The fungal family Botryosphaeriaceae, which includes genera such as Diplodia, Dothiorella, and Phaeobotryon, comprises species commonly associated with woody plants such as endophytes, pathogens, and saprophytes. The Xizang Autonomous Region of China, known for its rich forest resources, harbors significant fungal diversity. However, limited research has been conducted on plant-disease-associated fungi in this region. In this study, we employed morphological characteristics and molecular phylogenetic analyses of the internal transcribed spacer region of rDNA (ITS), the ribosomal large subunit (LSU), the translation elongation factor 1-alpha (tef1) gene, and the partial beta-tubulin (tub2) gene to identify fungal species. As a result, two new species, Diplodia salicicola sp. nov. and Phaeobotryon xizangense sp. nov., are proposed and described herein. Additionally, Di. corticola, Di. mutila, Do. acericola, Do. magnoliae, Do. vidmadera, Do. yunnana comb. nov., and Do. zanthoxyli are reported for the first time in Xizang. Our findings contribute to advancing the knowledge of fungal biodiversity in Xizang’s high-altitude ecosystems.

The Gram-negative bacterium Lonsdalea populi causes a lethal disease known as bark canker on Populus × euramericana in China and Europe. Typical symptoms of bark canker include an abundant white-colored fluid, which oozes from the infected tissues. The availability of the genomic sequence of the bacterium provided the necessary resource to launch genome-scale investigations into the mechanisms fundamental to pathogenesis. Functional analyses of a diverse group of genes encoding virulence factors and components of signaling pathways indicate that successful bark infection depends on specific responses by the pathogen to various stresses, including oxidative stress. Although physiology of resistance is well studied, the molecular processes underlying the defense responses and the genetic basis of resistance to L. populi and in other poplar species remain largely unknown. Control of the disease has relied on chemical measures. Due to the genetic amenability of Lonsdalea and poplar, this pathosystem will become an important model system to unravel molecular mechanisms of bacterial pathogenicity on woody plants. Increased understanding of pathogenesis and signaling in the interaction will facilitate the management of this kind of poplar canker.

Poplar, which is a dominant species in plant communities distributed in the northern hemisphere, is commonly used as a model plant in forestry studies. Poplar production can be inhibited by infections caused by bacteria, including Lonsdalea quercina subsp. populi, which is a gram-negative bacterium responsible for bark canker disease. However, the molecular basis of the pathogenesis remains uncharacterized. In this study, we annotated the two-component signal transduction systems (TCSs) encoded by the L. quercina subsp. populi N-5-1 genome and identified 18 putative histidine kinases and 24 response regulators. A large-scale mutational analysis revealed that 19 TCS genes regulated bacterial virulence against poplar trees. Additionally, the deletion of kdpE or overexpression of kdpD resulted in almost complete loss of bacterial virulence. We observed that kdpE and kdpD formed a bi-cistronic operon. KdpD exhibited autokinase activity and could bind to KdpE (K_d = 5.73 ± 0.64 μM). Furthermore, KdpE is an OmpR family response regulator. A chromatin immunoprecipitation sequencing analysis revealed that KdpE binds to an imperfect palindromic sequence within the promoters of 44 genes, including stress response genes Lqp0434, Lqp3037, and Lqp3270. A comprehensive analysis of TCS functions may help to characterize the regulation of poplar bark canker disease.

Poplar Cytospora canker, caused by Cytospora chrysosperma, is one of the most destructive and widespread poplar diseases worldwide, especially in northern China. However, our current understanding of its pathogenic mechanisms remains limited. Here, we show that trehalose biosynthetic genes, such as trehalose-6-phosphate synthase 1 ( CcTps1), trehalose-6-phosphate phosphatase ( CcTps2), and the regulatory subunit ( CcTps3), play important roles in the development and virulence of C. chrysosperma. The targeted deletion mutants showed reduced trehalose synthesis and were defective in hyphal growth and conidiation. Deletion of any of the three genes attenuated virulence in poplar twigs, and stronger poplar defense responses were triggered after inoculated by the mutants. Additionally, the mutants exhibited increased sensitivity to H₂O₂ and cell wall stressors. Taken together, the findings suggest that trehalose biosynthetic genes contribute to fungal development, stress responses, and full virulence in C. chrysosperma.

Bacteria employ two‐component systems (TCSs) to rapidly sense and respond to their surroundings often and during plant infection. Poplar canker caused by Lonsdalea populi is an emerging woody bacterial disease that leads to high mortality and poplar plantation losses in China. Nonetheless, the information about the underlying mechanism of pathogenesis remains scarce. Therefore, in this study, we reported the role of a TCS pair CpxA/CpxR in regulating virulence and stress responses in L. populi . The CpxA/R system is essential during infection, flagellum formation, and oxidative stress response. Specifically, the Cpx system affected flagellum formation by controlling the expression of flagellum‐related genes. CpxR, which was activated by phosphorylation in the presence of CpxA, participated in the transcriptional regulation of a chaperone sctU and the type III secretion system (T3SS)‐related genes, thereby influencing T3SS functions during L. populi infection. Phosphorylated CpxR directly manipulated the transcription of a membrane protein‐coding gene yccA and the deletion of yccA resulted in reduced virulence and increased sensitivity to H ₂ O ₂ . Furthermore, we mutated the conserved phosphorylation site of CpxR and found that CpxR ^D51A could no longer bind to the yccA promoter but could still bind to the sctU promoter. Together, our findings elucidate the roles of the Cpx system in regulating virulence and reactive oxygen species resistance and provide further evidence that the TCS is crucial during infection and stress response.

In recent years, Castanopsis carlesii, a keystone species in southern China’s forest ecosystems with high ecological and economic importance, has faced growing challenges from severe nut rot diseases. Gnomoniopsis (Gnomoniaceae, Diaporthales, Sordariomycetes, Ascomycota) represents a significant fungal genus that causes leaf spots, branch cankers, and fruit rot diseases. In this study, rotten nuts of C. carlesii were collected from Fujian Province, and fungal isolates were obtained using the tissue isolation method. Morphological characterization and molecular phylogenetic analysis, based on the combined sequences of the internal transcribed spacer region of rDNA (ITS), the translation elongation factor 1-alpha (tef1) gene, and the partial beta-tubulin (tub2) gene were used to identify these isolates. As a result, new isolates from diseased nuts of C. carlesii formed a distinct clade with Gnomoniopsis, and morphologically differentiated from the other species; hence, G. flava sp. nov. is proposed herein. Furthermore, pathogenicity tests involving three isolates of G. flava were conducted on healthy nuts of C. carlesii, confirming its role as the causal agent of this new plant disease. This study not only advances our understanding of species diversity within Gnomoniopsis but also lays the groundwork for developing control strategies for C. carlesii nut rot disease.