Service Overview Precision editing of CTL-2 in a premier genetic model for oxidative stress, antioxidant defense, and aging research

ctl-2 encodes the predominantly peroxisomal catalase of Caenorhabditis elegans, a heme-containing enzyme that converts hydrogen peroxide into water and oxygen. Peroxisomes generate peroxide continuously through their oxidases, so a dedicated catalase is required to keep the organelle — and the cytoplasm around it — below the threshold where peroxide starts damaging lipids, proteins, and DNA.

What makes ctl-2 stand out is the phenotype of its loss: animals age prematurely, with shortened lifespan, poor peroxide tolerance, and visible tissue deterioration. That is a direct, single-gene link between peroxide clearance and the rate of aging. CD BioSciences delivers custom ctl-2 alleles — knockouts, peroxisomal-targeting and heme-site point mutants, conditional configurations, and fluorescent tag knockins — with full genotype verification.

About the Target Gene: ctl-2 Key biological and practical facts to inform your edit design

Gene symbolctl-2 (Peroxisomal catalase (hydrogen-peroxide-degrading enzyme))
Protein productCTL-2 — peroxisomal catalase
Mammalian homologCAT (catalase)
Biological roleThe predominantly peroxisomal catalase of C. elegans, a heme enzyme that clears hydrogen peroxide generated by peroxisomal oxidases and by the dismutation of cytosolic superoxide. It protects peroxisome integrity and the surrounding cytoplasm from peroxide-driven damage.
Loss-of-function phenotypeLoss of ctl-2 produces a progeric (premature-aging) phenotype: shortened lifespan, reduced peroxide tolerance, accelerated tissue deterioration, and altered peroxisomal morphology — one of the clearest links between a single antioxidant enzyme and the pace of aging.
Why edit itctl-2 is the strongest single-gene demonstration in C. elegans that failing peroxide clearance accelerates aging: loss produces a progeric phenotype rather than a subtle stress defect. Because peroxisomal catalase is central to human peroxide handling, and peroxisome dysfunction underlies Zellweger-spectrum disorders, the model has direct translational relevance.
Recommended backgroundN2 (wild type). Deletion alleles are viable but show premature aging; we recommend scoring lifespan, peroxide survival, peroxisome morphology, and age-related tissue deterioration together.
Representative alleleDeletion alleles from the C. elegans knockout collections; custom CRISPR nulls, peroxisomal-targeting and heme-site point mutants, and tag knockins available on request.
CTL-2 in the C. elegans Hydrogen Peroxide Clearance Pathway activates inhibits acts on cleaves to restores prevents slows supports H2O2 accumulation ctl-2 ★ peroxisomal H2O2 → H2O + O2 Peroxisomal redox balance Oxidative damage Cellular decline Lifespan / survival loss of ctl-2 causes a progeric phenotype: short lifespan, poor peroxide tolerance, premature tissue decline.
Fig. 1 Catalase-mediated hydrogen peroxide clearance and its contribution to redox balance in C. elegans. The highlighted (amber) node marks the editing target.

ctl-2 at a glance: loss of ctl-2 causes a progeric phenotype: short lifespan, poor peroxide tolerance, premature tissue decline. Editing ctl-2 alone is a powerful way to dissect CTL-2 function in vivo, with conserved relevance to human CAT biology.

Our ctl-2 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 ctl-2 alleles.

Knockin & Tagging

Homology-directed repair (HDR) inserts GFP / HA / FLAG or other tags at the ctl-2 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 CTL-2.

Conditional & Reporter Alleles

Build tissue-specific, inducible, or temperature-sensitive configurations and reporter lines for spatiotemporal analysis of CTL-2 function.

Workflow of Our ctl-2 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 ctl-2 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 ctl-2 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 ctl-2 model adds value

  • Peroxisomal hydrogen peroxide clearance and organelle redox balance.
  • Premature-aging (progeric) phenotypes and age-related tissue deterioration.
  • Peroxisome biology and Zellweger-spectrum disorder relevance.
  • Human catalase (CAT) and peroxisomal disease modeling.
  • Peroxide challenge and oxidative-stress survival assays.
  • Lipid peroxidation, protein carbonylation, and damage-marker profiling.
  • Peroxisome-targeted antioxidant and prolongevity compound screening.

Deliverables What you receive with every project

  • Genetically verified ctl-2 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, stress-assay, or co-CRISPR selection backgrounds.
  • Optional: phenotype confirmation, stress assay setup, and imaging support.

Frequently Asked Questions

What type of ctl-2 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 ctl-2?

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 ctl-2 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.

Is a ctl-2 knockout a good premature-aging model?

Yes — it is one of the most direct ones available in C. elegans. Animals lacking CTL-2 show shortened lifespan, reduced peroxide tolerance, and accelerated tissue deterioration without any additional insult, so the aging phenotype is intrinsic rather than induced by a toxin. If you want to separate peroxisomal from cytosolic peroxide handling, we can build peroxisomal-targeting mutants or combine ctl-2 edits with ctl-1 or ctl-3 deletions.

Start Your ctl-2 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.

Contact Us

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. Petriv O. I., Rachubinski R. A. Lack of peroxisomal catalase causes a progeric phenotype in Caenorhabditis elegans. J Biol Chem, 2004, 279(29): 30633–30639.

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