Biology subjects

wang, Z.

Publications and source records attributed to wang, Z..

3 recordsLinked to original sources

bioRxiv2025

Unravelling termite evolution with 47 high-resolution genome assemblies

Termites are a lineage of social cockroaches abundant in tropical ecosystems where they are key decomposers of organic matter from wood to soil. Despite their ecological significance, only a handful of reference-quality termite genomes have been sequenced, which is insufficient to unravel the genetic mechanisms that have contributed to their ecological success. Here, we performed sequencing and hybrid assembly of 45 taxonomically and ecologically diverse termites and two cockroaches, resulting in haplotype-merged genome assemblies of 47 species, 22 of which were near-chromosome level. Next, we examined the link between termite dietary evolution and major genomic events. We found that Termitidae, which include [~]80% of described termite species, have larger genomes with more genes and a higher proportion of transposons than other termites. Our analyses identified a gene number expansion early in the evolution of Termitidae, including an expansion of the repertoire of CAZymes, the genes involved in lignocellulose degradation. Notably, this expansion of genomes and gene repertoires coincided with the origin of soil-feeding in Termitidae and remained unchanged in lineages that secondarily reverted to a wood-based diet. Overall, our sequencing effort multiplied the number of available termite genomes by six and provided unprecedented insights into the genome evolution of the most ancient lineage of social insects.

genomics↗

bioRxiv2023

Predication of the Post Mining Land Use Based on Random Forest and DBSCAN

Mine reclamation is one of the most important stages of the mining activities in line with the basic principles of sustainable development. In this study, different post-mining land uses are evaluated in the Hongliulin mining area, which is located in Shen mu country of China. 145 soil samples were collected in the May,2021 by using the soil auger, and the sampling depths were 0-20 cm. The sampling points contains 45 to be reclaimed samples and 100 existing classification land use types. 14 environmental factors including soil organic matter (SOM), total nitrogen (TN) and other soil nutrients and terrain factors were extracted and calculated based on laboratory test and digital elevation map. Meanwhile, random forest classier was utilized to determine the post-mining land use based on GINI index and 14 environmental factors by using 100 existing classification land use types. 82 of 100 samples were utilized to build the model and the other 18 samples were utilized to validate the accuracy of the classification model. Density-Based Spatial Clustering of Applications with Noise (DBSCAN) techniques were utilized to determine the specific land use types in cropland, shrub and grassland. the random forest classier showed a great prediction capability, with only 1 miss-classified sample in the validation data-set, the accuracy of the classification model was 95%. Among the 45 samples to be reclaimed, 15 samples were classified into cropland, 23 samples were classified into shrub and grassland, 5 samples were classified into arbor land, 2 samples were classified into solar station. By using DBSCAN, the 58 samples classified into cropland in terms of the post-mining were separated into cluster 1 and 2, cluster 1 comprises 24 samples while cluster 2 comprises 34 samples. Among the 61 samples classified into shrubland and grassland, Cluster -1 comprises 24 samples and Cluster 0 comprise 22 samples. The results could provide technological support for land reclamation determination. The content of TN of C1 is 5 times more than C2 and 4 times more than C3. Also, the K valve of C1 column is maximum and over 0.4, which means the soil particle is relatively smaller and the soil texture of it is sandy loam. The TWI of C1 is minimum, in consideration of a positive valve of profile curvature and a negative valve of plan curvature. In terms of the 45 to be reclaimed samples, 15 samples were classified into C1, 23 samples were classified into C2, 5 samples were classified into C3, 2 samples were classified into C4. The valve of K and content of soil nutrients of the samples classified to be C1 column(C1-C) is maximum. Simultaneously, the slope steepness({degrees}) is below 5{degrees} and is perceived as gentle surface. Cluster 1 comprises 24 samples and the average content of TN, AP and SOM is 0.566g/kg, 11.93mg/kg and 19.975g/kg respectively, while Cluster 2 comprises 34 samples and the average content of TN, AP and SOM is 0.304g/kg, 3.12mg/kg and 8.36g/kg respectively. The result may contribute to the land use planning and idle land utilization strategy.

ecology↗

bioRxiv2020

Extracellular histones stimulate collagen expression and potentially promote liver fibrogenesis via TLR4-MyD88 signalling pathway

