Abstract
RNA quality control pathways, particularly nonsense-mediated mRNA decay (NMD), function as critical antiviral defenses by degrading aberrant viral transcripts. However, how DNA geminiviruses counteract this RNA surveillance system remains largely unknown. Here we report that the Sri Lankan cassava mosaic virus (SLCMV) AC4 protein employs a novel strategy to suppress NMD: it targets the central regulator Upf1 for degradation. In Nicotiana benthamiana and Arabidopsis thaliana models, we demonstrate that SLCMV AC4 directly binds AtUpf1 via its N-terminal domain and triggers its depletion through the coordinated action of both the autophagy and ubiquitin-proteasome pathways. AC4 expression stabilized a broad range of endogenous NMD substrates and enhanced the accumulation and pathogenicity of a heterologous virus. Structural and functional analyses revealed that the N-terminal myristoylation motif of AC4 is indispensable for its function. While point mutations within this motif preserved Upf1 binding, they abrogated NMD suppression and Upf1 degradation, indicating the motif's essential role in assembling a functional degradation complex beyond mere interaction. Furthermore, we elucidate that AC4 activates autophagy by competitively disrupting the GAPC2-ATG3 interaction, thereby liberating ATG3 to promote autophagosome formation. Our findings unveil a sophisticated viral counter-defense mechanism in which a pathogen effector orchestrates the spatially coordinated degradation of a key host RNA surveillance factor, bridging the fields of plant-virus interactions, RNA biology, and host proteostasis.
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Claims 9
Claim · model-written summary
SLCMV AC4 directly binds AtUpf1 in Arabidopsis thaliana.
- Taxon
- Arabidopsis thaliana
Arabidopsis thalianae0 - Interactor
- Sri Lankan cassava mosaic virusSri Lankan cassava mosaic viruse2pathogen
- Gene
- AtUpf1e1
- Outcome
- binds AtUpf1e1
Organisms pictured · Representative pictures of the matched species, not figures from the paper.
Verbatim
e0“In Nicotiana benthamiana and Arabidopsis thaliana models”
e1“SLCMV AC4 directly binds AtUpf1 via its N-terminal domain”
e2“Sri Lankan cassava mosaic virus (SLCMV) AC4 protein”
Claim · model-written summary
SLCMV AC4 triggers depletion of AtUpf1 through coordinated autophagy and ubiquitin-proteasome pathways.
- Taxon
- Arabidopsis thalianaArabidopsis thalianae0
- Interactor
- Sri Lankan cassava mosaic virusSri Lankan cassava mosaic viruse2pathogen
- Gene
- AtUpf1e1
- Outcome
- depletione1
- Qualifier
- through the coordinated action of both the autophagy and ubiquitin-proteasome pathwayse1
Organisms pictured · Representative pictures of the matched species, not figures from the paper.
Verbatim
e0“In Nicotiana benthamiana and Arabidopsis thaliana models”
e1“SLCMV AC4 directly binds AtUpf1 via its N-terminal domain and triggers its depletion through the coordinated action of both the autophagy and ubiquitin-proteasome pathways”
e2“Sri Lankan cassava mosaic virus (SLCMV) AC4 protein”
Claim · model-written summary
AC4 expression stabilized a broad range of endogenous NMD substrates in Nicotiana benthamiana and Arabidopsis thaliana.
- Taxon
- Nicotiana benthamiana and Arabidopsis thalianaArabidopsis thaliana
Nicotiana benthamianae0 - Treatment
- AC4 expressione3
- Outcome
- endogenous NMD substratese3
- Direction
- stabilizede3
Not reportedComparator
Organisms pictured · Representative pictures of the matched species, not figures from the paper.
Verbatim
e0“In Nicotiana benthamiana and Arabidopsis thaliana models”
e3“AC4 expression stabilized a broad range of endogenous NMD substrates and enhanced the accumulation and pathogenicity of a heterologous virus”
Claim · model-written summary
AC4 enhanced the accumulation and pathogenicity of a heterologous virus.
