C. elegans isp-1 Functional Gene Editing Service

Service Overview Precision editing of ISP-1 in a premier genetic model for mitochondrial, dietary-restriction, and longevity research

isp-1 encodes the Rieske iron-sulfur protein of mitochondrial Complex III, the subunit that accepts electrons from ubiquinol and passes them to cytochrome c. Partial loss of ISP-1 throttles electron flow through the chain without collapsing oxidative phosphorylation.

That partial impairment is sufficient to extend adult lifespan, making isp-1 one of the strongest demonstrations that respiration rate causally controls aging. CD BioSciences delivers custom isp-1 alleles — knockouts, partial loss-of-function and iron-sulfur-binding point mutants, conditional configurations, and tag knockins — for mitochondrial aging research.

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

Gene symbol	isp-1 (Rieske iron-sulfur protein of mitochondrial Complex III)
Protein product	ISP-1 — Rieske iron-sulfur protein (Complex III)
Mammalian homolog	UQCRFS1 (Rieske iron-sulfur protein, Complex III)
Biological role	The Rieske iron-sulfur subunit of mitochondrial Complex III (cytochrome bc₁ complex). ISP-1 transfers electrons from ubiquinol to cytochrome c, so its impairment throttles the electron-transport chain downstream of the CoQ pool.
Loss-of-function phenotype	isp-1(qm150) reduces Complex III activity, slows development and reproduction, and markedly extends adult lifespan with enhanced resistance to oxidative and thermal stress.
Why edit it	isp-1 showed that manipulating a single electron-transport component is sufficient to change lifespan, anchoring mitochondrial function as a causal driver of aging. In humans, UQCRFS1 and other Complex III defects cause mitochondrial disease, making the worm model a tractable entry point.
Recommended background	N2 (wild type). isp-1(qm150) is viable and fertile but slow-growing; lifespan assays should control for developmental delay.
Representative allele	qm150 (canonical long-lived allele); null and additional alleles available.

Fig. 1 Mitochondrial electron-transport control of longevity in C. elegans, via retrograde (mitohormetic) signaling. The highlighted (amber) node marks the editing target.

isp-1 at a glance: isp-1(qm150) reduces Complex III activity; the resulting mild dysfunction markedly extends adult lifespan. Editing isp-1 alone is a powerful way to dissect ISP-1 function in vivo, with conserved relevance to human UQCRFS1 biology.

Our isp-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 isp-1 alleles.

Knockin & Tagging

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

Conditional & Reporter Alleles

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

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

Complex III function and lifespan determination.
Mitohormesis and retrograde mitochondrial signaling.
Iron-sulfur cluster biology and mitochondrial disease modeling.
Respiration rate, oxygen consumption, and ATP assays.
Oxidative and thermal stress resistance.
Epistasis with clk-1, nuo-6, mev-1, and UPRmt reporters.
Mitochondria-targeted compound and drug screening.

Deliverables What you receive with every project

Genetically verified isp-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, lifespan-assay, or co-CRISPR selection backgrounds.
Optional: phenotype confirmation, lifespan assay setup, and imaging support.

Frequently Asked Questions

What type of isp-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 isp-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 isp-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.

Should I request a null or a partial loss-of-function isp-1 allele?

For lifespan and healthspan work we recommend a partial loss-of-function allele in the range of qm150, which gives robust longevity while keeping the strain manageable. Null or severe alleles compromise development and respiration to a degree that confounds adult lifespan assays.

Start Your isp-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. Feng J., Bussière F., Hekimi S. Mitochondrial electron transport is a key determinant of life span in Caenorhabditis elegans. Dev Cell, 2001, 1(5): 633–644.

For research use only.