Yuqiang Liu

The endoplasmic reticulum (ER) is the largest intracellular membrane-bound organelle in eukaryotic cells, comprising an interconnected network of tubules and sheets. Lunapark (LNP) functions as an E3 ubiquitin ligase that targets RHD3, a dynamin-like GTPase essential for homotypic fusion of ER tubules, for proteasomal degradation, thereby modulating ER tubule stability. However, the regulatory mechanism governing LNP activity remains largely unknown. Here, we report the characterization of the rice oskish mutant, which exhibits aberrant aggregation of ER tubules and defective ER exit of seed storage proteins. OsKish is an ER-localized small protein that physically interacts with both OsLNPs and the RHD3-like (RHD3L) protein. OsKish stabilizes OsLNPs by suppressing their auto-ubiquitination; concomitantly, OsKish attenuates the membrane fusion activity of RHD3L, possibly by inhibiting its oligomerization. Altogether, our studies propose an OsKish–OsLNPs–RHD3L framework for fine-tuning homotypic ER tubule fusion in rice, providing mechanistic insights into the maintenance of ER architecture in plants.

Rice black-streaked dwarf virus (RBSDV) disease, caused by rice black-streaked dwarf virus and transmitted by the small brown planthopper (Laodelphax striatellus Fallén, SBPH), is a devastating viral disease severely impacting global rice production. The cultivation and promotion of resistant varieties is considered the most economical and effective control strategy. However, effectiveness of field-based resistance identification is hindered by environmental variability, seasonal limitations of SBPH outbreaks, and inconsistent virus pressure, leading to unreliable results. Therefore, we developed an efficient and reliable artificial inoculation system for RBSDV-resistant rice materials screening under controllable laboratory conditions. This system encompasses optimized procedures for material preparation, inoculation methodology, disease phenotyping and resistance evaluation. We directly inoculated 1st-2nd instar SBPH nymphs onto the RBSDV infected plants and obtained nymphs with high viruliferous rates. Then, to generate a stable laboratory virus source, these viruliferous nymphs were used to inoculate highly susceptible rice seedlings (e.g., Suyunuo). Subsequent inoculation cycles using these viruliferous rice seedlings consistently produced SBPH populations with high viruliferous rates (average about 42.4%). This system enables continuous, year-round resistance evaluation, breaking through the limitation of environmental dependence in field identification. This method will significantly accelerate the breeding of RBSDV disease resistant rice varieties.

The brown planthopper (BPH) poses a persistent threat to global rice production as one of the most devastating insect pests. Development and utilization of BPH-resistant rice cultivars are believed to be the most sustainable and eco-friendly control strategy, which has been successfully implemented in indica rice subspecies but remains underdeveloped in japonica rice. Here, we introgressed the BPH resistance gene Bph27(t) into elite japonica cultivars. Although the introgressed lines demonstrated robust BPH resistance throughout all developmental stages, they unexpectedly exhibited a brown anther phenotype accompanied by significantly reduced spikelet fertility. Histological analyses revealed that the brown anther phenotype and spikelet sterility in Bph27(t)-carrying japonica plants were likely caused by delayed tapetum degradation, leading to anther indehiscence. Furthermore, a brown anther locus, Ba1, was identified and localized to a 1.3 Mb region closely linked to Bph27(t). Genome assembly of the donor parent, Balamawee, revealed an approximately 1.1 Mb inversion in the fine-mapped region. By breaking the genetic linkage between Bph27(t) and Ba1, BPH-resistant japonica rice with high seed-setting rates was subsequently developed. The identification of Ba1 provides a new genetic resource to further explore the molecular mechanisms underlying rice anther development. Moreover, the development of novel BPH-resistant japonica germplasm lays the foundation for breeding high-yield and BPH-resistant japonica rice varieties.

