C. elegans bbs-2 Functional Gene Editing Service

Service Overview Precision editing of bbs-2 in a premier genetic model for sensory cilia, intraflagellar transport and ciliopathy

bbs-2 encodes BBS-2, a constituent subunit of the BBSome — the conserved eight-subunit complex that behaves as a vesicle coat adapted for cilia. In mammals BBS2 belongs to the stable core group alongside BBS1, BBS7 and BBS9.

In the nematode the gene is part of the DAF-19 X-box ciliogenic programme, and the protein sits at the ciliary transition zone as well as along the axoneme, where it moves bidirectionally with IFT. Loss leaves cilia assembled but functionally compromised, with transport no longer coordinated between motors. CD BioSciences delivers custom bbs-2 alleles — knockouts, interaction-surface mutants, patient-variant knockins and tag knockins — with full genotype verification.

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

Gene symbol	bbs-2 (BBS2, a core BBSome subunit required for complex assembly and basal body docking)
Protein product	BBS-2 — a core subunit of the BBSome ciliary coat
Mammalian homolog	BBS2; variants cause Bardet-Biedl syndrome 2
Biological role	BBS-2 is one of the subunits that make up the body of the BBSome. Structural and interaction mapping in mammalian systems places BBS2 among the group — with BBS1, BBS7 and BBS9 — that forms the stable core of the complex, rather than the peripheral subunits that come and go. In worms all eight bbs genes are X-box regulated and therefore part of the RFX transcription factor DAF-19 ciliogenic programme, and BBS-2 localises both to the transition zone at the base of the cilium and along the ciliary axoneme, moving bidirectionally by IFT.
Loss-of-function phenotype	Loss gives the recognisable BBSome pattern rather than an assembly failure: cilia form and are much longer than those of IFT complex B mutants, but carry structural defects toward the axoneme periphery, and the animals are dye-filling and chemotaxis defective. The mechanistic signature is that the IFT machinery loses coherence — the two motor populations no longer move one coordinated train along the axoneme.
Why edit it	The useful thing about working through BBS-2 rather than through an IFT subunit is that it separates assembly from function. Because the axoneme still builds, you can ask what a cilium can and cannot do once its transport system is running uncoordinated — a question that is hard to reach when the organelle never forms.
Recommended background	N2 (wild type). Null animals are viable and fertile. Because the defect is quantitative we recommend velocity measurements using a tagged IFT subunit plus chemotaxis indices, rather than dye filling as the primary endpoint.
Representative allele	Engineered deletion alleles plus available loss-of-function alleles from the CGC collection; custom CRISPR nulls, interaction-surface mutants that separate core assembly from cargo recognition, patient-variant knockins, and fluorescent or epitope tag knockins available on request.

Fig. 1 BBS-2, a core BBSome subunit that docks the complex at the basal body and couples it to the IFT machinery in C. elegans sensory cilia. The highlighted (amber) node marks the editing target.

bbs-2 at a glance: bbs-2 belongs to the stable BBSome core, so loss disrupts coordination without abolishing assembly. Editing bbs-2 alone is a powerful way to dissect BBS-2 function in vivo, with conserved relevance to human BBS2; variants cause Bardet-Biedl syndrome 2 biology.

Our bbs-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 bbs-2 alleles.

Knockin & Tagging

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

Conditional & Reporter Alleles

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

If you want to separate the two jobs this subunit does, an interaction-surface mutant is a better first construct than a deletion: it can leave the complex intact while blocking recognition of particular cargo classes. Pair it with a tagged subunit from the core group so you can confirm the complex still assembles in the mutant background.

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

BBSome core assembly and stability.
Basal body and transition zone recruitment.
Cargo recognition by the BBSome coat.
IFT-A / IFT-B coordination along the axoneme.
Bardet-Biedl syndrome variant modelling.
Chemotaxis and dye-filling phenotyping.
Comparative subunit mapping across species.

Deliverables What you receive with every project

Genetically verified bbs-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, cilia- and transition-zone marker, and co-CRISPR selection backgrounds.
Optional: phenotype confirmation, cilium morphology, live IFT imaging, dye-filling and chemotaxis analysis support.

Frequently Asked Questions

What type of bbs-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 bbs-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 bbs-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.

Are all the BBS subunits equivalent to knock out?

They overlap substantially but not completely, and treating them as interchangeable is a mistake. In nematodes every locus tested has ciliary abnormalities with a dye-filling defect, and the coordination phenotype is shared. But the severity differs by subunit, and in other systems some subunits are peripheral and dispensable for core assembly in ways the core group is not. If you are choosing one representative, say what you want to represent — core stability, cargo binding, or motor coordination — and pick accordingly rather than defaulting.

Start Your bbs-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.

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. Blacque O. E., Reardon M. J., Li C., McCarthy J., Mahjoub M. R., Ansley S. J., Badano J. L., Mah A. K., Beales P. L., Davidson W. S., Johnsen R. C., Audeh M., Plasterk R. H. A., Baillie D. L., Katsanis N., Quarmby L. M., Wicks S. R., Leroux M. R. Loss of C. elegans BBS-7 and BBS-8 protein function results in cilia defects and compromised intraflagellar transport. Genes & Development, 2004, 18(13): 1630–1640.

For research use only.