Tambocerus elongatus (Shen) (Hemiptera: Cicadellidae) is a devastating insect pest species of Camellia sinensis, significantly affecting the yield and quality of tea. Due to growing concerns over the irrational use of insecticides and associated food safety, it is crucial to better understand the innate resistance mechanism of tea trees to T. elongatus. This study aims to explore the responses of tea trees to different levels of T. elongatus infestation. We first focused on the primary metabolism and found that the amino acid levels decreased significantly with increasing T. elongatus infestation, while sugar accumulation showed an opposite trend. Moreover, secondary metabolite analysis showed a significant increase in flavonoid compounds and lignin content after T. elongatus infestation. Metabolomics analysis of the flavonoid compounds revealed a decrease in the proanthocyanidin level and an increase in anthocyanidin glycosides (anthocyanins and their derivatives) after T. elongatus infestation. T. elongatus infestation also caused a decrease in the abundance of non-ester catechins and an increase in the abundance of ester catechins. Furthermore, the gene expression analysis revealed that transcripts of genes involved in flavonoid biosynthesis, such as CsCHI, CsF3H, CsF3′H, CsFNS, CsFLS, and CsUFGT, were down-regulated, while genes involved in the lignin pathway were up-regulated by insect infestation, suggesting that lignin probably plays a pivotal role in tea plant response to T. elongatus infestation. Analysis of the expression of related genes indicates that the jasmonate (JA) pathway primarily responds to leafhopper damage. These findings suggest that the lignin pathway and JA play a preferential role in tea plant response to T. elongatus. Furthermore, the production of saccharides and the accumulation of anthocyanin glycosides in the flavonoid metabolic pathway are critical during this stress response. Further exploration of the roles of anthocyanin glycosides and lignin in tea tree resistance could provide a theoretical basis for understanding the defense mechanism of tea trees against T. elongatus damage.

The biological insecticide, Ectropis obliqua nucleopolyhedrovirus (EcobNPV), has been applied to control the major tea-pest Ectropis grisescens. Previously, the virus strain EcobNPV-QF4 showed higher a mortality rate (58.2% vs. 88.2%) and shorter median lethal-time (13.9 d vs. 15.4 d) on E. grisescens than the strain EcobNPV-QV. However, the mechanism of the difference in virulence between the two strains remains unclear. Using the leaf-disc method, we detected the virulence of the two strains on 3^rd-instar larvae, and found that median lethal-dose (LD₅₀) of EcobNPV-QF4 is 55-fold higher than that of EcobNPV-QV (4.35 × 10⁸ vs. 7.89 × 10⁶). Furthermore, fourteen larva transcriptomes of E. grisescens were subsequently sequenced at seven time-points after ingestion of the two virus strains, yielding 410.72 Gb of raw reads. Differential gene-expression analysis shows that 595, 87, 27, 108, 0, 12, and 290 genes were up-regulated in EcobNPV-QF4 at 0, 2, 6, 12, 24, 36 h and 48 h post ingestion (hpi), while 744, 68, 152, 8, 1, 0, 225 were down-regulated. KEGG enrichment showed that when the virus first invades (eats the leaf-discs), EcobNPV-QF4 mainly affects pathways such as ribosome (p-value = 2.47 × 10⁻²⁹), and at 48 hpi EcobNPV-QF4, causes dramatic changes in the amino-acid-synthesis pathway and ribosome pathway (p-value = 6.94 × 10⁻¹³) in E. grisescens. Among these, thirteen key genes related to immunity were screened. The present study provides the first ever comprehensive analysis of transcriptional changes in E. grisescens after ingestion of the two strains of EcobNPV.

