He Li

Bamboo is a rapidly renewable lignocellulosic resource widely used in construction, composites, and bio-based materials. However, its practical applications are often limited by high hygroscopicity, biological degradation, and dimensional instability under humid conditions. This review synthesizes current research on bamboo structure, microbial interactions, and material modification strategies to better understand how bamboo-associated microbiomes influence both deterioration and potential material enhancement. We summarize conventional chemical and thermal modification approaches that improve hydrophobicity, durability, and mechanical stability while also discussing their technical limitations. Emerging studies on bamboo-associated microbial communities reveal complex interactions between fungi, bacteria, and lignocellulosic substrates, including enzymatic degradation, nutrient cycling, and potential bioprotective functions. Advances in multi-omics technologies have further provided insights into the functional gene pools and metabolic pathways involved in bamboo–microbe interactions. Recent conceptual developments in microbiome engineering and engineered living materials (ELMs) suggest possible future directions for integrating microbial functionality into bamboo-based materials. However, direct experimental evidence for microbial enhancement of bamboo structural performance remains limited. Future interdisciplinary research integrating material science, microbial ecology, and synthetic biology will be essential to evaluate the feasibility and safety of such biohybrid systems.

Colletotrichum fructicola is the predominant pathogenic agent responsible for anthracnose in Camellia oleifera. RGS2 is a GTPase-activating protein that negatively regulates G-protein signaling by inactivating Gα subunits. In this study, we characterized the ortholog of CfRGS2 in C. fructicola to explore its pathogenic roles. Seven canonical RGS genes were identified through BLASTp and keyword searches. Conserved domains and subcellular localizations were predicted bioinformatically. A CfRGS2 knockout mutant was generated via overlap-PCR and PEG-mediated transformation, verified by PCR, and complemented by reintroducing the wild-type gene. Phenotypic characterization showed that the growth rates of mutants ΔCfrgs2-1 and ΔCfrgs2-2 were significantly reduced compared with those of the wild-type and complemented strains. On both PDA and minimal medium, the mutant strains exhibited significantly smaller colony diameters of 3.3 cm and 3.1 cm, respectively, relative to the control strains. Moreover, conidiation in the mutants was only 4% of that in the wild-type and complemented strains, and appressorium formation was reduced to 6%, with statistical analyses confirming high significance. Under cell wall stress induced by 400 μg/mL Congo red, the growth inhibition rates of ΔCfrgs2-1 and ΔCfrgs2-2 were 44% and 48%, respectively, significantly higher than those of the control strains. Pathogenicity assays demonstrated that the mutants failed to induce lesions on unwounded leaves and caused 47% and 30% smaller lesion areas on wounded apple fruits, respectively. In summary, C. fructicola possesses seven canonical RGS proteins that regulate G-protein signaling, among which CfRgs2 is implicated in growth, conidiation, the stress response to cell wall perturbation, and virulence.

Camellia oleifera is an important economic woody oil plant in many Asian countries, and the anthracnose caused by Colletotrichum fructicola is prevalent in its cultivation regions, causing significant losses annually. We previously found that CfGcn5-mediated H3 acetylation governs virulence of C. fructicola. To further elucidate the regulatory mechanism of CfGcn5, we carried out mass spectrometry analysis for CfGcn5-interacting proteins and identified CfAda3 protein for functional analysis. We found that CfAda3 was mainly localized in nucleus and cooperated with CfGcn5 to acetylate H3K18 for global gene transcription. Targeted gene deletion revealed that CfAda3 is involved in growth and conidiation. Similar to ΔCfgcn5 mutant, the ΔCfada3 mutant is defective in conidial germination, appressorial formation, autophagy, and in the response to environmental stresses. These combined effects result in its non-virulence on C. oleifera. In addition, we provided evidence showing that both NLS region and ADA3 domain are required for the localization and function of CfAda3. Moreover, we indicated that the interaction with CfGcn5 is essential but not sufficient for the normal localization and full function of CfAda3. Taken together, our studies not only illustrate the prominent roles of CfAda3 in growth, development, and virulence but also highlight how CfAda3 functions together with CfGcn5 in C. fructicola.

