Background: Numerous studies have highlighted that long non-coding RNAs (lncRNAs) can bind to microRNA (miRNA) sites as competing endogenous RNAs (ceRNAs), thereby affecting and regulating the expression of mRNAs and target genes. These lncRNA-associated ceRNAs have been theorized to play a significant role in cancer initiation and progression. However, the roles and functions of the lncRNA-miRNA-mRNA ceRNA network in squamous cell carcinoma of the tongue (SCCT) are still unclear. Methods: The miRNA, mRNA and lncRNA expression profiles from 138 patients with SCCT were downloaded from The Cancer Genome Atlas database. We identified the differential expression of miRNAs, mRNAs, and lncRNAs using the limma package of R software. We used the clusterProfiler package for GO and KEGG pathway annotations. The survival package was used to estimate survival analysis according to the Kaplan-Meier curve. Finally, the GDCRNATools package was used to construct the lncRNA-miRNA-mRNA ceRNA network.

Fusarium oxysporum f. sp. cubense (Foc) is the causal pathogen of Fusarium wilt of banana. To understand infection of banana roots by Foc race 4, we developed a green fluorescent protein (GFP)-tagged transformant and studied pathogenesis using fluorescence microscopy and confocal laser scanning microscopy. The transformation was efficient, and GFP expression was stable for at least six subcultures with fluorescence clearly visible in both hyphae and spores. The transformed Foc isolate also retained its pathogenicity and growth pattern, which was similar to that of the wild type. The study showed that: (i) Foc race 4 was capable of invading the epidermal cells of banana roots directly; (ii) potential invasion sites include epidermal cells of root caps and elongation zone, and natural wounds in the lateral root base; (iii) in banana roots, fungal hyphae were able to penetrate cell walls directly to grow inside and outside cells; and (iv) fungal spores were produced in the root system and rhizome. To better understand the interaction between Foc race 4 and bananas, nine banana cultivars were inoculated with the GFP-transformed pathogen. Root exudates from these cultivars were collected and their effect on conidia of the GFP-tagged Foc race 4 was determined. Our results showed that roots of the Foc race 4-susceptible banana plants were well colonized with the pathogen, but not those of the Foc race 4-resistant cultivars. Root exudates from highly resistant cultivars inhibited the germination and growth of the Fusarium wilt pathogen; those of moderately resistant cultivars reduced spore germination and hyphal growth, whereas the susceptible cultivars did not affect fungal germination and growth. The results of this work demonstrated that GFP-tagged Foc race 4 isolates are an effective tool to study plant-fungus interactions that could potentially be used for evaluating resistance in banana to Foc race 4 by means of root colonization studies. Banana root exudates could potentially also be used to identify cultivars in the Chinese Banana Germplasm Collection with resistance to the Fusarium wilt pathogen.

Summary P0 protein of some polerovirus members can target ARGONAUTE 1 ( AGO 1) to suppress RNA silencing. Although P0 harbors an F‐box‐like motif reported to be essential for interaction with S phase kinase‐associated protein 1 ( SKP 1) and RNA silencing suppression, it is the autophagy pathway that was shown to contribute to AGO 1 degradation. Therefore, the role of P0– SKP 1 interaction in silencing suppression remains unclear. We conducted global mutagenesis and comparative functional analysis of P0 encoded by Brassica yellows virus (BrYV) (P0 Br ). We found that several residues within P0 Br are required for local and systemic silencing suppression activities. Remarkably, the F‐box‐like motif mutant of P0 Br , which failed to interact with SKP 1, is destabilized in vivo . Both the 26S proteasome system and autophagy pathway play a role in destabilization of the mutant protein. Furthermore, silencing of a Nicotiana benthamiana SKP 1 ortholog leads to the destabilization of P0 Br . Genetic analyses indicated that the P0 Br – SKP 1 interaction is not directly required for silencing suppression activity of P0 Br , but it facilitates stability of P0 Br to ensure efficient RNA silencing suppression. Consistent with these findings, efficient systemic infection of Br YV requires P0 Br . Our results reveal a novel strategy used by BrYV for facilitating viral suppressors of RNA silencing stability against degradation by plant cells.

Summary Ascochyta blight ( AB ) is one of the major biotic stresses known to limit the chickpea production worldwide. To dissect the complex mechanisms of AB resistance in chickpea, three approaches, namely, transcriptome, small RNA and degradome sequencing were used. The transcriptome sequencing of 20 samples including two resistant genotypes, two susceptible genotypes and one introgression line under control and stress conditions at two time points (3rd and 7th day post inoculation) identified a total of 6767 differentially expressed genes ( DEG s). These DEG s were mainly related to pathogenesis‐related proteins, disease resistance genes like NBS ‐ LRR , cell wall biosynthesis and various secondary metabolite synthesis genes. The small RNA sequencing of the samples resulted in the identification of 651 mi RNA s which included 478 known and 173 novel mi RNA s. A total of 297 mi RNA s were differentially expressed between different genotypes, conditions and time points. Using degradome sequencing and in silico approaches, 2131 targets were predicted for 629 mi RNA s. The combined analysis of both small RNA and transcriptome datasets identified 12 mi RNA ‐ mRNA interaction pairs that exhibited contrasting expression in resistant and susceptible genotypes and also, a subset of genes that might be post‐transcriptionally silenced during AB infection. The comprehensive integrated analysis in the study provides better insights into the transcriptome dynamics and regulatory network components associated with AB stress in chickpea and, also offers candidate genes for chickpea improvement.