Plants are subject to attack by diverse pests and pathogens. Few genes conferring broad-spectrum resistance to both insects and pathogens have been identified. Because of the growth–defense tradeoff, it is often challenging to balance biotic stress resistance and yield for crops. Here, we report that OsWRKY36 suppresses the resistance to insects and pathogens via transcriptional repression of Phenylalanine Ammonia Lyases ( PALs ), a key enzyme in phenylpropanoid pathway in rice. Knocking out OsWRKY36 causes elevated lignin biosynthesis and increased sclerenchyma thickness of leaf sheath, leading to enhanced resistance to multiple pests and pathogens. Additionally, loss of OsWRKY36 also derepresses the transcription of Ideal Plant Architecture 1 ( IPA1 ) and MONOCULM2 ( MOC2 ), resulting in increased spikelet number per panicle and tiller number. These findings provide mechanistic insights into biotic stress tolerance in rice and offer a promising strategy to breed rice cultivars with broad-spectrum resistance to insects and pathogens while maintaining stable yield.

Plant defense responses against insect pests are intricately regulated by highly complex regulatory networks. Post-translational modifications (PTMs) of histones modulate the expression of genes involved in various biological processes. However, the role of PTMs in conferring insect resistance remains unclear. Through the screening of a T-DNA insertion activation-tagged mutant collection in rice, we identified the mutant planthopper susceptible 1 (phs1), which exhibits heightened expression of SET domain group 703 (SDG703). This overexpression is associated with increased susceptibility to the small brown planthopper (SBPH), an economically significant insect pest affecting rice crops. SDG703 is constitutively expressed in multiple tissues and shows substantial upregulation in response to SBPH feeding. SDG703 demonstrates the activity of histone H3K9 methyltransferase. Transcriptomic analysis revealed the downregulation of genes involved in effector-triggered immunity (ETI) and pattern-triggered immunity (PTI) in plants overexpressing SDG703. Among the downregulated genes, the overexpression of SDG703 in plants resulted in a higher level of histone H3K9 methylation compared to control plants. Collectively, these findings indicate that SDG703 suppresses the expression of defense-related genes through the promotion of histone methylation, consequently leading to reduced resistance against SBPH. The defense-related genes regulated by histone methylation present valuable targets for developing effective pest management strategies in future studies. Furthermore, our study provides novel insight into the epigenetic regulation involved in plant-insect resistance.

Increasing planting density is one of the most effective ways to improve crop yield. However, one major factor that limits crop planting density is the weakened immunity of plants to pathogens and insects caused by dim light (DL) under shade conditions. The molecular mechanism underlying how DL compromises plant immunity remains unclear. Here, we report that DL reduces rice (Oryza sativa) resistance against brown planthopper (BPH; Nilaparvata lugens) by elevating ethylene (ET) biosynthesis and signaling in a Phytochrome B (OsPHYB)-dependent manner. The DL-reduced BPH resistance is relieved in osphyB mutants, but aggravated in OsPHYB overexpressing plants. Further, we found that DL reduces the nuclear accumulation of OsphyB, thus alleviating Phytochrome Interacting Factor Like14 (OsPIL14) degradation, consequently leading to the up-regulation of 1-Aminocyclopropane-1-Carboxylate Oxidase1 (OsACO1) and an increase in ET levels. In addition, we found that nuclear OsphyB stabilizes Ethylene Insensitive Like2 (OsEIL2) by competitively interacting with EIN3 Binding F-Box Protein (OsEBF1) to enhance ET signaling in rice, which contrasts with previous findings that phyB blocks ET signaling by facilitating Ethylene Insensitive3 (EIN3) degradation in other plant species. Thus, enhanced ET biosynthesis and signaling reduces BPH resistance under DL conditions. Our findings provide insights into the molecular mechanism of the light-regulated ET pathway and host-insect interactions and potential strategies for sustainable insect management.

