SUMOylation-modified Pelota-Hbs1 RNA surveillance complex restricts the infection of potyvirids in plants

RNA quality control nonsense-mediated decay is involved in viral restriction in both plants and animals.However,it is not known whether two other RNA quality control pathways,nonstop decay and no-go decay,are capable of restricting viruses in plants.Here,we show that the evolutionarily conserved Pelota–Hbs1 complex negatively regulates infection of plant viruses in the family Potyviridae(termed potyvirids),the largest group of plant RNA viruses that accounts for more than half of the viral crop damage worldwide.Pelota enables the recognition of the functional G1-2A6-7 motif in the P3 cistron,which is conserved in almost all potyvirids.This allows Pelota to target the virus and act as a viral restriction factor.Furthermore,Pelota interacts with the SUMO E2-conjugating enzyme SCE1 and is SUMOylated in planta.Blocking Pelota SUMOylation disrupts the ability to recruit Hbs1 and inhibits viral RNA degradation.These findings reveal the functional importance of Pelota SUMOylation during the infection of potyvirids in plants.

Geminiviral C2 proteins inhibit active autophagy to facilitate virus infection by impairing the interaction of ATG7 and ATG8

Autophagy is a conserved intracellular degradation process that plays an active role in plant response to virus infections.Here we report that geminiviruses counteract activated autophagymediated antiviral defense in plant cells through the C2 proteins they encode.We found that,in Nicotiana benthamiana plants,tomato leaf curl Yunnan virus(TLCYnV)infection upregulated the transcription levels of autophagy-related genes(ATGs).Overexpression of NbATG5,NbATG7,or NbATG8a in N.benthamiana plants decreased TLCYnV accumulation and attenuated viral symptoms.Interestingly,transgenic overexpression of NbATG7 promoted the growth of N.benthamiana plants and enhanced plant resistance to TLCYnV.We further revealed that the C2 protein encoded by TLCYnV directly interacted with the ubiquitinactivating domain of ATG7.This interaction competitively disrupted the ATG7–ATG8 binding in N.benthamiana and Solanum lycopersicum plants,thereby inhibiting autophagy activity.Furthermore,we uncovered that the C2-mediated autophagy inhibition mechanism was conserved in three other geminiviruses.In summary,we discovered a novel counter-defensive strategy employed by geminiviruses that enlists their C2 proteins as disrupters of ATG7–ATG8 interactions to defeat antiviral autophagy.

Geminivirus satellite-encoded βC1 activates UPR,induces bZIP60 nuclear export,and manipulates the expression of bZIP60 downstream genes to benefit virus infection

UPR is a conserved response in eukaryotes and can alleviate endoplasmic reticulum(ER)stresses induced by abiotic and biotic stresses.The interactions between UPR and plant RNA viruses have been documented,while the interplays between UPR and plant DNA viruses remain unknown.Using tomato yellow leaf curl China virus(TYLCCNV)and its associated betasatellite(TYLCCNB)as a model,we indicate that TYLCCNBβC1 is a major inducer of UPR and can upregulate the expression of b ZIP60,a transcription factor in Nicotiana benthamiana plants.Treatment using ER stress inducers or overexpression of Nbb ZIP60 increasesβC1 accumulation and benefits TYLCCNV/TYLCCNB infection in N.benthamiana plants,and vice versa.In the TYLCCNV/TYLCCNB-infected or theβC1-expressing cells,Nbb ZIP60 is exported from the nucleus to the nuclear periphery via the XPO1 pathway,and blocking the XPO1 pathway inhibited TYLCCNV/TYLCCNB infection.We have found that the Nbb ZIP60-regulated pro-survival genes could promote virus infection,and the pro-death gene plays a contrasting role in virus infection.This study reveals that geminivirus infection activates UPR and utilizes the up-regulated molecular chaperons to promote viral infection,and then induces the nuclear export of Nbb ZIP60 to evade plant defense response,which is a distinct virulence strategy exploited by plant pathogens.