C. elegans mec-7 Functional Gene Editing Service

Service Overview Precision editing of mec-7 in a premier genetic model for gentle touch sensation, mechanotransduction channel function and touch receptor neuron biology

mec-7 encodes MEC-7, a beta-tubulin expressed almost exclusively in the six touch receptor neurons of C. elegans, where it partners MEC-12 alpha-tubulin to build the unusual 15-protofilament microtubules that fill the sensory processes.

Without it the processes still grow and are still filled with microtubules, but those have eleven protofilaments and the neurons do not respond to touch, so the requirement is for the specialised polymer rather than for a bundle as such. The promoter is the standard driver for touch neuron labelling. CD BioSciences delivers custom mec-7 alleles — knockouts, substitutions and tag knockins — with full genotype verification.

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

Gene symbol	mec-7 (a beta-tubulin expressed almost exclusively in the touch receptor neurons, where it builds the unusual 15-protofilament microtubules)
Protein product	MEC-7 — touch neuron beta-tubulin, building block of the 15-protofilament microtubules
Mammalian homolog	the beta-tubulin family, human TUBB, TUBB2A, TUBB2B, TUBB3 and TUBB4B; MEC-7 is a divergent isotype whose expression is largely restricted to the six touch receptor neurons
Biological role	The sensory processes of the touch neurons are packed with microtubules that have fifteen protofilaments instead of the usual eleven, and MEC-7 is the beta-tubulin that builds them. It is a beta-tubulin of 440 amino acids expressed at high level in the touch neurons and, unlike its partner MEC-12, almost nowhere else. In animals lacking MEC-7 the touch processes still grow out and are still filled with microtubules, but those microtubules have eleven protofilaments and the neurons do not respond to touch, which is the evidence that the unusual protofilament number, and not merely the presence of a bundle, is what the transduction machinery requires. Its promoter is also the standard tool for labelling the six touch cells.
Loss-of-function phenotype	Loss gives touch insensitivity with morphologically intact, normally positioned neurons; the only structural correlate is the replacement of 15-protofilament microtubules with 11-protofilament ones. Animals are viable and otherwise coordinated, and the defect is confined to the touch circuit.
Why edit it	It is the canonical example of a specialised tubulin isotype serving a single sensory modality, and it gives a clean separation between having a cytoskeleton and having the right cytoskeleton. The promoter is also the most convenient reagent in the whole pathway: if anything needs to be expressed specifically in the six touch receptor neurons, a mec-7 promoter fusion is the default choice, so a tagged or modified locus has value well beyond the mutant phenotype.
Recommended background	Standard N2 background. Behavioural scoring is sufficient for a null, but we recommend electron microscopy for any allele intended to address polymer geometry, since light-level markers cannot distinguish fifteen from eleven protofilaments and a normal-looking fluorescent bundle may still be structurally wrong.
Representative allele	Classical alleles including mec-7(e1343); custom CRISPR nulls, isotype-specific tag knockins, and defined substitutions in the regions that differ from the ubiquitous beta-tubulins.

Fig. 1 MEC-7, the touch-neuron beta-tubulin that pairs with MEC-12 alpha-tubulin to build the unusual 15-protofilament microtubules needed for transduction in C. elegans. The highlighted (amber) node marks the editing target.

mec-7 at a glance: mec-7 loss replaces 15-protofilament microtubules with 11-protofilament ones and abolishes touch response. Editing mec-7 alone is a powerful way to dissect MEC-7 function in vivo, with conserved relevance to human the beta-tubulin family, human TUBB, TUBB2A, TUBB2B, TUBB3 and TUBB4B; MEC-7 is a divergent isotype whose expression is largely restricted to the six touch receptor neurons biology.

Our mec-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 mec-7 alleles.

Knockin & Tagging

Homology-directed repair (HDR) inserts GFP / HA / FLAG or other tags at the mec-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 MEC-7.

Conditional & Reporter Alleles

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

Deleting the gene is straightforward, but note that the genome carries several beta-tubulin genes, so a knockout gives an isotype-specific defect rather than a cytoskeletal collapse, and the phenotype should be read as loss of the specialised polymer rather than loss of microtubules. If the goal is a neuronal marker rather than a mutant, a C-terminal tag knockin is usually preferable to a promoter fusion, because endogenous regulation keeps expression restricted; we suggest confirming that the tag does not alter protofilament number when the strain is to be used for structural work.

Workflow of Our mec-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 mec-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 mec-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 mec-7 model adds value

15-protofilament microtubules in mechanosensory neurons.
Specialised tubulin isotypes in sensory function.
Cytoskeletal basis of mechanotransduction.
Touch receptor neuron labelling and morphology.
Separation of neurite outgrowth from sensory function.
Microtubule protofilament number and its determinants.
Comparison with vertebrate beta-tubulin isotypes.

Deliverables What you receive with every project

Genetically verified mec-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, touch neuron GFP / mCherry marker, degenerin channel tag, and co-CRISPR selection backgrounds.
Optional: phenotype confirmation, ten-touch behavioural scoring, touch neuron morphology and 15-protofilament microtubule assessment, and channel puncta imaging.

Frequently Asked Questions

What type of mec-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 mec-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 mec-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.

Do the 15-protofilament microtubules carry the gating force?

They are required, but the mechanism is not settled and the simple force-transmission model has problems. The evidence for a requirement is strong: in mec-7 and mec-12 mutants the processes still extend and are still filled with microtubules, but those are 11-protofilament polymers and the neurons are touch insensitive, so the specialised bundle is necessary. What remains open is whether it transmits force to the channel or simply provides the stiffness and geometry the channel needs, and the finding that bulk touch-induced strain is unchanged in extracellular-matrix mutants suggests that simple longitudinal stretching is not the whole story. For practical purposes, treat the bundle as a necessary structural component and design experiments that can distinguish a placement defect from a force-transmission defect, for example by scoring channel puncta alongside behaviour.

Start Your mec-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. Savage C., Hamelin M., Culotti J. G., Coulson A., Albertson D. G., Chalfie M. mec-7 is a beta-tubulin gene required for the production of 15-protofilament microtubules in Caenorhabditis elegans. Genes & Development, 1989, 3(6): 870–881.

For research use only.