White-backed planthopper (WBPH) is one of the most serious pests in rice production. Breeding resistant varieties is the most economical and effective strategy to control the white-backed planthopper. In this study, we found that Guangxi wild rice variety ‘Y11’ had high resistance to white-backed planthopper. The number and survival rate of WBPH were significantly less than the susceptible variety ‘Guanghui 998’. These results showed that ‘Y11’ displayed higher antixenosis and antibiosis against WBPH. Subsequently, ‘Y11’ was as the donor parent and an indica cultivar ‘Guanghui 998’ was as the recurrent parent by continuous backcrossing and selfing to obtain the BC3F9 population. Furthermore, to identify the quantitative trait locus (QTL) for white-backed planthopper resistance, we completed the evaluation of this population for WBPH resistance at seedling stage and constructed the genome-wide linkage map. Three QTLs were detected on the three different rice chromosomes, and designed as qWBPH2Y11, qWBPH6Y11, and qWBPH11Y11, respectively. The LOD values were 4.8, 2.5, and 3.7, which accounted for 9.3%, 2.3%, and 5.6% of the phenotypic variation, respectively. All of the resistance alleles were from resistant parent ‘Y11’. Plant harboring qWBPH2 Y11 was selected from BC3F9 population to continuously backcross with ‘Guanghui 998’. The near isogenic line of qWBPH2 Y11 was developed by molecular marker assisted selection, which displayed higher resistance to WBPH than the background parent ‘Guanghui 998’. The mapping of WBPH resistance QTLs and the development of the near isogenic line in this study will be helpful for cloning resistance genes and breeding resistant in rice cultivars.

Plants have evolved a sophisticated defense system that employs various hormone pathways to defend against attacks by insect pests. Cytokinin (CK) plays an important role in plant growth and stress tolerance, but the role of CKs in plant–insect interaction remains largely unclear. Here, we report that CKs act as a positive regulator in rice resistance against brown planthopper (BPH), a devastating insect pest of rice. We found that BPH feeding promotes CK biosynthesis and signaling in rice. Exogenous application of CKs significantly increased the rice resistance to BPH. Increasing endogenous CKs by knocking out cytokinin oxidase/dehydrogenase (OsCKXs) led to enhanced resistance to BPH. Moreover, the levels of the plant hormone jasmonic acid (JA) and the expression of JA-responsive genes were elevated by CK treatment and in OsCKXs knockout plants. Furthermore, JA-deficient mutant og1 was more susceptible to BPH, and CK-induced BPH resistance was suppressed in og1. These results indicate that CK-mediated BPH resistance is JA-dependent. Our findings provide the direct evidence for the novel role of CK in promoting insect resistance, and demonstrate that CK-induced insect resistance is JA-dependent. These results provide important guidance for effective pest management strategies in the future.

Rice stripe virus (RSV) is one of the most destructive viral diseases affecting rice production. However, so far, only one RSV resistance gene has been cloned, the molecular mechanisms underlying host-RSV interaction are still poorly understood. Here, we show that increasing levels or signaling of brassinosteroids (BR) and jasmonic acid (JA) can significantly enhance the resistance against RSV. On the contrary, plants impaired in BR or JA signaling are more susceptible to RSV. Moreover, the enhancement of RSV resistance conferred by BR is impaired in OsMYC2 (a key positive regulator of JA response) knockout plants, suggesting that BR-mediated RSV resistance requires active JA pathway. In addition, we found that RSV infection suppresses the endogenous BR levels to increase the accumulation of OsGSK2, a key negative regulator of BR signaling. OsGSK2 physically interacts with OsMYC2, resulting in the degradation of OsMYC2 by phosphorylation and reduces JA-mediated defense to facilitate virus infection. These findings not only reveal a novel molecular mechanism mediating the crosstalk between BR and JA in response to virus infection and deepen our understanding about the interaction of virus and plants, but also suggest new effective means of breeding RSV resistant crops using genetic engineering. Brassinosteroids (BR) and jasmonic acid (JA) play critical roles in responding to various stresses. However, the roles of BR and JA, particularly, the crosstalk between these two phytohormones in viral resistance is still very limited. In this work, we found that both BR and JA positively regulate RSV resistance, and JA pathway is necessary for BR-mediated RSV resistance in rice. RSV infection significantly inhibits the BR signaling pathway and increases the accumulation of OsGSK2. OsGSK2 interacts with and phosphorylates OsMYC2, resulting in the degradation of OsMYC2 and suppression of the JA-mediated RSV resistance response to facilitate virus infection. These findings revealed the molecular mechanism of crosstalk between the BR and JA in response to virus infection and deepen our understanding about the mechanism of RSV resistance.