- Taxon
- Nicotiana benthamiana and Arabidopsis thalianaArabidopsis thalianaNicotiana benthamianae0
- Treatment
- AC4 expressione3
- Interactor
- heterologous viruse3pathogen
- Outcome
- accumulation and pathogenicitye3
- Direction
- enhancede3
Not reportedComparator
Organisms pictured · Representative pictures of the matched species, not figures from the paper.
Verbatim
e0“In Nicotiana benthamiana and Arabidopsis thaliana models”
e3“AC4 expression stabilized a broad range of endogenous NMD substrates and enhanced the accumulation and pathogenicity of a heterologous virus”
Claim · model-written summary
The N-terminal myristoylation motif of AC4 is indispensable for its function.
- Taxon
- Nicotiana benthamiana and Arabidopsis thalianaArabidopsis thalianaNicotiana benthamianae0
- Outcome
- functione4
- Qualifier
- the N-terminal myristoylation motif of AC4e4
Organisms pictured · Representative pictures of the matched species, not figures from the paper.
Verbatim
e0“In Nicotiana benthamiana and Arabidopsis thaliana models”
e4“Structural and functional analyses revealed that the N-terminal myristoylation motif of AC4 is indispensable for its function”
Claim · model-written summary
Point mutations within the myristoylation motif abrogated AC4 suppression of NMD and Upf1 degradation.
- Taxon
- Nicotiana benthamiana and Arabidopsis thalianaArabidopsis thalianaNicotiana benthamianae0
- Treatment
- point mutations within this motife5
- Outcome
- NMD suppression and Upf1 degradatione5
- Direction
- abrogatede5
Not reportedComparator
Organisms pictured · Representative pictures of the matched species, not figures from the paper.
Verbatim
e0“In Nicotiana benthamiana and Arabidopsis thaliana models”
e5“While point mutations within this motif preserved Upf1 binding, they abrogated NMD suppression and Upf1 degradation”
Claim · model-written summary
Point mutations within the myristoylation motif preserved AC4 binding to Upf1.
- Taxon
- Nicotiana benthamiana and Arabidopsis thalianaArabidopsis thalianaNicotiana benthamianae0
- Treatment
- point mutations within this motife5
- Outcome
- Upf1 bindinge5
- Direction
- preservede5
Not reportedComparator
Organisms pictured · Representative pictures of the matched species, not figures from the paper.
Verbatim
e0“In Nicotiana benthamiana and Arabidopsis thaliana models”
e5“While point mutations within this motif preserved Upf1 binding, they abrogated NMD suppression and Upf1 degradation”
Claim · model-written summary
AC4 activates autophagy by competitively disrupting the GAPC2-ATG3 interaction.
- Taxon
- Nicotiana benthamiana and Arabidopsis thalianaArabidopsis thalianaNicotiana benthamianae0
- Gene
- GAPC2e6
- Outcome
- activates autophagye6
- Qualifier
- by competitively disrupting the GAPC2-ATG3 interactione6
Organisms pictured · Representative pictures of the matched species, not figures from the paper.
Verbatim
e0“In Nicotiana benthamiana and Arabidopsis thaliana models”
e6“AC4 activates autophagy by competitively disrupting the GAPC2-ATG3 interaction, thereby liberating ATG3 to promote autophagosome formation”
Claim · model-written summary
Liberated ATG3 promotes autophagosome formation.
- Taxon
- Nicotiana benthamiana and Arabidopsis thalianaArabidopsis thalianaNicotiana benthamianae0
- Gene
- ATG3e6
- Outcome
- autophagosome formatione6
- Direction
- promotee6
- Qualifier
- thereby liberating ATG3e6
Organisms pictured · Representative pictures of the matched species, not figures from the paper.
Verbatim
e0“In Nicotiana benthamiana and Arabidopsis thaliana models”
e6“AC4 activates autophagy by competitively disrupting the GAPC2-ATG3 interaction, thereby liberating ATG3 to promote autophagosome formation”
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See all 73 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.