Changxiang Zhu

Rice stripe virus (RSV) causes substantial rice (Oryza sativa) yield losses and poses a serious threat to agricultural production. Auxin is a pivotal hormone in orchestrating the antagonism between plant growth and defense. Conversely, pathogen manipulation of auxin signaling promotes disease and inhibits plant growth, but how this hormone influences immunity is not fully understood. Here, we report that RSV infection results in dwarfism and short crown roots in rice and reduces the sensitivity of rice plants to NAA. The RSV-encoded nonstructural protein 3 (NS3) interacts with Aux/IAA repressor protein OsIAA25, disrupting its degradation by the auxin receptor transport inhibitor response 1 (OsTIR1). Additionally, NS2 and NS3 can form heterodimers to enhance the ability to stabilize OsIAA25. Plants overexpressing OsIAA25 or OsIAA25P98L, a single-amino-acid substitution of leucine for proline at position 98, exhibit growth and development defects similar to RSV-infected plants and increased susceptibility to RSV infection. By contrast, OsIAA25 knockout plants display an opposite phenotype, indicating that OsIAA25 positively regulates RSV infection. Thus, our findings establish a mechanism by which RSV proteins guide virus infection and affect plant growth by interfering with the auxin signaling pathway through their interaction with rice OsIAA25.

The tomato chlorosis virus (ToCV) is one of the most destructive plant viruses affecting tomato crops, leading to significant agricultural losses. As an obligate parasite, ToCV depends on the macromolecular machinery of host cells for replication. The ubiquitin 26S proteasome system maintains the intracellular protein homeostasis, which is essential for plant growth and development. Our study found that the CPm protein of ToCV interacted with SlPAD1, a component of the 26S proteasome, to enhance viral infection. This interaction disrupts the binding between SlPAD1 and SlPA4, thereby impairing the 26S proteasome function. In addition, SlPAD1 and SlPA4 positively regulate plant resistance to ToCV. Our findings reveal a mechanism by which ToCV proteins facilitate infection by interfering with 26S proteasome function.

Alginate oligosaccharides (AOSs), important plant immunity inducers, are widely used in agriculture because of their important role in the biological control of crop diseases. However, the mechanism by which AOSs induce plant resistance to pathogens is not clear. Here, we report AOS with a degree of polymerization of 2–5, which was obtained by a newly reported enzyme Aly2. AOS treatment exhibited high activity in enhancing resistance to Phytophthora infestans (P. infestans). AOS significantly induced reactive oxygen species (ROS) accumulation, calcium influx, stomata closure, and callose deposition. The salicylic acid (SA) synthesis-related gene and the defense-related genes were upregulated after AOS treatment. A transcriptome file generated from AOS-treated seedlings verified the SA pathway and suggested the presence of chitin elicitor receptor kinase (CERK). The subsequent results showed that AtCERK1 binds AOS tightly, suggesting that AtCERK1 is responsible for AOS recognition. This study laid a theoretical foundation for the broad application of AOS.

Plant viruses rely on host factors for successful infection. Non‐specific lipid transfer proteins (nsLTPs) play critical roles in plant−pathogen interactions; however, their functions and underlying molecular mechanisms in viral infections remain largely unknown. Jasmonic acid (JA) is a crucial regulatory hormone in the process of plant resistance to viral infection. In this study, we screened and verified that StLTP6, a previously identified pro‐viral factor, interacts with the silencing suppressor triple gene block1 (TGB1) of potato virus S (PVS). The PVS TGB1 induces the expression of StLTP6, and both co‐localize in the cytoplasm. Furthermore, StLTP6 interacts with allene oxide cyclase and inhibits its accumulation, thereby suppressing JA synthesis and attenuating RNA silencing antiviral resistance. In summary, we elucidated the molecular mechanism by which PVS TGB1 interacts with StLTP6 to facilitate PVS infection. These findings broaden our understanding of the biological roles of nsLTPs and provide a new antiviral target for potato research.

