Protein trafficking
Spike glycosylation and palmitoylation trafficking
Open access · cc by · source: Europe PMC
Glycosylation motifs and cysteine palmitoylation steer SARS-CoV-2 spike maturation, Golgi trafficking, and fusion.
Study at a glance
- Design
- Animal / in-vitro — Mutagenesis and 2BP inhibition of SARS-CoV-2 spike glycosylation/palmitoylation trafficking
- N
- Cell-based spike trafficking/fusion assays — no single primary analytic N
- Population
- Cells expressing wild-type or mutant SARS-CoV-2 spike
- Outcome
- Spike intracellular trafficking, packaging, and ACE2-mediated fusion
Structured fields used in claim comparison tables when every cited study has a complete layer.
Key findings
LYQD mutants altered S2 glycosylation mobility; palmitoylation at cysteine clusters I/II was required for efficient S pp/virus production, Golgi/plasma-membrane targeting, and cell fusion.
Methodology
Mutated LYQD and cysteine clusters in SARS-CoV-2 S, inhibited palmitoylation with 2BP, and tracked glycosylation, localization, packaging, and ACE2-mediated fusion.
Limitations
Not a clinical antiviral trial; much work uses S pseudoviruses rather than full virus genetics for every assay.
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.
LYQD mutants altered S2 glycosylation mobility; palmitoylation at cysteine clusters I/II was required for efficient S pp/virus production, Golgi/plasma-membrane targeting, and cell fusion.
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.
SARS-CoV-2 spike LYQD mutants changed S2 glycosylation mobility, and palmitoylation at cysteine clusters I/II was required for efficient particle production, Golgi/plasma-membrane targeting, and ACE2-mediated fusion (2-bromopalmitate inhibition). Mobility shifts on S2 are a western-style glycosylation readout; much of the work uses spike pseudoviruses rather than full-virus genetics for every assay.
Evidence for the claim as stated.
Westerns here answer different biochemical questions. Caveolar work asks which subunits co-purify; N–p50 asks which domain is required for association and HR; USP8 asks whether Smo is ubiquitinated; spike work asks whether glycan occupancy and palmitoylation change S2 mobility and trafficking. A darker band is not a universal 'more protein' story across those designs.
Evidence for the claim as stated.
Enteroid polarity reversed within hours without BME, with β1 integrin orienting apical pathogen access. Spike LYQD mutants altered S2 glycosylation mobility, and palmitoylation at cysteine clusters I/II was required for Golgi/plasma-membrane targeting and ACE2-mediated fusion. Those localisation phenotypes are IF/trafficking stains; enteroids are not a clinical gut, and much spike work uses pseudoviruses.
Evidence for the claim as stated.
Permeabilized-sperm SNARE timing and live epithelial polarity/spike trafficking disagree about how much native membrane regulation is still present. In-vitro sperm may miss in-vivo layers; enteroids and pseudovirus spike assays only approximate infection of a human airway or gut.
Evidence for the claim as stated.
Two papers barely use flow cytometry as the core method. Spike glycosylation/palmitoylation trafficking used LYQD and cysteine-cluster mutants plus 2-bromopalmitate, scoring S2 mobility, packaging and ACE2 fusion — cell-based trafficking, not a leukocyte panel. Naegleria fowleri work assembled an ~30 Mb AT-rich genome and listed pathogenicity candidates that still need infection-model tests.
Evidence for the claim as stated.
Foxp3+ gating is a means to an epigenetic comparison (TSDR demethylation versus unstable induced Foxp3), whereas spike and Naegleria papers are trafficking genetics and a genome assembly. Treating every hit as a flow-cytometry methods paper hides those mismatches.
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 · How do proteins find plasmodesmata?
- Supports · How does monoubiquitin turn down Rab5?
Westerns here answer different biochemical questions. Caveolar work asks which subunits co-purify; N–p50 asks which domain is required for association and HR; USP8 asks whether Smo is ubiquitinated; spike work asks whether glycan occupancy and palmitoylation change S2 mobility and trafficking. A darker band is not a universal 'more protein' story across those designs.
- Supports · What proteins build the caveolar coat?
- Supports · Plant TIR domain binds viral elicitor
- Supports · How does USP8 turn on Smoothened?
Permeabilized-sperm SNARE timing and live epithelial polarity/spike trafficking disagree about how much native membrane regulation is still present. In-vitro sperm may miss in-vivo layers; enteroids and pseudovirus spike assays only approximate infection of a human airway or gut.
- Supports · SNARE timing in sperm acrosome exocytosis
- Supports · Apical-out enteroids for pathogen access
Foxp3+ gating is a means to an epigenetic comparison (TSDR demethylation versus unstable induced Foxp3), whereas spike and Naegleria papers are trafficking genetics and a genome assembly. Treating every hit as a flow-cytometry methods paper hides those mismatches.
- Supports · Epigenetic locking of Foxp3 in Tregs
- Supports · Pathogenicity factors in Naegleria fowleri
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Same topic cluster — not a recommendation engine.