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.
| Gene symbol | ctl-2 (Peroxisomal catalase (hydrogen-peroxide-degrading enzyme)) |
|---|---|
| Protein product | CTL-2 — peroxisomal catalase |
| Mammalian homolog | CAT (catalase) |
| Biological role | The 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 phenotype | Loss 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 it | ctl-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 background | N2 (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 allele | Deletion 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 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.
gRNA-guided Cas9 cutting with NHEJ repair to introduce frameshift indels, generating premature stop codons and null / strong-loss-of-function ctl-2 alleles.
Homology-directed repair (HDR) inserts GFP / HA / FLAG or other tags at the ctl-2 locus for endogenous expression and subcellular localization studies.
Introduce specific amino-acid substitutions to dissect functional domains and separate catalytic from scaffolding roles of CTL-2.
Build tissue-specific, inducible, or temperature-sensitive configurations and reporter lines for spatiotemporal analysis of CTL-2 function.
Define target (knockout / knockin / point mutation), select gRNA(s) and HDR template, confirm against the latest genome build.
Design, validate, and synthesize high-specificity guide RNAs targeting the ctl-2 locus.
Build Cas9 / gRNA delivery construct and, for knockin, the homology-arm repair template.
Perform gonadal microinjection of N2 animals with CRISPR components and co-CRISPR selection markers.
PCR, Sanger / sequencing, and phenotype confirmation to isolate edited animals and verify alleles.
Provide homozygous / balanced ctl-2 strains plus a full genotype and methods report.
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.
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.
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.
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.
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 UsReferences
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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