In plants, recognition between resistance gene (R) and virus induces a local hypersensitive response (HR), which is accompanied by systemic acquired resistance (SAR). The dominant resistance gene N in tobacco confers resistance to tobacco mosaic virus (TMV) at both locally inoculated tissues and systemically infected tissues. However, the mechanisms underlying HR- and SAR-mediated viral inhibition are not fully revealed. In this study, we find that Nicotiana glutinosa RNA-binding protein (NgRBP) is an RNA silencing suppressor which enhances TMV-triggered HR. Stronger HR could result in stronger local and systemic RNA silencing as well as SAR. Enhanced RNA silencing in the systemically infected leaves induced by the NgRBP gene is compromised by transient expression of NahG. These results indicate that RNA silencing is activated by HR and plays a crucial role in local and systemic virus resistance. Our results reveal a crosstalk between N gene-mediated virus resistance and RNA silencing which would deepen our understanding of the established HR and SAR models.

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.

Tomato chlorosis virus (ToCV) severely threatens tomato production worldwide. P27 is known to be involved in virion assembly, but its other roles in ToCV infection are unclear. In this study, we found that removal of p27 reduced systemic infection, while ectopic expression of p27 promoted systemic infection of potato virus X in Nicotiana benthamiana. We determined that Solanum lycopersicum catalases (SlCAT) can interact with p27 in vitro and in vivo and that amino acids 73 to 77 of the N-terminus of SlCAT represent the critical region for their interaction. p27 is distributed in the cytoplasm and nucleus, and its coexpression with SlCAT1 or SlCAT2 changes its distribution in the nucleus. Furthermore, we found that silencing of SlCAT1 and SlCAT2 can promote ToCV infection. In conclusion, p27 can promote viral infection by binding directly to inhibit anti-ToCV processes mediated by SlCAT1 or SlCAT2.

Tomato chlorosis virus (ToCV) is a member of the genus Crinivirus in the family Closteroviridae . It has a wide host range and wide distribution, causing serious harm to the vegetable industry. The autophagy pathway plays an important role in plant resistance to virus infection. Viruses and plant hosts coevolve in defence and antidefence processes around autophagy. In this study, the interaction between ToCV p22 and Nicotiana benthamiana B‐cell lymphoma2‐associated athanogenes5 Nicotiana benthamiana (NbBAG5) was examined. Through overexpression and down‐regulation of NbBAG5, results showed that NbBAG5 could negatively regulate ToCV infection. NbBAG5 was found to be localized in mitochondria and can change the original localization of ToCV p22, which is colocalized in mitochondria. NbBAG5 inhibited the expression of mitophagy‐related genes and the number of autophagosomes, thereby regulating viral infection by affecting mitophagy. In summary, this study demonstrated that ToCV p22 affects autophagy by interacting with NbBAG5, established the association between viral infection, BAG proteins family, and the autophagy pathway, and explained the molecular mechanism by which ToCV p22 interacts with NbBAG5 to inhibit autophagy to regulate viral infection.

Main conclusion For the first time it is reported that members of the nsLTP protein family could promote viral infection by inhibiting virus-induced RNA silencing. Abstract Non-specific lipid transfer proteins (nsLTPs) are a class of soluble proteins with low relative molecular weight and widely present in higher plants. The role of nsLTPs in biotic and abiotic stresses has been studied, but no report has shown that nsLTPs play a role in the process of viral infection. We report the function and mechanism of the classical nsLTP protein StLTP6 in viral infection. We found that StLTP6 expression was remarkably upregulated in potato infected with potato virus Y and potato virus S. The infection efficiency and virus content of StLTP6-overexpressed potato and Nicotiana benthamiana were remarkable increased. Further study found that the overexpression of StLTP6 inhibited the expression of multiple genes in the RNA silencing pathway, thereby inhibiting virus-induced RNA silencing. This result indicated that StLTP6 expression was induced during viral infection to inhibit the resistance of virus-induced RNA silencing and promote viral infection. In summary, we reported the role of StLTP6 in viral infection, broadening the biological function range of the nsLTP family and providing valuable information for the study of viral infection mechanism.