BACKGROUNDLiver fibrosis progressing to liver cirrhosis and hepatic carcinoma is very common and causes more than one million deaths annually. Fibrosis develops from recurrent liver injury but the molecular mechanisms are not fully understood. Recently, the Toll-like receptor (TLR) 4-MyD88 signalling pathway has been reported to contribute to fibrosis. Extracellular histones are the ligands of TLR4 but their roles in liver fibrosis have not been investigated. AIMThis study aims to investigate the roles and potential mechanisms of extracellular histones in liver fibrosis. METHODSIn vitro, the LX2 cells, a human hepatic stellate cell (HSC) line, were treated with histones in the presence or absence of non-anticoagulant heparin (NAHP) for neutralising histones or TLR4-blocking antibody. The cells resultant expression of collagen I was detected using Western blotting and immunofluorescent staining. In vivo, the CCl4-induced liver fibrosis model was generated in male 6 week old ICR mice and in TLR4 or MyD88 knockout and parental mice. Circulating histones were detected and the effect of NAHP was evaluated. RESULTSExtracellular histones strongly stimulated LX2 cells to produce collagen I. The histone-enhanced collagen expression was significantly reduced by NAHP and TLR4 blocking antibody. In CCl4-treated wild type mice, circulating histones were dramatically increased and maintained high levels during the whole course of fibrosis-induction. Injection of NAHP not only reduced alanine aminotransferase (ALT) and liver injury scores, but also significantly reduced fibrogenesis. Since the TLR4-blocking antibody reduced histone-enhanced collagen I production in HSC, the CCl4 model with TLR-4 and MyD88 knockout mice was used to demonstrate the roles of the TLR4-MyD88 signalling pathway in CCl4-induced liver fibrosis. The levels of liver fibrosis were indeed significantly lower than in these knockout mice than the wild type parental mice. CONCLUSIONThis study demonstrated that extracellular histones are able to stimulate HSC to produce collagen I and TLR4 is involved in this process. The in vivo findings support the novel concept that high levels of circulating histones potentially stimulate TLR4 receptor to enhance fibrogenesis via the TLR4-MyD88 signalling pathway. NAHP detoxify extracellular histones and thus has a potential therapeutic role by reducing liver injury and fibrogenesis. Core tipThis work fills the gap between recurrent liver injury and liver fibrosis. When liver cells die, histones will be released. High levels of extracellular histones not only cause a secondary liver injury, but also activate the TLR4-MyD88 signalling pathway to enhance collagen I production and liver fibrosis. Binding of non-anticoagulant heparin (NAHP) to extracellular histones reduces histone toxicity, alleviates liver injury and prevent histones from activating the TLR4-MyD88 signalling pathway. These results may explain why NAHP reduces liver fibrosis in this animal model although further investigations are required. ARTICLE HIGHLIGHTSO_ST_ABSResearch backgroundC_ST_ABSCurrently, the molecular mechanisms of liver fibrosis are not fully understood. Recurrent liver injury or inflammation initiate wound healing process along with fibrogenesis. However, what initiates this process is not clear. When cells die, damage-associated molecular patterns (DAMPs) will be released. Histones are the most abundant DAMP and are also the ligands for TLR4, which in turn has been demonstrated to be involved in bile duct ligation-induced liver fibrosis. Lipopolysaccharides (LPS) has been proposed to be a ligand for TLR4. Since recurrent liver injury does not naturally produce LPS but abundant extracellular histones, this study sought to investigate the potential roles of extracellular histones as TLR4 ligands in liver fibrosis. Research motivationSince our laboratory has been involved in studying the roles of DAMPs in critical illnesses, extracellular histones in liver fibrosis is of great interest in terms of biological and clinical significance. Research objectivesOur study aimed to clarify the roles of extracellular histones in fibrogenesis in vitro and in vivo. Research methodsIn our study, a HSC cell line and animal models of liver fibrosis were employed. Intervention studies with NAHP to detoxify histones and TLR4 blocking antibodies to inhibit TLR4 was performed. In addition, TLR4 and MyD88 knockout mice were used to support that the theory that the TLR4-MyD88 signalling pathway is involved in liver fibrosis in the CCl4 mouse model. Research resultsO_LIDemonstrated that high levels of circulating histones exist when fibrosis is induced by CCl4 in the mouse model. C_LIO_LIDemonstrated in vitro that extracellular histones are able to stimulate HSC cells to produce collagen I. C_LIO_LIDemonstrated that NAHP is able to inhibit histone-enhanced collagen production in the HSC cell line, and reduce liver injury and fibrosis in the animal model. C_LIO_LIDemonstrated that TLR4 is involved in histone-enhanced collagen I production in HSC cells. In vivo, the TLR4-MyD88 signalling pathway was demonstrated to be involved in liver fibrosis, but whether circulating histones are the major activators of the pathway is not fully clear. C_LI Research conclusionRecurrent liver injury releases extracellular histones which potentially activate TLR4-MyD88 signalling pathway to promote liver fibrosis. The ability of NAHP to detoxify circulating histones holds the potential for the treatment of liver injury and prevention of liver fibrosis. Research perspectivesFuture studies demonstrating the contributions of circulating histones in activating the TLR4-MyD88 signalling pathway in vivo will validate their role in liver fibrosis. Development of better anti-histone reagents to reduce liver injury and prevent liver fibrosis will hold great potential in the management of diseases with recurrent liver injury.

pathology↗