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"Yi, Yun Yun"
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Factors affecting variations of soil pH in different horizons in hilly regions
Soil pH is a key factor that controls soil nutrient availability, soil microbial activities, and crop growth and development. However, studies on the soil pH variations of cultivated lands in different horizons at the regional scale remain limited. In this work, 348 soil samples were collected from three soil horizons (A, B, and C) at 120 sites over the hilly region of Chongqing, southwestern China. Six topographic indicators, four climate parameters, and parent material were considered. Classification and regression trees (CARTs) were applied to investigate the relationships between soil pH and the variables in the A, B, and C horizons. Model performances were evaluated by root mean square error (RMSE), relative root mean square error (RRMSE), and coefficient of determination (R2). Results showed that soil pH increased obviously from the A to C horizons. Soil pH was predicted well by the forcing factors with the CART models in all horizons. RMSE, RRMSE, and R2 varied between 0.37 and 0.435, between 5.93 and 7.23%, and between 0.71 and 0.80, respectively. The relative importance of the studied variables to soil pH differed with the horizons. Annual temperature range (ATR), terrain wetness index (TWI), and Melton ruggedness number were critical factors that controlled soil pH variability in the A horizon. Parent material, precipitation of warmest quarter (PWQ), ATR, and TWI were important variables in the B horizon. Parent material, PWQ, ATR, and precipitation were key factors in the C horizon. The results are expected to provide valuable information for designing appropriate measurements for agricultural practices and preventing soil acidification.
Journal Article
Emergence of plasmid-mediated colistin resistance mechanism MCR-1 in animals and human beings in China: a microbiological and molecular biological study
Until now, polymyxin resistance has involved chromosomal mutations but has never been reported via horizontal gene transfer. During a routine surveillance project on antimicrobial resistance in commensal Escherichia coli from food animals in China, a major increase of colistin resistance was observed. When an E coli strain, SHP45, possessing colistin resistance that could be transferred to another strain, was isolated from a pig, we conducted further analysis of possible plasmid-mediated polymyxin resistance. Herein, we report the emergence of the first plasmid-mediated polymyxin resistance mechanism, MCR-1, in Enterobacteriaceae.
The mcr-1 gene in E coli strain SHP45 was identified by whole plasmid sequencing and subcloning. MCR-1 mechanistic studies were done with sequence comparisons, homology modelling, and electrospray ionisation mass spectrometry. The prevalence of mcr-1 was investigated in E coli and Klebsiella pneumoniae strains collected from five provinces between April, 2011, and November, 2014. The ability of MCR-1 to confer polymyxin resistance in vivo was examined in a murine thigh model.
Polymyxin resistance was shown to be singularly due to the plasmid-mediated mcr-1 gene. The plasmid carrying mcr-1 was mobilised to an E coli recipient at a frequency of 10−1 to 10−3 cells per recipient cell by conjugation, and maintained in K pneumoniae and Pseudomonas aeruginosa. In an in-vivo model, production of MCR-1 negated the efficacy of colistin. MCR-1 is a member of the phosphoethanolamine transferase enzyme family, with expression in E coli resulting in the addition of phosphoethanolamine to lipid A. We observed mcr-1 carriage in E coli isolates collected from 78 (15%) of 523 samples of raw meat and 166 (21%) of 804 animals during 2011–14, and 16 (1%) of 1322 samples from inpatients with infection.
The emergence of MCR-1 heralds the breach of the last group of antibiotics, polymyxins, by plasmid-mediated resistance. Although currently confined to China, MCR-1 is likely to emulate other global resistance mechanisms such as NDM-1. Our findings emphasise the urgent need for coordinated global action in the fight against pan-drug-resistant Gram-negative bacteria.
Ministry of Science and Technology of China, National Natural Science Foundation of China.
Journal Article
Integrated meta-omics reveals new ruminal microbial features associated with feed efficiency in dairy cattle
Background
As the global population continues to grow, competition for resources between humans and livestock has been intensifying. Increasing milk protein production and improving feed efficiency are becoming increasingly important to meet the demand for high-quality dairy protein. In a previous study, we found that milk protein yield in dairy cows was associated with the rumen microbiome. The objective of this study was to elucidate the potential microbial features that underpins feed efficiency in dairy cows using metagenomics, metatranscriptomics, and metabolomics.
