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Reactive oxygen species (ROS) play important roles in defence response of host plants versus pathogens. While generation and detoxification of ROS is well understood, how varied ability of different isolates of pathogens to overcome host ROS, or ROS contribution to a particular isolate's pathogenicity, remains largely unexplored. Here, we report that transcriptional regulation of the ROS pathway, in combination with the insulin pathway, increases the pathogenicity of invasive species Bursaphelenchus xylophilus. The results showed a positive correlation between fecundity and pathogenicity of different nematode isolates. The virulent isolates from introduced populations in Japan, China and Europe had significantly higher fecundity than native avirulent isolates from the USA. Increased expression of Mn-SOD and reduced expression of catalase/ GPX-5 and H 2 O 2 accumulation during invasion are associated with virulent strains. Additional H 2 O 2 could improve fecundity of Bu. xylophilus. Furthermore, depletion of Mn-SOD decreased fecundity and virulence of Bu. xylophilus, while the insulin pathway is significantly affected. Thus, we propose that destructive pathogenicity of Bu. xylophilus to pines is partly owing to upregulated fecundity modulated by the insulin pathway in association with the ROS pathway and further enhanced by H 2 O 2 oxidative stress. These findings provide a better understanding of pathogenic mechanisms in plant-pathogen interactions and adaptive evolution of invasive species. This article is part of the theme issue 'Biotic signalling sheds light on smart pest management'.

Objective: To investigate the role and mechanism of Nur77 in lung adenocarcinoma cell apoptosis and autophagy. Methods: Five cases of lung adenocarcinoma tissues which were confirmed by pathology and para-cancerous tissues were collected from the Affiliated Southwest Hospital of Youjiang Medical University for Nationalities (People's Hospital of Bai.se). The expression of Nur77 in lung adenocarcinoma and para-cancerous tissues was detected with immunofluorescence. Nur77-associated pathways were analyzed with bioinformatics analysis. Human bronchial epithelial (BEAS-2B) cells and human lung cancer (A549) cells were cultured in vitro and designated as BEAS-2B and A549 groups, respectively. In both groups, Nur77 mRNA expression was measured with RT-qPCR, the expression of Nur77, LC3, PI3K, p-PI3K, AKT, and p-AKT was assessed with western blotting, and the fluorescence intensity of Nur77 was determined with immunofluorescence. A549 cells were transfected with si-NC or si-Nur77, referred to as si-NC or si-Nur77 groups, respectively, and non-transfected cells serving as the control group (Con). Nur77 expression was analyzed with RT-qPCR, and the expression of Nur77, LC3, PI3K, p-PI3K, AKT, p-AKT, cas-pase-3, Bax, and Bcl-2 was examined using Western blot. Cell apoptosis was assessed by flow cytometry.Results: Lung adenocar-cinoma tissues exhibited higher levels of Nur77 protein expression compared to para-cancerous tissues. Bioinformatics analysis demonstrated a correlation between Nur77 and the PI3K/AKT pathway. The mRNA and protein expression of Nur77 (P<((.((((1) and the ratio of LC3 II /LC3 I, p-AKT/AKT (P<((.((5), and p-PI3K/PI3K (P<((.((1) were higher in the A549 group than in the BEAS-2B group. Compared with the si-NC group, the si-Nur77 group exhibited decreased Bcl-2 expression (P<((.((5), increased Caspase-3 and Bax expression (P<((.((1), and elevated LC3 I /LC3 I ratio (P<((.((1), along with reduced p-AKT/ AKT (P<((.((5) and p-PI3K/PI3K (P<((.((1) ratios and significantly enhanced apoptosis (P<((.((5).Conclusion: Nur77 down-regulation accelerates autophagy and apoptosis in lung cancer cells, which may be achieved by the inhibition of the PI3K/AKT pathway. [ABSTRACT FROM AUTHOR]

