- Home
- Services
- Products
- Featured Products:
- Applications
- About Us
- Contact Us
dpy-5 encodes an intermediate-group cuticle procollagen synthesised by the hypodermis and secreted into the cuticle before each molt. Animals lacking DPY-5 are shorter and fatter than wild type, with altered annuli spacing, slower post-embryonic growth and a reduced brood, yet remain viable and fertile.
The locus is also a classic genetic marker on linkage group I and a probe for extracellular-matrix processing: DPY-5 carries an Arg-X-X-Arg motif cleaved by the proprotein convertase BLI-4, and mutating that site causes a dominant Dumpy phenotype while suppressing bli-4 blistering. CD BioSciences supplies dpy-5 strains with full genotype verification and body-shape phenotyping.
| Gene symbol | dpy-5 (an intermediate-group cuticle procollagen of C. elegans expressed exclusively in hypodermal cells and cleaved by the proprotein convertase BLI-4) |
|---|---|
| Protein product | DPY-5 — intermediate-group cuticle procollagen processed by BLI-4 |
| Mammalian homolog | no one-to-one human ortholog; member of the ~160-gene nematode cuticle collagen family, whose short interrupted Gly-X-Y blocks flanked by conserved cysteines resemble the vertebrate fibril-associated collagens (COL12A1 / COL9A1 branch) |
| Biological role | During every cuticle synthesis period the collagen genes are transcribed in a fixed temporal series that is repeated at each molt. dpy-5 belongs to the intermediate group together with dpy-13: its mRNA peaks about two hours before the new cuticle is secreted, whereas the early group (dpy-2, dpy-3, dpy-7, dpy-8, dpy-10) peaks about four hours before. The two groups build different substructures — the early collagens localise in the annuli of the outermost cuticle layer, directly above the hypodermal actin bundles, while DPY-5 settles below and between the annuli. A dpy-5::gfp fusion is expressed only in hypodermal cells from mid-to-late L1 to adulthood, with notably variable expression in the V-lineage-derived seam cells. The protein carries an Arg-X-X-Arg motif recognised by a proprotein convertase; mutating that site produces a dominant Dumpy phenotype, and every dpy-5 allele isolated acts as a dominant suppressor of the blistering caused by loss of the convertase bli-4. |
| Loss-of-function phenotype | Loss of dpy-5 gives the classical Dumpy phenotype: adults are shorter and fatter than wild type, the spacing and width of the annuli are altered, post-embryonic growth rate is reduced and brood size is lower. The reference allele e61 is a nonsense substitution, whereas e907 removes the entire coding region and behaves as the null. Animals are viable and fertile, and the phenotype is fully penetrant and scorable on a dissecting microscope without any reagent, which is why the locus has been carried in genetic mapping strains for decades. |
| Why edit it | dpy-5 earns its place for two different reasons. As a tool, it is one of the standard visible markers of C. elegans genetics: it sits on linkage group I, is recessive, needs no assay to score, and appears in classic multiply-marked mapping strains, so an edited allele can be placed by inspection as well as by sequencing. As a target, it is a clean entry into extracellular-matrix biogenesis, because the same locus reports on two separable processes — collagen trimer assembly in the hypodermis and the proteolytic processing step carried out by BLI-4. That second point is unusual: a point mutation in the cleavage motif makes the animal Dumpy in a dominant fashion and simultaneously suppresses bli-4 blistering, so a single engineered substitution lets you separate processing from structural incorporation. |
| Recommended background | Standard N2 background. Two practical cautions. First, Dumpy body shape masks or suppresses other visible markers: the Roller phenotype conferred by rol-6(su1006) is suppressed in several Dumpy and Unc backgrounds, so do not plan a dpy-5 knockout into a strain that relies on a Roller marker for array maintenance. Second, body shape is sensitive to culture conditions, so score body length and annuli on synchronised young adults raised in parallel with an N2 control rather than comparing across batches. |
| Representative allele | The reference allele dpy-5(e61), a nonsense substitution, and the null dpy-5(e907), which removes the entire coding region. Because the locus is annotated with a single exon, a sequence-defined full coding-region deletion is straightforward to produce and reproduces the e907 configuration exactly. We also offer recreation of the e61 stop allele, substitution of the Arg-X-X-Arg processing motif, and endogenous GFP or epitope tag knockin for hypodermal expression analysis. |
dpy-5 at a glance: dpy-5 is a hypodermis-specific intermediate-group cuticle procollagen; null animals are viable and Dumpy. Editing dpy-5 alone is a powerful way to dissect DPY-5 function in vivo, with conserved relevance to human no one-to-one human ortholog; member of the ~160-gene nematode cuticle collagen family, whose short interrupted Gly-X-Y blocks flanked by conserved cysteines resemble the vertebrate fibril-associated collagens biology.
gRNA-guided Cas9 cutting with NHEJ repair to introduce frameshift indels, generating premature stop codons and null / strong-loss-of-function dpy-5 alleles.
Homology-directed repair (HDR) inserts GFP / HA / FLAG or other tags at the dpy-5 locus for endogenous expression and subcellular localization studies.
Introduce specific amino-acid substitutions to dissect functional domains and separate catalytic from scaffolding roles of DPY-5.
Build tissue-specific, inducible, or temperature-sensitive configurations and reporter lines for spatiotemporal analysis of DPY-5 function.
The locus is annotated with a single exon, so the simplest design is a paired-guide deletion that removes the coding region in one step and reproduces the e907 null; we confirm the junction by sequencing. Three further configurations are worth considering. If the question is processing rather than structure, a point substitution in the Arg-X-X-Arg motif gives the dominant Dumpy allele and is the reagent of choice for bli-4 epistasis. If the question is expression, an endogenous GFP fusion reports hypodermal transcription through every post-embryonic stage and reproduces the variable seam-cell pattern described for dpy-5::gfp. If the locus is to be used as a marker, we deliver the deletion allele already backcrossed so that the body-shape phenotype is separated from any background effect. All alleles are viable, so no balancer is required.
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 dpy-5 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 dpy-5 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 — Dumpy is one of the most reliable visible phenotypes in C. elegans. Null animals are shorter and fatter than wild type from the L1 stage onward, so the phenotype can be scored on a dissecting microscope without staining or imaging equipment. Two points determine whether the experiment is clean. The allele is recessive, so the phenotype appears only in homozygous animals: expect to pick F2 or later, and confirm homozygosity by sequencing rather than by shape alone, because body length varies with culture conditions and with the bacterial food source. And the effect is quantitative as well as categorical, so if you intend to publish body-length data, measure synchronised young adults alongside an N2 control processed in parallel. Note also that a Dumpy background suppresses the Roller phenotype of rol-6(su1006), so a dpy-5 knockout is a poor choice for a strain that depends on a Roller marker to maintain an extrachromosomal array. If you need both, tell us at design stage and we will place the edits so the markers do not interfere.
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. Thacker C., Peters K., Srayko M., Rose A. M. The bli-4 locus of Caenorhabditis elegans encodes structurally distinct kex2 / subtilisin-like endoproteases essential for early development and adult morphology. Genes & Development, 1995, 9(8): 956–971.
For research use only.
Copyright © 2026 CD BioSciences. All rights reserved.
