expression change with conditions.
Representative allele	Classic alleles including e1372 and deletion alleles; daf-7p::gfp reporter configurations, endogenous GFP knockins, and custom CRISPR nulls available on request.

Fig. 1 The DAF-7 / TGF-β branch of the C. elegans dauer pathway, from ASI sensory neurons to the developmental decision. The highlighted (amber) node marks the editing target.

daf-7 at a glance: daf-7 is the ASI-derived TGF-beta license signal; loss gives dauer-constitutive arrest, longevity and fat accumulation. Editing daf-7 alone is a powerful way to dissect DAF-7 function in vivo, with conserved relevance to human TGFB1 biology.

Our daf-7 Editing Strategies Choose the allele that matches your experimental question

Gene Knockout

gRNA-guided Cas9 cutting with NHEJ repair to introduce frameshift indels, generating premature stop codons and null / strong-loss-of-function daf-7 alleles.

Knockin & Tagging

Homology-directed repair (HDR) inserts GFP / HA / FLAG or other tags at the daf-7 locus for endogenous expression and subcellular localization studies.

Point Mutation

Introduce specific amino-acid substitutions to dissect functional domains and separate catalytic from scaffolding roles of DAF-7.

Conditional & Reporter Alleles

Build tissue-specific, inducible, or temperature-sensitive configurations and reporter lines for spatiotemporal analysis of DAF-7 function.

Workflow of Our daf-7 Editing Service From sequence to validated strain in a streamlined pipeline

Strategy Design

Define target (knockout / knockin / point mutation), select gRNA(s) and HDR template, confirm against the latest genome build.

gRNA Synthesis

Design, validate, and synthesize high-specificity guide RNAs targeting the daf-7 locus.

Vector & Template Construction

Build Cas9 / gRNA delivery construct and, for knockin, the homology-arm repair template.

Microinjection

Perform gonadal microinjection of N2 animals with CRISPR components and co-CRISPR selection markers.

Screening & Verification

PCR, Sanger / sequencing, and phenotype confirmation to isolate edited animals and verify alleles.

Delivery & Report

Provide homozygous / balanced daf-7 strains plus a full genotype and methods report.

Key Features Why researchers choose CD BioSciences for C. elegans editing

High-efficiency, optimized CRISPR / Cas9 platform for C. elegans.
Whole-process technical traceability and transparent timelines.
Flexible editing: knockout, knockin, tagging, and point mutation.
Full genotype verification before strain delivery.
One-stop model development integrated with our C. elegans portfolio.
Competitive pricing and short turnaround.
Direct access to scientists and prompt inquiry response.
Reliable, convenient global shipping of frozen stocks.

Applications Where a custom daf-7 model adds value

TGF-β ligand biology and neuroendocrine signaling.
Dauer formation, pheromone sensing, and developmental plasticity.
Environmental integration: food, crowding, and temperature cues.
daf-7 reporter construction and live readout of sensory state.
Epistasis with the DAF-3 / DAF-5 output cassette.
Longevity, stress resistance, and fat-storage phenotyping.
Sensory-to-endocrine signaling and neurobiology of the ASI neurons.

Deliverables What you receive with every project

Genetically verified daf-7 edited strain(s) (homozygous or balanced).
Detailed genotyping report (editing strategy, allele sequence, verification data).
Methods summary and rearing / storage recommendations.
Optional: crosses into reporter, dauer-assay, or co-CRISPR selection backgrounds.
Optional: phenotype confirmation, dauer assay setup, and imaging support.

Frequently Asked Questions

What type of daf-7 allele will I get from a knockout project?

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.

Can you add a GFP or epitope tag to endogenous daf-7?

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.

How long does a typical daf-7 editing project take?

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.

Should I use a daf-7p::gfp array or an endogenous tag knockin?

For quantitative work, the endogenous knockin is usually better: it keeps the native promoter, all regulatory elements, and single-copy expression, so fluorescence tracks the physiological decision signal rather than array-to-array variation. Arrays are faster and brighter, which can help when the signal is weak or for screening. We can build either, and we routinely deliver the endogenous knockin together with a matched untagged control.

Start Your daf-7 Editing Project

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.

References
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. Ren P., Lim C. S., Johnsen R., Albert P. S., Pilgrim D. B., Riddle D. L. Control of C. elegans larval development by neuronal expression of a TGF-beta homolog. Science, 1996, 274(5291): 1389–1391.

For research use only.