Camellia oleifera, known as the tea-oil tree, is a multifunctional woody oil crop renowned as the "Oriental olive". During 2023-2024, in Jishou City (28°17'N, 109°29'E), Hunan Province, China, 100% of tea-oil tree plants and over 40% of the leaves on each plant exhibited typical anthracnose symptoms. Initially, infected areas displayed yellowish regions. As the disease progressed, brown necrotic lesions with dark brown margin and tiny, dark dots emerged. Diseased leaves were collected, rinsed under running water, and cut into small pieces (5×5 mm) from the edges of the lesions. These pieces were surface-disinfected with 70% ethanol for 30 seconds, followed by 2% NaOCl for 2 minutes, and then rinsed three times with sterile water. The disinfected samples were placed on potato dextrose agar (PDA supplemented with 100 mg/L streptomycin sulphate) and incubated at 28℃ in the dark. After 3 days, mycelia plugs from the infected tissues were transferred to fresh PDA for subculturing. Twenty isolates displaying two distinct morphological types were obtained. One representative strain from each morphology type (designated as LinC-A and LinC-B) was randomly selected for further study. On PDA, LinC-A developed cottony, raised colonies that were initially white on the obverse and yellowish on the reverse. Over time, the colonies turned reddish to deep red at the center, with red pigmentation on the reverse side. LinC-B colonies were initially white to yellowish on the obverse and deep yellow on the reverse, later turning yellowish to deep pink on both sides, producing pink pigmentation. Conidia of both strains were single-celled, hyaline, fusiform with acute ends, and smooth-walled. The average conidial size of LinC-A was 12.9 ± 1.6 × 5.8 ± 1.6 μm (n=100), while that of LinC-B was 15.6 ± 2.2 × 6.4 ± 0.7 μm (n=100). Additionally, brown setae were observed surrounding dark brown acervulus. For molecular identification, the ITS region and four other genes (GAPDH, CHS-1, ACT, and TUB2), were amplified and sequenced. The sequences were deposited in GenBank (ITS: PQ825943, PQ825944; GAPDH: PQ827013, PQ827014; CHS-1: PQ827015, PQ827016; ACT: PQ827017, PQ827018; TUB2: PQ827019, PQ827020). Phylogenetic analysis based on the combined ITS, GAPDH, CHS-1, ACT, and TUB2 sequences confirmed that both LinC-A and LinC-B clustered with C. fioriniae strains, consistent with the homology search results. Therefore, based on morphological and molecular evidence, LinC-A and LinC-B were identified as C. fioriniae. To fulfill Koch's postulates, pathogenicity tests were conducted using conidial suspensions of 1×106 conidia/mL on tea-oil tree plants. A 50 μL aliquot of the suspension conidia was applied on each leaf, while control leaves were inoculated with an equivalent volume of sterile distilled water. Inoculated plants were maintained in humid chambers at 28℃ under a 12-hour light-dark cycle. Six leaves were used for each of the three replicates. After five days, all inoculated leaves developed anthracnose symptoms, whereas control leaves remained asymptomatic. C. fioriniae was re-isolated and re-identified from the inoculated leaves, confirming its pathogenicity. Previous studies have reported C. fructicolca, C. gloeosporioides, C. camelliae, C. aeschynomenes, C. karstii, C. siamense, C. kahawae, and C. horii as pathogens of tea-oil tree in China (Li et al., 2016, 2017, 2019; Wei et al., 2023). This is the first report of C. fioriniae causing anthracnose on tea-oil tree plants.

During interactions, pathogenic fungi are subjected to endoplasmic reticulum (ER) stress from the host plants, resulting in the activation of the unfolded protein response (UPR) pathway. We identified the bZIP transcription factor CfHac1 in C. fructicola, which is a pathogenic organism implicated in a variety of plant diseases, and we found it to be crucial for the ER stress response and pathogenicity. However, the role of CfHac1 in regulating the degradation of ER-associated misfolded proteins remains unclear. In this study, we discovered that the CfHAC1 gene regulates conidial production, appressorium formation, response to ER stress, and pathogenicity through unconventional splicing. Further research revealed that the CfHAC1 gene also affects the ubiquitination of ER-associated misfolded proteins and mediates their degradation. We further identified two ubiquitin ligase genes, CfHRD1 and CfHRD3, that exhibit significant down-regulation in the ΔCfhac1 mutant strain. Subsequent investigations revealed that the CfHAC1 gene affects CfHRD1 and CfHRD3 expression through unconventional splicing, with both genes managing the degradation of ER-associated misfolded proteins via ubiquitination and influencing C. fructicola pathogenicity. Taken together, our results reveal a mechanism by which the transcription factor CfHac1 affects the expression of the ubiquitin ligase genes CfHRD1 and CfHRD3, leading to the ubiquitination and degradation of ER-associated misfolded proteins and pathogenicity. This provides a theoretical basis for the development of novel agents targeting key genes within this pathway.

Anthracnose, caused by Colletotrichum species, induces significant economic damages to crop plants annually, especially for Camellia oleifera. During infection, the counter-defence mechanisms of plant pathogens against ROS-mediated resistance, however, remain poorly understood. By employing Weighted Gene Co-expression Network Analysis (WGCNA), we identified ACTIVATOR PROTEIN-1 (AP-1), a bZIP transcription factor, as significant to infection. And deletion of CfAP1 inhibited aerial hyphae formation and growth under oxidative stress. Furthermore, RNA-seq analysis post H₂O₂ treatment revealed 33 significantly down-regulated genes in the AP-1 deficient strain, including A12032, a dual specificity phosphatase (DSP) homologous to MSG5 from Saccharomyces cerevisiae. This ΔCfmsg5 strain showed enhanced oxidative tolerance, reduced ROS scavenging, and negative regulation of the CWI MAPK cascade under oxygen stress, suggesting its involvement in oxidative signal transduction. Importantly, we provide evidence that CfMsg5 regulates growth, endoplasmic reticulum stress, and several unfolded protein response genes upregulated in ΔCfmsg5. Collectively, this study identified core components during C. fructicola infection and highlights a potential regulatory module involving CfAp1 and CfMsg5 in response to host ROS bursts. It provides new insights into fungal infection mechanisms and potential targets like CfAP1 and CfMSG5 for managing anthracnose diseases.