Tomato chlorosis virus p22 interacts with <scp>NbBAG5</scp> to inhibit autophagy and regulate virus infection

Shang, Kaijie; Xiao, Li; Zhang, Xianping; Zang, Lianyi; Zhao, Dan; Wang, Chenchen; Wang, Xipan; Zhou, Tao; Zhu, Changxiang; Zhu, Xiaoping

doi:10.1111/mpp.13311

Cited by 5 publications

(3 citation statements)

References 53 publications

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“…According to the plasmid construction method used in our laboratory ( Shang et al., 2023 ), the StlncRNA13558 gene was ligated to the restriction site region between the 35S promoter and Nos terminator of the pCa plasmid to obtain the pCa- StlncRNA13558 overexpression plasmid. The StPRL gene was ligated to the restriction site region between the 35S promoter and the Nos terminator of the pCa-GFP plasmid to obtain the pCa-StPRL-GFP overexpression plasmid.…”

Section: Methodsmentioning

confidence: 99%

Abscisic-acid-responsive StlncRNA13558 induces StPRL expression to increase potato resistance to Phytophthora infestans infection

Shang,

Wang,

Cao

et al. 2024

Front. Plant Sci.

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Late blight, caused by Phytophthora infestans, is one of the most serious diseases affecting potatoes (Solanum tuberosum L.). Long non-coding RNAs (lncRNAs) are transcripts with a length of more than 200 nucleotides that have no protein-coding potential. Few studies have been conducted on lncRNAs related to plant immune regulation in plants, and the molecular mechanisms involved in this regulation require further investigation. We identified and screened an lncRNA that specifically responds to P. infestans infection, namely, StlncRNA13558. P. infestans infection activates the abscisic acid (ABA) pathway, and ABA induces StlncRNA13558 to enhance potato resistance to P. infestans. StlncRNA13558 positively regulates the expression of its co-expressed PR-related gene StPRL. StPRL promotes the accumulation of reactive oxygen species and transmits a resistance response by affecting the salicylic acid hormone pathway, thereby enhancing potato resistance to P. infestans. In summary, we identified the potato late blight resistance lncRNA StlncRNA13558 and revealed its upstream and downstream regulatory relationship of StlncRNA13558. These results improve our understanding of plant-pathogen interactions’ immune mechanism and elucidate the response mechanism of lncRNA-target genes regulating potato resistance to P. infestans infection.

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Section: Methodsmentioning

confidence: 99%

Abscisic-acid-responsive StlncRNA13558 induces StPRL expression to increase potato resistance to Phytophthora infestans infection

Shang,

Wang,

Cao

et al. 2024

Front. Plant Sci.

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“…One such example is observed in the case of tomato chlorosis virus (ToCV) infection. The P22 protein of ToCV interacts with the N. benthamiana B-cell lymphoma2-associated athanogenes5 (NbBAG5), an evolutionarily conserved protein mainly involved in plant growth and stress response, and induces NbBAG5 expression, leading to the inhibition of autophagy and favoring viral infection [ 74 ]. Another report revealed that the interaction of P3 and/or P3N-PIPO of PVY with BI-1 decreases the expression of the ATG6, thereby inhibiting the autophagic degradation of viral NIb and enhancing viral replication [ 75 ].…”

Section: Autophagy–virus Interplay In Plants: From Antiviral Recognit...mentioning

confidence: 99%

The Great Game between Plants and Viruses: A Focus on Protein Homeostasis

Sun

Jing

Wang

et al. 2023

IJMS

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Plant viruses are tiny pathogenic obligate parasites that cause significant damage to global crop production. They exploit and manipulate the cellular components of host plants to ensure their own survival. In response, plants activate multiple defense signaling pathways, such as gene silencing and plant hormone signaling, to hinder virus propagation. Growing evidence suggests that the regulation of protein homeostasis plays a vital role in the ongoing battle between plants and viruses. The ubiquitin-proteasome-degradation system (UPS) and autophagy, as two major protein-degradation pathways, are widely utilized by plants and viruses in their arms race. One the one hand, these pathways act as essential components of plant’s antiviral defense system by facilitating the degradation of viral proteins; on the other hand, viruses exploit the UPS and autophagy to create a favorable intracellular environment for viral infection. This review aims to provide a comprehensive summary of the events involved in protein homeostasis regulation during viral infection in plants. Gaining knowledge in this area will enhance our understanding of the complex interplay between plants and viruses.

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“…Autophagy also targets plant viruses and it is a major player in antiviral innate immunity [69][70][71][72][73][74][75]. Several plant viruses manipulate the autophagy machinery to inhibit antiviral defenses in plants [76][77][78][79][80]. However, plant viruses also exploit autophagy for pro-viral functions [65,81,82].…”

Section: Introductionmentioning

confidence: 99%

Subversion of selective autophagy for the biogenesis of tombusvirus replication organelles inhibits autophagy

Kang,

Lin,

Nagy

2024

PLoS Pathog

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Elaborate viral replication organelles (VROs) are formed to support positive-strand RNA virus replication in infected cells. VRO formation requires subversion of intracellular membranes by viral replication proteins. Here, we showed that the key ATG8f autophagy protein and NBR1 selective autophagy receptor were co-opted by Tomato bushy stunt virus (TBSV) and the closely-related carnation Italian ringspot virus. Knockdown of ATG8f or NBR1 in plants led to reduced tombusvirus replication, suggesting pro-viral function for selective autophagy. BiFC and proximity-labeling experiments showed that the TBSV p33 replication protein interacted with ATG8f and NBR1 to recruit them to VROs. In addition, we observed that several core autophagy proteins, such as ATG1a, ATG4, ATG5, ATG101 and the plant-specific SH3P2 autophagy adaptor proteins were also re-localized to TBSV VROs, suggesting that TBSV hijacks the autophagy machinery in plant cells. We demonstrated that subversion of autophagy components facilitated the recruitment of VPS34 PI3 kinase and enrichment of phospholipids, such as phosphatidylethanolamine and PI3P phosphoinositide in the VRO membranes. Hijacking of autophagy components into TBSV VROs led to inhibition of autophagic flux. We also found that a fraction of the subverted ATG8f and NBR1 was sequestered in biomolecular condensates associated with VROs. We propose that the VRO-associated condensates trap those autophagy proteins, taking them away from the autophagy pathway. Overall, tombusviruses hijack selective autophagy to provide phospholipid-rich membranes for replication and to regulate the antiviral autophagic flux.

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Tomato chlorosis virus p22 interacts with NbBAG5 to inhibit autophagy and regulate virus infection

Cited by 5 publications

References 53 publications

Abscisic-acid-responsive StlncRNA13558 induces StPRL expression to increase potato resistance to Phytophthora infestans infection

Abscisic-acid-responsive StlncRNA13558 induces StPRL expression to increase potato resistance to Phytophthora infestans infection

The Great Game between Plants and Viruses: A Focus on Protein Homeostasis

Subversion of selective autophagy for the biogenesis of tombusvirus replication organelles inhibits autophagy

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