C. elegans che-1 Functional Gene Editing Service

Service Overview Precision editing of che-1 in a premier genetic model for chemosensation, olfaction, taste and sensory neuron identity

che-1 encodes CHE-1, a C2H2 zinc-finger transcription factor expressed selectively in the ASE chemosensory neurons. It binds a 12-bp ASE motif in target cis-regulatory regions and is related to the Drosophila Glass protein.

CHE-1 is a terminal selector: it switches on the entire ASE identity battery, positively autoregulates to stay on, and is sufficient to drive ASE genes elsewhere. ASE neurons are still born in che-1 nulls but never acquire their identity. CD BioSciences delivers custom che-1 alleles — knockouts, DNA-binding point mutants, autoregulatory site edits and degron or tag knockins — with full genotype verification.

About the Target Gene: che-1 Key biological and practical facts to inform your edit design

Gene symbol	che-1 (a C2H2 zinc-finger transcription factor that acts as the terminal selector of ASE taste neuron identity)
Protein product	CHE-1 — C2H2 zinc-finger terminal selector of the ASE chemosensory neurons
Mammalian homolog	Related to the Drosophila Glass transcription factor; no single unambiguous one-to-one vertebrate ortholog, and the conserved feature is the terminal-selector logic rather than the protein sequence
Biological role	CHE-1 is the transcription factor that makes an ASE neuron an ASE neuron. It encodes a C2H2 zinc-finger protein expressed selectively in the two ASE taste neurons, and it acts as a terminal selector: it binds a 12-base-pair ASE motif in the cis-regulatory regions of its targets and switches on the whole terminal identity battery, including neuropeptide receptors, the guanylyl cyclases GCY-5, GCY-6 and GCY-7, the cation channel TAX-2 and the transcription factor CEH-36. Two features make it a genuine selector rather than a one-off activator. It positively autoregulates, so once on it stays on, and it is sufficient: expressing CHE-1 in other neuron classes drives ectopic expression of ASE identity genes. Expression is initiated by the nuclear receptor NHR-67/TLX but not maintained by it, and CHE-1 is continuously required in adults to hold ASE identity.
Loss-of-function phenotype	In che-1 null mutants the ASE neurons are still generated and still look neuronal — a pan-neuronal marker is expressed and the anatomy is only partly affected — but they never acquire terminal identity. Expression of the shared and subtype-specific markers is lost, including GCY-7, GCY-5, LIM-6, COG-1, CEH-36 and FLP-6, and the animals are chemotaxis defective for the water-soluble cues ASE detects. Notably, transient depletion of CHE-1 in an adult causes a permanent loss of CHE-1 expression, ASE identity and chemotactic behaviour, because the autoregulatory loop does not restart.
Why edit it	CHE-1 is the best-characterised terminal selector in any system and the source of the general model that one transcription factor can maintain a whole neuronal identity indefinitely. The autoregulation makes it a tractable system for studying the stability of cell identity, and the finding that transient depletion is irreversible is a rare experimental demonstration of a bistable switch in a living animal. The logic is conserved: the Drosophila ortholog Glass is likewise a terminal selector, for photoreceptors.
Recommended background	N2 (wild type). Nulls are viable and the neurons are still born, which makes this one of the cleanest available separations of neuron generation from neuron identity. We recommend a pan-neuronal marker plus at least two ASE identity markers, since loss of identity without loss of the cell is the defining result, and an auxin-inducible degron tag if you want to test maintenance rather than establishment.
Representative allele	Classical null alleles from the CGC collection plus engineered deletion alleles; custom CRISPR nulls, zinc-finger and ASE-motif-binding point mutants, endogenous autoregulatory site mutations, auxin-inducible degron knockins and fluorescent or epitope tag knockins available on request.

Fig. 1 CHE-1, the C2H2 zinc-finger terminal selector that binds 12-bp ASE motifs and locks in the receptor and channel battery of the ASE taste neurons in C. elegans. The highlighted (amber) node marks the editing target.

che-1 at a glance: che-1 loss leaves ASE neurons born but without terminal identity or taste-driven chemotaxis. Editing che-1 alone is a powerful way to dissect CHE-1 function in vivo, with conserved relevance to human Related to the Drosophila Glass transcription factor; no single unambiguous one-to-one vertebrate ortholog, and the conserved feature is the terminal-selector logic rather than the protein sequence biology.

Our che-1 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 che-1 alleles.

Knockin & Tagging

Homology-directed repair (HDR) inserts GFP / HA / FLAG or other tags at the che-1 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 CHE-1.

Conditional & Reporter Alleles

Build tissue-specific, inducible, or temperature-sensitive configurations and reporter lines for spatiotemporal analysis of CHE-1 function.

The most distinctive allele available here targets the autoregulatory loop rather than the protein. CRISPR mutation of the CHE-1 binding site in the endogenous che-1 locus leaves the protein intact but collapses its own expression in adults, which separates the establishment and maintenance functions in a way no coding mutation can. Pair a degron tag with it if you want to test the irreversible-depletion result directly.

Workflow of Our che-1 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 che-1 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 che-1 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 che-1 model adds value

Terminal selector control of neuronal identity.
Establishment versus lifelong maintenance of cell fate.
Positive autoregulation and bistable cell identity.
ASE taste neuron specification and left-right asymmetry.
Transcription factor binding at a defined cis motif.
Conservation of selector logic with Drosophila Glass.
Chemotaxis to water-soluble chemical cues.

Deliverables What you receive with every project

Genetically verified che-1 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, sensory neuron and cilia marker, and co-CRISPR selection backgrounds.
Optional: phenotype confirmation, chemotaxis and avoidance assays, dye-filling, thermotaxis and dauer formation analysis support.

Frequently Asked Questions

What type of che-1 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 che-1?

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 che-1 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.

Do che-1 mutants lose the ASE neurons entirely?

No — and that distinction is the whole point of the gene. The ASE neurons are generated normally and still express pan-neuronal markers, with only partially affected anatomy; what they fail to do is acquire terminal identity. Every ASE marker tested is lost, from shared genes to subtype-specific ones such as GCY-7 in ASEL and GCY-5 in ASER. So the phenotype is a neuron that exists but does not know what it is, which is much more informative for identity studies than a cell that simply fails to be born. Score a pan-neuronal marker alongside an ASE marker to demonstrate this directly.

Start Your che-1 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. Uchida O., Nakano H., Koga M., Ohshima Y. The C. elegans che-1 gene encodes a zinc finger transcription factor required for specification of the ASE chemosensory neurons. Development, 2003, 130(7): 1215–1224.

For research use only.