Protein trafficking
How do proteins find plasmodesmata?
Open access · cc by · source: Europe PMC
PDLP1 is a type I membrane protein targeted to plasmodesmata; altering PDLP dosage changes GFP cell-to-cell trafficking.
Study at a glance
- Design
- Animal / in-vitro — GFP localization and topology/knockout assays of PDLP plasmodesmal proteins
- N
- Plant cell-biology localization and trafficking assays — no single sample N
- Population
- Arabidopsis and other plants expressing PDLP family proteins
- Outcome
- Plasmodesmal targeting of PDLPs and effects on cell-to-cell GFP movement
Structured fields used in claim comparison tables when every cited study has a complete layer.
Key findings
PDLP1 family proteins target plasmodesmata; PDLP1a has cytoplasmic C-tail and apoplastic DUF26 domains; combined KOs increase GFP movement.
Methodology
GFP-tagged cell-wall membrane proteins from Arabidopsis proteomes were localized across plant species; PDLP topology and knockout trafficking phenotypes were tested.
Limitations
Does not fully catalog every plasmodesmal protein or all cargoes regulated by PDLPs.
How this study connects
Role on claims
Each row is a claim on a concept or method page where this paper supports, challenges, or qualifies the statement. Roles are hand-checked — not a model guess.
Multiple empirical papers in this library examine protein trafficking with mechanistic biological findings.
Evidence for the claim as stated.
PDLP1 family proteins target plasmodesmata; PDLP1a has cytoplasmic C-tail and apoplastic DUF26 domains; combined KOs increase GFP movement.
Evidence for the claim as stated.
Systems and scales differ across protein trafficking studies (species, tissues, methods), so mechanisms should not be over-generalised.
Evidence for the claim as stated.
In Arabidopsis, combined PDLP knockouts increased GFP cell-to-cell movement, while GFP-tagged PDLP1 family proteins targeted plasmodesmata (PDLP1a: cytoplasmic C-tail, apoplastic DUF26). The KO phenotype is trafficking of a reporter, not a full catalogue of every plasmodesmal cargo.
Evidence for the claim as stated.
Loss-of-function tools are not interchangeable. CK1ε used shRNA plus inhibitors in mammalian cancer models; USP8 used Drosophila RNAi; IFN work used receptor knockouts and siRNA in macrophages; PDLP used plant combined KOs. A 'knockdown paper' in flies is not the same genetic lesion as a mouse IFNAR1 knockout or an Arabidopsis double mutant.
Evidence for the claim as stated.
GFP-tagged PDLP1 family proteins targeted plasmodesmata across plant species; PDLP1a has a cytoplasmic C-tail and apoplastic DUF26 domains, and combined knockouts increased GFP cell-to-cell movement. Localisation here is a trafficking address, not a complete plasmodesmal proteome.
Evidence for the claim as stated.
Confocal is used here for polarity reversal (enteroids), plasmodesmal targeting (PDLP), and vesicle itineraries (Bt OMVs in ~15 min; E. coli OMVs to NOD sensors). Those are different spatial questions — which face of an epithelium, which plant cell-wall channel, which endocytic route — and cannot be pooled as one 'trafficking phenotype'.
Evidence for the claim as stated.
Open questions
Tensions this paper is part of
From concept pages' “where studies disagree.” Disagreement means the same question; scope means different assays, populations, or outcomes.
Systems and scales differ across protein trafficking studies (species, tissues, methods), so mechanisms should not be over-generalised.
- Supports · Spike glycosylation and palmitoylation trafficking
- Supports · How does monoubiquitin turn down Rab5?
Loss-of-function tools are not interchangeable. CK1ε used shRNA plus inhibitors in mammalian cancer models; USP8 used Drosophila RNAi; IFN work used receptor knockouts and siRNA in macrophages; PDLP used plant combined KOs. A 'knockdown paper' in flies is not the same genetic lesion as a mouse IFNAR1 knockout or an Arabidopsis double mutant.
Confocal is used here for polarity reversal (enteroids), plasmodesmal targeting (PDLP), and vesicle itineraries (Bt OMVs in ~15 min; E. coli OMVs to NOD sensors). Those are different spatial questions — which face of an epithelium, which plant cell-wall channel, which endocytic route — and cannot be pooled as one 'trafficking phenotype'.
Related papers in this topic
Same topic cluster — not a recommendation engine.