Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1008889 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25753002.fastq.gz | Fastqsanger.gz | |||
| SRR25753003.fastq.gz | Fastqsanger.gz |
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Project description:Fire disturbances are becoming more common, more intense, and further-reaching across the globe, with consequences for ecosystem functioning. Importantly, fire can have strong effects on the soil microbiome, including community and functional changes after fire, but surprisingly little is known regarding the role of soil fire legacy in shaping responses to recent fire. To address this gap, we conducted a manipulative field experiment administering fire across 32 soils with varying fire legacies, including combinations of 1-7 historic fires and 1-33 years since most recent fire. We analyzed soil metatranscriptomes, determining for the first time how fire and fire legacy interactively affect metabolically-active soil taxa, the microbial regulation of important carbon (C), nitrogen (N) and phosphorus (P) cycling, expression of carbohydrate-cycling enzyme pathways, and functional gene co-expression networks. Experimental fire strongly downregulated fungal activity while upregulating many bacterial and archaeal phyla. Further, fire decreased soil capacity for microbial C and N cycling and P transport, and drastically rewired functional gene co-expression. Perhaps most importantly, we highlight a novel role of soil fire legacy in regulation of microbial C, N, and P responses to recent fire. We observed a greater number of functional genes responsive to the interactive effects of fire and fire legacy than those affected solely by recent fire, indicating that many functional genes respond to fire only under certain fire legacy contexts. Therefore, without incorporating fire legacy of soils, studies will miss important ways that fire shapes microbial roles in ecosystem functioning. Finally, we showed that fire caused significant downregulation of carbon metabolism and nutrient cycling genes in microbiomes under abnormal soil fire histories, producing a novel warning for the future: human manipulation of fire legacies, either indirectly through global change-induced fire intensification or directly through fire suppression, can negatively impact soil microbiome functional responses to new fires.
2024-08-12 | GSE274211 | GEO
Project description:Fire is a crucial event regulating the structure and functioning of many ecosystems. Yet few studies focused on how fire affects both the taxonomic and functional diversity of soil microbial communities, along with plant diversity and soil carbon (C) and nitrogen (N) dynamics. Here, we analyze these effects for a grassland ecosystem 9-months after an experimental fire at the Jasper Ridge Global Change Experiment (JRGCE) site in California, USA. Fire altered soil microbial communities considerably, with community assembly process analysis indicating that environmental selection pressure was higher in burned sites. However, a small subset of highly connected taxa were able to withstand the disturbance. In addition, fire decreased the relative abundances of most genes associated with C degradation and N cycling, implicating a slow-down of microbial processes linked to soil C and N dynamics. In contrast, fire stimulated plant growth, likely enhancing plant-microbe competition for soil inorganic N. To synthesize our findings, we performed structural equation modeling, which showed that plants but not microbial communities were responsible for the significantly higher soil respiration rates in burned sites. In conclusion, fire is well-documented to considerable alter the taxonomic and functional composition of soil microorganisms, along with the ecosystem functioning, thus arousing feedback of ecosystem responses to affect global climate.
2022-02-19 | GSE126737 | GEO
Project description:Background & Aims. As a T cell-mediated disease of the colonic epithelium, ulcerative colitis (UC) is likely to share pathogenic elements with other T cell-mediated inflammatory diseases. Recently we showed T cell-mediated rejection of kidney and heart transplants share large scale molecular changes. We hypothesized that UC would manifest a similar disturbance, and that these features would correlate with response to infliximab. Results. UC biopsies manifested coordinate transcript changes resembling rejecting transplants, with T cell, IFNG-induced, macrophage, and injury transcripts increasing while parenchymal transcripts decreased. The disturbance expressed as principal component 1 correlated with conventional assessments e.g. Mayo scores, serum albumin, and lymphoplasmacytic infiltrate. When assessed in published microarray studies, the disturbance predicted response to infliximab: patients with intense disturbance did not achieve clinical response, although quantitative improvement was usually seen even in non-responders. Similar changes were seen in CrohnM-bM-^@M-^Ys colitis (CDc). Conclusions. The molecular phenotype of UC manifests a large scale coordinate disturbance reflecting changes in inflammatory cells and parenchymal elements that correlates with conventional features and predicts response to infliximab. We studied 56 colon biopsies from patients with colitis, including 43 with UC, characterizing the clinical and histological features, and defined the mRNA phenotype with Affymetrix expression microarrays. We measured the expression of previously defined pathogenesis-based transcript sets representing effector T cells, macrophages, IFNG effects, and parenchymal injury response and dedifferentiation. We also studied 48 microarray files from human colon biopsies from the Gene Expression Omnibus database, classified by response to infliximab therapy to look for molecular changes that predict unresponsiveness.
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Project description:Mammalian species have co-evolved with intestinal microbial communities that can shape development and adapt to environmental changes, including antibiotic perturbation or nutrient flux. In humans, especially children, microbiota disruption is common, yet the dynamic microbiome recovery from early-life antibiotics is still uncharacterized. Using a mouse model mimicking pediatric antibiotic use, we found that therapeutic-dose pulsed antibiotic treatment (PAT) with a beta-lactam or macrolide altered both host and microbiota development. Early-life PAT accelerated total mass and bone growth, and resulted in progressive changes in gut microbiome diversity, population structure, and metagenomic content, with microbiome effects dependent on the number of courses and class of antibiotic. While control microbiota rapidly adapted to a change in diet, PAT slowed the ecological progression, with delays lasting several months in response to the macrolide. This study identifies key markers of disturbance and recovery, which may help provide therapeutic targets for microbiota restoration following antibiotic treatment. C57BL/6J mice received three antibiotic courses: at days 10-15, 28-31, and 37-40 of life, amoxicillin or tylosin.Livers were collected at age 22 weeks, RNA was extracted, and transcriptional differences were measured by microarray analysis.
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Project description:The oomycete Phytophthora palmivora infects a wide range of tropical crops worldwide. Like other filamentous plant pathogens, it secretes effectors to colonise plant tissues. Here we characterise FIRE, an RXLR effector that contains a canonical mode I 14-3-3 phospho-sensor binding motif that is conserved in effectors of several Phytophthora species. FIRE is phosphorylated in planta and interacts with multiple 14-3-3 proteins. Binding is sensitive to the R18 14-3-3 inhibitor. FIRE promotes plant susceptibility and co-localises with its target around haustoria. This work uncovers a new type of oomycete effector target mechanism. It demonstrates that substrate mimicry for 14-3-3 proteins is a cross-kingdom effector strategy used by both prokaryotic and eukaryotic plant pathogens to suppress host immunity.
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Project description:Intensity of press disturbance determined soil community stability to pulse disturbance
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