Biology subjects

Gao, Y.

Publications and source records attributed to Gao, Y..

At least 19 recordsLinked to original sources

bioRxiv2018

Transcriptome profiling of pathogen-specific CD4 T cells identifies T-cell-intrinsic caspase-1 as an important regulator of Th17 differentiation

One sentence summaryOur study revealed that DCs shape distinct pathogen-specific CD4 T cell transcriptome and from which, we discovered an unexpected role for T-cell-intrinsic caspase-1 in promoting Th17 differentiation.\n\nABSTRACTDendritic cells (DCs) are critical for priming and differentiation of pathogen-specific CD4 T cells. However, to what extent innate cues from DCs dictate transcriptional changes in T cells leading to effector heterogeneity remains elusive. Here we have used an in vitro approach to prime naive CD4 T cells by DCs stimulated with distinct pathogens. We have found that such pathogen-primed CD4 T cells express unique transcriptional profiles dictated by the nature of the priming pathogen. In contrast to cytokine-polarized Th17 cells that display signatures of terminal differentiation, pathogen-primed Th17 cells maintain a high degree of heterogeneity and plasticity. Further analysis identified caspase-1 as one of the genes upregulated only in pathogen-primed Th17 cells but not in cytokine-polarized Th17 cells. T-cell-intrinsic caspase-1, independent of its function in inflammasome, is critical for inducing optimal pathogen-driven Th17 responses. More importantly, T cells lacking caspase-1 fail to induce colitis following transfer into RAG-deficient mice, further demonstrating the importance of caspase-1 for the development of pathogenic Th17 cells in vivo. This study underlines the importance of DC-mediated priming in identifying novel regulators of T cell differentiation.

immunology↗

bioRxiv2018

Unilateral relapse of Behcet’s disease-associated uveitis does not appear to cause asymmetric tear protein profiles

Purpose: To explore whether unilateral relapse of Bechets disease uveitis (BDU) causes differences in the tear proteome between the diseased and the contralateral quiescent eye.\n\nExperimental design: To minimize interindividual variations, bilateral tear samples were collected from the same patient (n=15) with unilateral relapse of BDU. A data-independent acquisition (DIA) strategy was used to identify proteins that differed between active and quiescent eyes.\n\nResults: A total of 1,797 confident proteins were identified in the tear samples, of which 371 are also highly expressed in various tissues and organs. Sixty-two (3.5%) proteins differed in terms of expression between tears in active and quiescent eyes, similar to the number of differentially expressed proteins (74, 4.1%) identified in a randomized grouping strategy. Furthermore, the intrapair trend of the differentially expressed proteins was not consistent and none of the proteins showed the same trend in more than 9 pairs of eyes.\n\nConclusions and clinical relevance: Unilateral relapse of BDU does not appear to cause asymmetric changes in the tear proteome between active and contralateral quiescent eyes. Tear fluid is a valuable source for biomarker studies of systemic diseases.\n\nStatement of clinical relevanceTears are an easily, noninvasively accessible body fluid that is a valuable source of biomarkers for various diseases. Behcets disease uveitis (BDU) has high potential to cause blindness and represents the leading cause of morbidity in BD patients, especially in frequently relapsing cases. Here, we adopted a method combining a \"dry\" method for tear preservation and nano-LC-DIA-MS/MS system to explore whether unilateral relapse of BDU causes differences in the tear proteome between the diseased and the contralateral quiescent eye, with the aim of evaluating tear fluid as a source for biomarker studies of uveitis relapse.

molecular biology↗

bioRxiv2018

Using QC-Blind for quality control and contamination screening of bacteria DNA sequencing data without reference genome

Quality control in next generation sequencing has become increasingly important as the technique becomes widely used. Tools have been developed for filtering possible contaminants in the sequencing data of species with known reference genome. Unfortunately, reference genomes for all the species involved, including the contaminants, are required for these tools to work. This precludes many real-life samples that have no information about the complete genome of the target species, and are contaminated with unknown microbial species.\n\nIn this work we propose QC-Blind, a novel quality control pipeline for removing contaminants without any use of reference genomes. The pipeline requires only very little information from the marker genes of the target species. The entire pipeline consists of unsupervised read assembly, contig binning, read clustering and marker gene assignment.\n\nWhen evaluated on in silico, ab initio and in vivo datasets, QC-Blind proved effective in removing unknown contaminants with high specificity and accuracy, while preserving most of the genomic information of the target bacterial species. Therefore, QC-Blind could serve well in situations where limited information is available for both target and contamination species.\n\nIMPORTANCEAt present, many sequencing projects are still performed on potentially contaminated samples, which bring into question their accuracies. However, current reference-based quality control method are limited as they need either the genome of target species or contaminations. In this work we propose QC-Blind, a novel quality control pipeline for removing contaminants without any use of reference genomes. When evaluated on in silico, ab initio and in vivo datasets, QC-Blind proved effective in removing unknown contaminants with high specificity and accuracy, while preserving most of the genomic information of the target bacterial species. Therefore, QC-Blind is suitable for real-life samples where limited information is available for both target and contamination species.

bioinformatics↗

bioRxiv2018

Histologically derived fiber response functions for diffusion MRI vary across white matter fibers - an ex vivo validation study in the squirrel monkey brain