Tea anthracnose is a major disease of tea plant (Camellia sinensis) in all tea-growing regions in China, with the southern tea region being particularly susceptible. Over the past decade, more than 20 species belonging to Colletotrichum have been identified as causal agents of tea anthracnose besides its actual pathogen Discula theae-sinensis. Although researchers have increasingly regarded Colletotrichum spp. as the primary pathogens of tea anthracnose, there is still controversy over whether they cause tea anthracnose. By employing spore isolation methods, here we identified a fungal strain causing typical tea anthracnose disease but not belonging to the genus Colletotrichum. Upon spore isolation of tea anthracnose pathogens, various methods were employed to determine the pathogenicity of the isolate cultures. Eventually, a single isolate was obtained through the spore isolation method, which was subsequently identified as Sinodiscula theae-sinensis (Discula theae-sinensis) based on its morphological and molecular characteristics. The pathogenicity assay revealed that with either wound or non-wound inoculation the isolate exhibited typical lesions that were identical to those observed on the original diseased leaves. Furthermore, all the re-isolation strains obtained from the inoculated leaves was identical to the original strain. The pathogen of tea anthracnose was further confirmed as S. theae-sinensis by Koch's validation. Additionally, the symptomatic manifestations of the inoculation by S. theae-sinensis and Colletotrichum camelliae were also compared. The symptoms induced by C. camelliae are distinct from those observed in anthracnose. This study clarified the causal pathogen of tea anthracnose, thus a crucial foundation for the identification, prevention, and control of tea anthracnose.

Ectropis grisescens (Lepidoptera: Geometridae) is a destructive pest in tea plantations, leading to significant economic losses through defoliation. Existing control strategies, including chemical insecticides and biological agents, are often limited by environmental concerns, resistance, and variable efficacy. Recent evidence suggests that bacteria influence insect physiology and could be leveraged for pest management, but the postmortem microbial ecology of E. grisescens remains uncharacterized. In this study, we employed 16S rRNA sequencing to investigate temporal changes in the bacterial communities of E. grisescens cadavers at 0, 7, and 21 days following cryogenic mortality. Our results indicate a time-dependent decline in microbial diversity, while species richness initially increased before subsequent reduction. The dominant endosymbiont Wolbachia gradually diminished after host death, whereas Enterobacter remained abundant. Notably, non-dominant genera including Lysinibacillus and Sporosarcina exhibited a transient increase in abundance at day 7 before reverting to control levels by day 21. This study presents the first comprehensive analysis of postmortem microbial succession in a lepidopteran system, highlighting dynamic shifts in bacterial composition and offering potential avenues for microbiome-based pest management strategies.

Ectropis obliqua nucleopolyhedrovirus (EcobNPV) is an important biocontrol agent against Ectropis obliqua and E. grisescens. A previously isolated strain, EcobNPV-QF4, exhibits significantly higher virulence than the original strain EcobNPV-QV, yet the molecular basis for this difference remains unclear. Leaf-dipping bioassays demonstrated that EcobNPV-QF4 caused significantly higher larval mortality than EcobNPV-QV from 10 dpi onward, reaching 97.9% versus 33.8% at 16 dpi, and higher pupal mortality (100% versus 47.3%), confirming its superior virulence across both larval and pupal stages. To investigate the transcriptional dynamics underlying virulence variation, we performed a comparative time-course transcriptomic analysis of E. grisescens infected with either strain at 0, 2, 6, 12, 24, 36, and 48 h post-infection. The reliability of the RNA-seq data was validated by qRT-PCR for selected expressed genes. The results showed that, relative to EcobNPV-QV, the EcobNPV-QF4 strain exhibits a transcriptional strategy characterized by comprehensive and accelerated activation: the transcriptional initiation of its functional modules is globally advanced by approximately 6 h compared with EcobNPV-QV, and genes associated with midgut escape, virion assembly, and viral DNA replication are preferentially and coordinately expressed, resulting in a more synchronized transcriptional profile. Based on these findings, we hypothesize that the enhanced virulence of EcobNPV-QF4 is not attributable to a single factor but rather reflects a synergistic, multitiered acceleration of transcriptional progression that may compress the infection cycle and enhance viral dissemination efficiency. These findings provide critical insights into the molecular mechanisms that may underlie baculovirus virulence and provide a basis for future mechanistic studies.