Background: Autophagy is an evolutionary conserved important process for the turnover of intracellular substances in eukaryotes and is closely related to the development of atrial fibrillation (AF). The aim of this study is to identify and validate potential autophagy-related genes (ARGs) of AF through bioinformatics analysis and experimental validation. Methods: We downloaded two data sets from the Gene Expression Omnibus (GEO) database, GSE14975 and GSE31821. After merging the data of the two microarrays, adjusting the batch effect, and integrating the differentially expressed genes (DEGs) with ARGs to obtain differentially expressed autophagy-related genes (DEARGs). Functional and pathway enrichment analyses were carried out based on Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG). Use the STRING database to construct a protein–protein interaction (PPI) network. Finally, mRNA expression levels of DEARGs were validated in right atrial tissue samples from AF patients and non-AF controls by qRT-PCR. Results: Through bioinformatics analysis, we finally identified 11 DEARGs (CDKN1A, CXCR4, DIRAS3, HSP90AB1, ITGA3, PRKCD, TP53INP2, DAPK2, IFNG, PTK6, and TNFSF10) in AF using [log2 (fold change)] > 0.5 and P < 0.05. In the pathway enrichment analysis, the most significantly enriched pathway was the autophagy pathway. The results of validation showed that the expression levels of CXCR4, DAPK2, and TNFSF10 corroborating with our computational findings, and the results were statistically significant (P< 0.05). Conclusion: Our study demonstrates that these 11 potential crucial ARGs, especially CXCR4, DAPK2, and TNFSF10, may be potential biomarkers and therapeutic targets in AF, which will help the personalized treatment of AF patients. [ABSTRACT FROM AUTHOR]

This study aimed to explore the influence of Tryptophanyl-tRNA synthetase (WARS) expression on the proliferation and migration of uveal melanoma (UM) cells, and the potential mechanisms. Bioinformatics analysis based on Gene Expression Omnibus (GEO) database showed that WARS expression in metastatic cancer was significantly higher than that in no-metastatic group. Kaplan-Meier analysis based on The Cancer Genome Atlas (TCGA) database showed that high WARS expression was associated with lower survival. Biological function experiments showed that overexpression of WARS in OCM-1A cells can promote cell proliferation, migration, and invasion, whereas knockdown of WARS in C918 cells showed the opposite effect. Finally, we observed that the up-regulation of WARS induced the activation of phosphatidylinositol 3-kinase/AKT (PI3K/AKT) signaling, whilst depletion of WARS resulted in opponent outcomes. Taken together, our results illustrated that WARS was overexpressed in UM cells and contributed to the viability and motility of UM cells via modulating PI3K/AKT signaling pathway. Knockdown of WARS suppresses UM cell proliferation, migration, and invasion [ABSTRACT FROM AUTHOR]

Graphical abstract Highlights • A ratiometric fluorescent sensor has been applied for detecting UDG. • This method can selectively detect UDG with a low detection limit. • The system is label-free, simple, fast, and economic. • The kinetic parameter and the UDG inhibition effect have been evaluated. Abstract As one of critical base excision repair enzymes, uracil-DNA glycosylase (UDG) can specifically repair uracil-induced DNA damage to maintain the genome integrity of organisms. Moreover, abnormal expression of UDG is related to various cancers and other serious diseases. Therefore, it is essential to accurately and sensitively monitor UDG activity. In this work, a ratiometric fluorescence method using poly-(thymine) DNA template copper nanoclusters (Cu NCs) and 4′,6-diamidino-2-phenylindole (DAPI) as the output signals is developed for simple, selective, and sensitive detection of UDG. A double-stranded DNA (dsDNA) consisting of a uracil-containing single chain and a trigger sequence is designed as a substrate dsDNA. Meanwhile, another dsDNA comprising 30 pairs of A-T bases ((AT) 30 dsDNA) is designed to be partially complementary to the trigger chain. The (AT) 30 dsDNA itself has no blunt or recessed 3′ end and cannot be cut by exonuclease III (Exo III). With the Exo III-assisted amplification, adding UDG results in the success synthesis of red-emissive Cu NCs, while the dsDNAs in the system are hydrolyzed and the fluorescence signal of DAPI is weak. In contrast, without addition of UDG, the fluorescence intensity of Cu NCs is low, while the DAPI emits significantly enhanced fluorescence signal. The proposed method presents a detection limit of 5.0 × 10−5 U mL−1 and can be applied to the HeLa cell lysate sample with satisfactory results. Additionally, the kinetic parameter is studied and the UDG inhibition effect is evaluated. In summary, this work provides a potential platform for DNA repair enzyme-related analysis and clinical diagnosis. [ABSTRACT FROM AUTHOR]

