ctl-1 encodes one of the three C. elegans catalases, the heme enzymes that disproportionate hydrogen peroxide into water and molecular oxygen. It deals with the peroxide produced downstream of superoxide dismutation and by peroxisomal metabolism, closing the second half of the reactive-oxygen-species clearance chain that begins with superoxide dismutase.
The result that makes ctl-1 important is that removing it shortens the extended lifespan of daf-2 and clk-1 mutants. Antioxidant capacity, in other words, is a required input to these longevity programs rather than a passive readout of them. CD BioSciences delivers custom ctl-1 alleles — knockouts, heme-binding and catalytic point mutants, conditional configurations, and tag knockins — with full genotype verification.
| Gene symbol | ctl-1 (Catalase (hydrogen-peroxide-degrading peroxisomal enzyme)) |
|---|---|
| Protein product | CTL-1 — catalase (CaTaLase family) |
| Mammalian homolog | CAT (catalase) |
| Biological role | One of three C. elegans catalases, the heme-containing enzymes that disproportionate hydrogen peroxide into water and molecular oxygen. CTL-1 handles the peroxide produced by superoxide dismutation and by peroxisomal metabolism, and it is required for the full lifespan extension seen in insulin/IGF and clk-1 longevity mutants. |
| Loss-of-function phenotype | Loss of ctl-1 reduces catalase activity and peroxide tolerance and shortens the extended lifespan of daf-2 and clk-1 mutants, showing that peroxide clearance is a required component of those longevity programs rather than a bystander. |
| Why edit it | ctl-1 supplies direct genetic evidence that antioxidant capacity is a limiting input to longevity, not merely a correlate: removing one catalase is enough to blunt the lifespan extension produced by two of the best-characterized longevity pathways. Human catalase deficiency and CAT variants are associated with diabetes, hypertension, and age-related disease. |
| Recommended background | N2 (wild type). Deletion alleles are viable; we recommend scoring peroxide (H2O2) survival alongside lifespan, and for longevity epistasis work combining with daf-2 or clk-1 reduction-of-function backgrounds. |
| Representative allele | Deletion alleles from the C. elegans knockout collections; custom CRISPR nulls, heme-binding-site point mutants, and catalase-activity reporter configurations available on request. |
ctl-1 at a glance: loss of ctl-1 blunts the extended lifespan of daf-2 and clk-1 mutants and lowers peroxide tolerance. Editing ctl-1 alone is a powerful way to dissect CTL-1 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-1 alleles.
Homology-directed repair (HDR) inserts GFP / HA / FLAG or other tags at the ctl-1 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-1.
Build tissue-specific, inducible, or temperature-sensitive configurations and reporter lines for spatiotemporal analysis of CTL-1 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-1 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-1 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.
Because removing it does more than make animals stress-sensitive: it shortens the long lifespan of daf-2 and clk-1 mutants back toward wild type. That means the peroxide-clearing capacity supplied by CTL-1 is part of the mechanism by which those pathways extend life, not simply a general health measure. The practical consequence is that ctl-1 edits are most informative when scored in a long-lived background rather than in wild type alone.
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. Taub J., Lau J. F., Ma C., Hahn J. J., Hoque R., Rothblatt J., Chalfie M. A cytosolic catalase is needed to extend adult lifespan in C. elegans daf-C and clk-1 mutants. Nature, 1999, 399(6732): 162–166.
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