Results
Comparison of metagenomic and metatranscriptomic data revealed that the latter was a better approach to uncover the associations between rumen microbial functions and host performance. Co-occurrence network analysis of the rumen microbiome revealed differential microbial interaction patterns between the animals with different feed efficiency, with high-efficiency animals having more and stronger associations than low-efficiency animals. In the rumen of high-efficiency animals,
Selenomonas
and members of the
Succinivibrionaceae
family positively interacted with each other, functioning as keystone members due to their essential ecological functions and active carbohydrate metabolic functions. At the metabolic level, analysis using random forest machine learning suggested that six ruminal metabolites (all derived from carbohydrates) could be used as metabolic markers that can potentially differentiate efficient and inefficient microbiomes, with an accuracy of prediction of 95.06%.
Conclusions
The results of the current study provided new insights into the new ruminal microbial features associated with feed efficiency in dairy cows, which may improve the ability to select animals for better performance in the dairy industry. The fundamental knowledge will also inform future interventions to improve feed efficiency in dairy cows.
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Journal Article
Polystyrene nanoplastics disrupt the intestinal microenvironment by altering bacteria-host interactions through extracellular vesicle-delivered microRNAs
Nanoplastics (NP) are emerging environmental pollutants with potential risks to human health. This study investigates how polystyrene-NP exposure disrupts the intestinal microenvironment and barrier function through bacteria-host interactions. Using in vivo models and bacterial sorting technology, we show that NP accumulation in the mouse intestine alters the expression of intestinal miR-501-3p and miR-700-5p, compromising tight junction protein ZO-1 and mucin (MUC)−13 expression, thereby increasing intestinal permeability. NP increases miR-98-3p, miR-548z, miR-548h-3o, miR-548d-3p, miR-548az-5p, miR-12136, and miR-101-3p levels in extracellular vesicles (EVs) derived from goblet-like cells, which can interfere with ZO-1 expression. NP also induces gut microbiota dysbiosis, characterized by elevated
Ruminococcaceae
abundance and altered EV characteristics from goblet cells.
Lachnospiraceae
internalize NP, and their EVs suppress MUC-13 expression. These findings reveal a mechanism by which NP compromises intestinal integrity and indirectly alters intestinal microbiota composition, potentially leading to adverse health outcomes.
Nanoplastics are a concern for health and safety. Here, the authors show polystyrene nanoplastics disrupt intestinal integrity and gut microbiota composition by altering microRNA expression in extracellular vesicles, highlight a potential pathway through which nanoplastic exposure affects gut health.
Journal Article
Dying tumor cell-derived exosomal miR-194-5p potentiates survival and repopulation of tumor repopulating cells upon radiotherapy in pancreatic cancer
Background
Tumor repopulation is a major cause of radiotherapy failure. Previous investigations highlighted that dying tumor cells played vital roles in tumor repopulation through promoting proliferation of the residual tumor repopulating cells (TRCs). However, TRCs also suffer DNA damage after radiotherapy, and might undergo mitotic catastrophe under the stimulation of proliferative factors released by dying cells. Hence, we intend to find out how these paradoxical biological processes coordinated to potentiate tumor repopulation after radiotherapy.
Methods
Tumor repopulation models in vitro and in vivo were used for evaluating the therapy response and dissecting underlying mechanisms. RNA-seq was performed to find out the signaling changes and identify the significantly changed miRNAs. qPCR, western blot, IHC, FACS, colony formation assay, etc. were carried out to analyze the molecules and cells.
Results
Exosomes derived from dying tumor cells induced G1/S arrest and promoted DNA damage response to potentiate survival of TRCs through delivering miR-194-5p, which further modulated E2F3 expression. Moreover, exosomal miR-194-5p alleviated the harmful effects of oncogenic HMGA2 under radiotherapy. After a latent time, dying tumor cells further released a large amount of PGE2 to boost proliferation of the recovered TRCs, and orchestrated the repopulation cascades. Of note, low-dose aspirin was found to suppress pancreatic cancer repopulation upon radiation via inhibiting secretion of exosomes and PGE2.
Conclusion
Exosomal miR-194-5p enhanced DNA damage response in TRCs to potentiate tumor repopulation. Combined use of aspirin and radiotherapy might benefit pancreatic cancer patients.
Journal Article