Abstract
Accumulated experimental evidence has shown that viruses recruit the host intracellular machinery to establish infection. It has recently been shown that the potyvirus Turnip mosaic virus (TuMV) transits through the late endosome (LE) for viral genome replication, but it is still largely unknown how the viral replication vesicles labelled by the TuMV membrane protein 6K2 target LE. To further understand the underlying mechanism, we studied the involvement of the vacuolar sorting receptor (VSR) family proteins from Arabidopsis in this process. We now report the identification of VSR4 as a new host factor required for TuMV infection. VSR4 interacted specifically with TuMV 6K2 and was required for targeting of 6K2 to enlarged LE. Following overexpression of VSR4 or its recycling-defective mutant that accumulates in the early endosome (EE), 6K2 did not employ the conventional VSR-mediated EE to LE pathway, but targeted enlarged LE directly from cis-Golgi and viral replication was enhanced. In addition, VSR4 can be N-glycosylated and this is required for its stability and for monitoring 6K2 trafficking to enlarged LE. A non-glycosylated VSR4 mutant enhanced the dissociation of 6K2 from cis-Golgi, leading to the formation of punctate bodies that targeted enlarged LE and to more robust viral replication than with glycosylated VSR4. Finally, TuMV hijacks N-glycosylated VSR4 and protects VSR4 from degradation via the autophagy pathway to assist infection. Taken together, our results have identified a host factor VSR4 required for viral replication vesicles to target endosomes for optimal viral infection and shed new light on the role of N-glycosylation of a host factor in regulating viral infection.
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Claims 10
Claim · model-written summary
VSR4 specifically interacted with TuMV 6K2.
- Taxon
- Arabidopsis
Arabidopsise1 - Interactor
- TuMV
Turnip mosaic viruse0pathogen - Gene
- VSR4e0
- Outcome
- interacted specifically with TuMV 6K2e0
Not reportedDirection
Organisms pictured · Representative pictures of the matched species, not figures from the paper.
Verbatim
e0“VSR4 interacted specifically with TuMV 6K2”
e1“Arabidopsis”
Claim · model-written summary
VSR4 was required to target 6K2 to enlarged late endosomes.
- Taxon
- ArabidopsisArabidopsise1
- Interactor
- TuMVTurnip mosaic viruse0pathogen
- Gene
- VSR4e0
- Outcome
- targeting of 6K2 to enlarged LEe0
Not reportedDirection
Organisms pictured · Representative pictures of the matched species, not figures from the paper.
Verbatim
e0“VSR4 interacted specifically with TuMV 6K2 and was required for targeting of 6K2 to enlarged LE.”
e1“Arabidopsis”
Claim · model-written summary
Overexpressed VSR4 or its recycling-defective mutant redirected 6K2 from cis-Golgi directly to enlarged late endosomes.
- Taxon
- ArabidopsisArabidopsise1
- Treatment
- overexpression of VSR4 or its recycling-defective mutante0
- Gene
- VSR4e0
- Outcome
- targeted enlarged LE directly from cis-Golgie0
- Comparator
- conventional VSR-mediated EE to LE pathwaye0
Not reportedDirection
Organisms pictured · Representative pictures of the matched species, not figures from the paper.
Verbatim
e0“Following overexpression of VSR4 or its recycling-defective mutant that accumulates in the early endosome (EE), 6K2 did not employ the conventional VSR-mediated EE to LE pathway, but targeted enlarged LE directly from cis-Golgi”
e1“Arabidopsis”
Claim · model-written summary
Overexpression of VSR4 or its recycling-defective mutant enhanced viral replication.
- Taxon
- ArabidopsisArabidopsise1
- Treatment
- overexpression of VSR4 or its recycling-defective mutante0
- Interactor
- TuMVTurnip mosaic viruse2pathogen
- Gene
- VSR4e0
- Outcome
- viral replicatione0
- Direction
- enhancede0
Not reportedComparator
Organisms pictured · Representative pictures of the matched species, not figures from the paper.
Verbatim
e0“Following overexpression of VSR4 or its recycling-defective mutant that accumulates in the early endosome (EE), 6K2 did not employ the conventional VSR-mediated EE to LE pathway, but targeted enlarged LE directly from cis-Golgi and viral replication was enhanced.”
e1“Arabidopsis”
e2“identification of VSR4 as a new host factor required for TuMV infection.”
