Aug 2026· Molecular Horticulture· Vol 6· 0 citations· 79 references
Medicine
TL;DR
The first spatiotemporal atlas of RKN-infected tomato roots is established and genes associated with giant cell formation are identified, laying a foundation for further research on the establishment of RKN feeding sites, providing novel insights into RKN pathogenic mechanisms, and potentially guiding novel control strategies.
Abstract
Root-knot nematodes (RKNs; Meloidogyne spp.) are destructive agricultural parasites, but although giant cell formation is required for establishing parasitism, the mechanism of action has not been fully elucidated. Spatial transcriptomics enables precise spatiotemporal analyses of gene expression, facilitating studies of cell heterogeneity. We performed spatial transcriptomic sequencing on Moneymaker tomato root galls caused by M. incognita infection at 3, 5, and 7 days post-inoculation to investigate RKN-induced giant cell formation. Five major cell types were identified; of these, giant cell clusters were localized predominantly in the xylem, stele, and meristem. Four novel giant cell-specific marker genes were confirmed through RNA in situ hybridization. Pseudotime analysis revealed genes potentially associated with giant cell formation. Virus-induced gene silencing (VIGS) of four genes encoding a cyclin-dependent kinase, two cell division cycle-associated proteins, and a MYB3R-1-like transcription factor—hypothesized to maintain the cell cycle or gene expression during mitosis—resulted in significantly fewer galls and significantly smaller giant cells. This study established the first spatiotemporal atlas of RKN-infected tomato roots and identified genes associated with giant cell formation, laying a foundation for further research on the establishment of RKN feeding sites, providing novel insights into RKN pathogenic mechanisms, and potentially guiding novel control strategies.
Molecular insights of host–pathogen interactions offer decoding of sustainable strategies for developing resilient cultivars and effective management of false smut disease, highlighting stage-specific pathogenicity genes and rice defense mechanisms that control false smut disease development.
P. Parmar, B. Bashyal· Plant Molecular Biology· 0 citations
A single-cell leaf transcriptomic atlas of Vitis vinifera during early E. necator infection revealed cell-type-specific temporal dynamics of defense-related gene expression, with epidermal cells showing delayed transcriptional activation relative to other cell types.
Yasheng Xi, Kai Wu, Bofan Liu et al.· Horticulturae· 0 citations
Root-knot nematodes (
Meloidogyne
spp.) are devastating plant pathogens that cause substantial economic losses worldwide. This study uses RNA-seq to profile the transcriptomic responses of
M. incognita
to the culture supernatant of
Streptomyces
sp. TR27, a strain previously shown to induce 67.6% calibrated mortality against
M. incognita
second-stage juveniles at 48 h. At 12 h post treatment, 231 differentially expressed genes (DEG) were identified, including 114 up-regulated and 117 down-regulated genes. Down-regulated genes were enriched in the pathways related to lysosome (lysosomal ATPase, acid hydrolase, and membrane protein) and steroid hormone metabolism. Gene set enrichment analysis (GSEA) further revealed the transcriptional suppression of oxidative phosphorylation (Complexes I-V) and ribosomal protein coding genes at 12 h post treatment. These findings suggest that the
Streptomyces
sp. TR27 supernatant is associated with multi-pathway transcriptional perturbations, including lysosomal homeostasis dysregulation, steroid hormone metabolism impairment, and potential inhibition of mitochondrial energy production and protein translation. This transcriptional signature provides candidate cellular targets and a hypothetical framework for developing actinobacteria-derived biocontrol agents, pending functional validation of direct compound-target interactions.
Ling Qu, R. Han, Z. Rao et al.· Nematology· 0 citations
Auxin Response Factors (ARFs) are of vital importance in plant growth and vascular development. Class A ARFs are the core auxin-driven drivers of embryogenesis, vascular pattern development, (pro)cambial stem cell initiation and xylem cell fate specification, while class B ARFs may attenuate or fine-tune auxin-mediated development. The potential roles of class C ARFs in vascular development and xylogenesis, however, remain largely unexplored. In this study, we identified Eucalyptus grandis ARF10 (EgrARF10) as a potential regulator of secondary cell wall (SCW) development. We show that EgrARF10 is nucleus-localised and strongly associated with SCW biosynthetic genes and transcription factors across co-expression and multi-omic networks. Mining of published spatial and single cell transcriptomic data revealed preferential expression of EgrARF10 in vessel and fusiform organizer cells of secondary xylem tissue, while EgrARF10 orthologs in other species exhibit diverse cell type-specific expression ranging from root cap vascular and metaxylem to cork cambium. Heterologous overexpression of EgrARF10 in hybrid poplar did not alter overall growth or morphology but resulted in a significant reduction in stem lignification, accompanied by relative increases in D-glucose, D-xylose and D-mannose, indicating altered SCW composition. While the molecular mechanism by which EgrARF10 acts remains unknown, these findings provide the first evidence for the role of a class C ARF in xylem SCW biology.
Ipeleng Makhura, R. Ployet, A. Myburg et al.· Tree Genetics & Genomes· 0 citations
Bacterial wilt (BW), caused by Ralstonia solanacearum, is a highly destructive disease in tomato, and resistance to BW is attenuated under high temperature (HT). However, limited information is available with respect to the molecular basis of tomato-R. solanacearum interactions under HT. Here, we conducted transcriptomic analysis on the root-stem junction tissues of tomatoes exhibiting varying levels of BW resistance at 0, 12, 24, and 48hours post-inoculation (hpi) with R. solanacearum under 33 °C. Weighted gene co-expression network analysis (WGCNA) revealed two modules containing key genes that participated in disease resistance under HT. A total of 91 core genes were identified as potentially coordinating immune signaling and metabolic homeostasis during the interactions between tomato and R. solanacearum. Ultimately, we identified HsfA9 as a key transcription factor potentially involved in bacterial wilt resistance under HT. Our findings provide a valuable resource for elucidating the molecular mechanism underlying of R. solanacearum-tomato interactions under HT, thereby facilitating the development of effective strategies in disease control and prevention.
Jing Li, Wenhao Zhong, Qiaoping Mo et al.· Plant Science· 0 citations
Rhizoctonia solani AGI-IA is a polyphagous necrotrophic fungal pathogen that causes sheath blight disease in rice. Efforts are being made to identify pathogenicity-associated genes in R. solani and modulate them to develop a disease control strategy. Here, we investigate the roles of some predicted pathogenicity-associated genes of R. solani that have previously been reported to be upregulated during infection in rice. The tobacco rattle virus-based host-induced gene silencing of the selected pathogenicity-associated genes revealed that silencing of Rs_MEP1, a zinc-containing Peptidase_M43 domain-metalloprotease, severely compromises R. solani infection in tomato. Moreover, double-stranded RNA-mediated silencing of Rs_MEP1 prevented R. solani infection in rice. The signal sequence trap assay indicated the secretory nature of Rs_MEP1, while the reporter assay suggested its localization in the plant apoplast. Notably, agrobacterium-mediated transient overexpression of Rs_MEP1 induces necrotic cell death responses in plants. We provide evidence that Rs_MEP1 interacts with GH19 family of rice chitinases and potentially modulates their functions. Overall, our study emphasizes that Rs_MEP1 facilitates R. solani in promoting necrotic responses and targets rice GH19 chitinases to impart disease susceptibility in plants.