FUS1 is a tumor suppressor gene that has been found to be frequently lost in a variety of solid tumors. In this study, we aimed to investigate the expression status of the FUS1 gene in acute myeloid leukemia (AML), as well as its clinical significance. We further explored the correlation between the expression of FUS1 and miR-378 in AML. We detected expression of the FUS1 transcript in bone marrow mononuclear cells from 23 controls and 158 newly diagnosed AML patients by real-time quantitative polymerase chain reaction. Downregulated FUS1 expression was found in 139 out of 158 (87.97%) AML cases; this rate was significantly lower than that in all 23 controls (p = 0.012). Receiver operating characteristic curve analysis revealed that the FUS1 transcript level could discriminate AML patients from controls effectively (area under the ROC curve = 0.663). Kaplan-Meier analysis demonstrated that non-M3-AML patients with a low FUS1 expression had a shorter overall survival (p = 0.049) and leukemia-free survival (p = 0.051) than those with a high FUS1 expression. Furthermore, we studied the correlation between the expression of FUS1 and miR-378 in 53 newly diagnosed AML patients. We found that the correlation coefficient was –0.346, which showed that FUS1 and miR-378 were negatively correlated in AML patients (p = 0.011). These results indicate that the low expression of FUS1 is a common molecular event in AML. [ABSTRACT FROM AUTHOR]

The cytochrome P450 enzymes encoded by the Halloween genes - spook ( spo), phantom ( phm), disembodied ( dib), shadow ( sad), and shade ( shd) - catalyze a series of hydroxylation steps resulting in the active molting hormone 20-hydroxyecdysone (20E). This study investigated 20E and ecdysone titers and the expression profile of Halloween genes and ecdysone receptor ( EcR) during larval, pupal, and adult stages in seabuckthorn carpenterworm, Holcocerus hippophaecolus Hua ( Lepidoptera: Cossidae). Hh-spo, Hh-phm, Hh-dib, and Hh-sad showed predominant expression in the prothoracic gland at the larval stage, whereas Hh-shd and Hh-EcR were significantly expressed in the fat body. The mRNA levels of Hh-spo, Hh-phm, Hh-dib, Hh-shd, Hh-sad, and Hh-EcR were lowest from late October to middle April, when the insects were in overwintering dormancy, but began to increase from May each year, when the insects were terminating quiescence. Concomitant with the changes in these genes, 20E and ecdysone titers gradually increased during the 4-year life cycle of H. hippophaecolus. These data indicate that the seasonal expressions of Hh-spo, Hh-phm, Hh-shd, and Hh-EcR play crucial roles in quiescence of the overwintering period, and are responsible for the long larval phase and the exact timing and amplitude of the ecdysteroid titer required for the coordination of growth and development in H. hippophaecolus. [ABSTRACT FROM AUTHOR]

In this study, we report the c DNA cloning and sequence determination of H h- JHAMT from the seabuckthorn carpenterworm, H olcocerus hippophaecolus, by using rapid amplification of c DNA ends. The full-length c DNA of putative H h- JHAMT was 1659 bp and contained a highly conserved Motif I, SAM motif I, which showed that Hh- JHAMT like enzyme was a member of SAM-dependent MTases. Moreover, putative Hh- JHAMT had high homology to the other members of the JHAMT peptide family: 59% with S podoptera litura, 54% with B ombyx mori and 54% with H elicoverpa armigera. Multiple alignments and phylogenetic analysis revealed that H h- JHAMT was closely related to JHAMT from Lepidoptera. Real-time quantitative PCR experiments showed that H h- JHAMT m RNA expression was highest in the corpora allata ( CA) complex, and was also detected at high levels during earlier larval and adult stages. The JHAMT m RNA level gradually declined during larval development, and the lowest amount of expression was observed in the pupal stage, while it increased to a higher level during adult stages. The pattern of H h- JHAMT expression was similar to the mode of JH biosynthesis. These results provided information concerning molecular characteristics of H h- JHAMT, whose expression profile suggests that the H h- JHAMT gene might be changed with larval development, metamorphosis and adult reproduction of the H . hippophaecolus. [ABSTRACT FROM AUTHOR]