Claim · model-written summary
VSR4 N-glycosylation was required for protein stability.
- Taxon
- ArabidopsisArabidopsise1
- Gene
- VSR4e0
- Outcome
- its stabilitye0
- Qualifier
- N-glycosylatede0
Not reportedDirection
Organisms pictured · Representative pictures of the matched species, not figures from the paper.
Verbatim
e0“VSR4 can be N-glycosylated and this is required for its stability”
e1“Arabidopsis”
Claim · model-written summary
VSR4 N-glycosylation was required to monitor 6K2 trafficking to enlarged late endosomes.
- Taxon
- ArabidopsisArabidopsise1
- Gene
- VSR4e0
- Outcome
- monitoring 6K2 trafficking to enlarged LEe0
- Qualifier
- N-glycosylatede0
Not reportedDirection
Organisms pictured · Representative pictures of the matched species, not figures from the paper.
Verbatim
e0“VSR4 can be N-glycosylated and this is required for its stability and for monitoring 6K2 trafficking to enlarged LE.”
e1“Arabidopsis”
Claim · model-written summary
A non-glycosylated VSR4 mutant enhanced dissociation of 6K2 from cis-Golgi.
- Taxon
- ArabidopsisArabidopsise1
- Material
- non-glycosylated VSR4 mutante0
- Treatment
- non-glycosylated VSR4 mutante0
- Gene
- VSR4e0
- Outcome
- dissociation of 6K2 from cis-Golgie0
- Direction
- enhancede0
Not reportedComparator
Organisms pictured · Representative pictures of the matched species, not figures from the paper.
Verbatim
e0“A non-glycosylated VSR4 mutant enhanced the dissociation of 6K2 from cis-Golgi”
e1“Arabidopsis”
Claim · model-written summary
The non-glycosylated VSR4 mutant led to punctate bodies targeting enlarged late endosomes.
- Taxon
- ArabidopsisArabidopsise1
- Treatment
- non-glycosylated VSR4 mutante0
- Outcome
- formation of punctate bodies that targeted enlarged LEe0
Not reportedComparatorDirection
Organisms pictured · Representative pictures of the matched species, not figures from the paper.
Verbatim
e0“A non-glycosylated VSR4 mutant enhanced the dissociation of 6K2 from cis-Golgi, leading to the formation of punctate bodies that targeted enlarged LE”
e1“Arabidopsis”
Claim · model-written summary
Non-glycosylated VSR4 yielded more robust viral replication than glycosylated VSR4.
- Taxon
- ArabidopsisArabidopsise2
- Treatment
- non-glycosylated VSR4 mutante1
- Interactor
- TuMVTurnip mosaic viruse3pathogen
- Outcome
- viral replicatione0
- Direction
- more robuste0
- Comparator
- glycosylated VSR4e0
Organisms pictured · Representative pictures of the matched species, not figures from the paper.
Verbatim
e0“more robust viral replication than with glycosylated VSR4”
e1“A non-glycosylated VSR4 mutant”
e2“Arabidopsis”
e3“identification of VSR4 as a new host factor required for TuMV infection.”
Claim · model-written summary
TuMV protects N-glycosylated VSR4 from autophagic degradation to assist infection.
- Taxon
- ArabidopsisArabidopsise1
- Interactor
- TuMVTurnip mosaic viruse0pathogen
- Gene
- VSR4e0
- Outcome
- protects VSR4 from degradation via the autophagy pathwaye0
- Qualifier
- to assist infectione0
Not reportedDirection
Organisms pictured · Representative pictures of the matched species, not figures from the paper.
Verbatim
e0“TuMV hijacks N-glycosylated VSR4 and protects VSR4 from degradation via the autophagy pathway to assist infection.”
e1“Arabidopsis”
The same questions in other papers
loss of function · Turnip mosaic virus · ArabidopsisPositive and negative results
2 papers in the same direction as this paper · 3 in the opposite direction
- positive
- positive
- positive
2 papers more in this group
See all 6 papers →Claims are grouped by organism, treatment and what was measured or targeted. A paper counts as positive when any of its claims in the group is positive.