Understanding the relationship between the diffusion-weighted MRI signal and the arrangement of white matter fibers is fundamental for accurate voxel-wise reconstruction of the fiber orientation distribution (FOD) and subsequent fiber tractography. Spherical deconvolution reconstruction techniques model the diffusion signal as the convolution of the FOD with a response function which represents the signal profile of a single fiber orientation. Thus, given the signal and a fiber response function, the FOD can be estimated in every imaging voxel by deconvolution. However, the selection of the appropriate response function remains relatively un-studied, and requires further validation. In this work, using 3D histologically-defined FODs and the corresponding diffusion signal from three ex vivo squirrel monkey brains, we derive the ground truth response functions. We find that the histologically-derived response functions differ from those conventionally used. Next, we find that response functions statistically vary across brain regions, which suggests that the practice of using the same kernel throughout the brain is not optimal. Additionally, response functions vary significantly across subjects. We show that different kernels lead to different FOD reconstructions, which in turn can lead to different tractography results depending on algorithmic parameters, with large variations in the accuracy of resulting reconstructions. Together, this suggests that there is room for improvement in estimating and understanding the relationship between the diffusion signal and the underlying FOD.

neuroscience↗

bioRxiv2018

Tau accumulation activates STAT1 triggering memory deficits via suppressing NMDA receptor expression

Intracellular tau accumulation forming neurofibrillary tangles is hallmark pathology of Alzheimer's disease (AD), but how tau accumulation induces synapse impairment is elusive. By overexpressing human full-length wildtype tau (termed hTau) to mimic tau abnormality as seen in the brain of sporadic AD patients, we found that hTau accumulation activated JAK2 to phosphorylate STAT1 (Signal Transducer and Activator of Transcription 1) at Tyr701 leading to STAT1 dimerization, nuclear translocation and its activation. STAT1 activation suppressed expression of N-methyl-D-aspartate receptors (NMDARs) through direct binding to the specific GAS element of GluN1, GluN2A and GluN2B promoters, while knockdown STAT1 by AAV-Cre in STAT1flox/flox mice or expressing dominant negative Y701F-STAT1 efficiently rescued hTau-induced suppression of NMDARs expression with amelioration of synaptic functions and memory performance. These findings indicate that hTau accumulation impairs synaptic plasticity through JAK2/STAT1-induced suppression of NMDARs expression, revealing a novel mechanism for hTau-associated synapse and memory deficits.

neuroscience↗

bioRxiv2018

Rapidly Assessing the Quality of Targeted Proteomics Experiments Through Monitoring Stable-isotope Labeled Standards

Targeted proteomics experiments based on selected reaction monitoring (SRM) have gained wide adoption in clinical biomarker, cellular modeling and numerous other biological experiments due to their highly accurate and reproducible quantification. The quantitative accuracy in targeted proteomics experiments is reliant on the stable-isotope, heavy-labeled peptide standards which are spiked into a sample and used as a reference when calculating the abundance of endogenous peptides. Therefore, the quality of measurement for these standards is a critical factor in determining whether data acquisition was successful. With improved MS instrumentation that enables the monitoring of hundreds of peptides in hundreds to thousands of samples, quality assessment is increasingly important and cannot be performed manually. We present Q4SRM, a software tool that rapidly checks the signal from all heavy labeled peptides and flags those that fail quality control metrics. Using four metrics, the tool detects problems both with individual SRM transitions and the collective group of transitions that monitor a single peptide. The programs speed enables its use at the point of data acquisition and can be ideally run immediately upon the completion of an LC-SRM-MS analysis.

bioinformatics↗

bioRxiv2018

Limits to anatomical accuracy of diffusion tractography using modern approaches

Diffusion MRI fiber tractography is widely used to probe the structural connectivity of thebrain, with a range of applications in both clinical and basic neuroscience. Despite widespread use, tractography has well-known pitfalls that limits the anatomical accuracy of this technique. Numerous modern methods have been developed to address these shortcomings through advances in acquisition, modeling, and computation. To test whether these advances improve tractography accuracy, we organized the ISBI 2018 3D Validation of Tractography with Experimental MRI (3D-VoTEM) challenge. We made available three unique independent tractography validation datasets - a physical phantom and two ex vivo brain specimens - resulting in 176 distinct submissions from 9 research groups. By comparing results over a wide range of fiber complexities and algorithmic strategies, this challenge provides a more comprehensive assessment of tractographys inherent limitations than has been reported previously. The central results were consistent across all sub-challenges in that, despite advances in tractography methods, the anatomical accuracy of tractography has not dramatically improved in recent years. Taken together, our results independently confirm findings from decades of tractography validation studies, demonstrate inherent limitations in reconstructing white matter pathways using diffusion MRI data alone, and highlight the need for alternative or combinatorial strategies to accurately map the fiber pathways of the brain.

neuroscience↗

bioRxiv2018

deGSM: memory scalable construction of large scale de Bruijn Graph

MotivationDe Bruijn graph, a fundamental data structure to represent and organize genome sequence, plays important roles in various kinds of sequence analysis tasks such as de novo assembly, high-throughput sequencing (HTS) read alignment, pan-genome analysis, metagenomics analysis, HTS read correction, etc. With the rapid development of HTS data and ever-increasing number of assembled genomes, there is a high demand to construct de Bruijn graph for sequences up to Tera-base-pair level. It is non-trivial since the size of the graph to be constructed could be very large and each graph consists of hundreds of billions of vertices and edges. Current existing approaches may have unaffordable memory footprints to handle such a large de Bruijn graph. Moreover, it also requires the construction approach to handle very large dataset efficiently, even if in a relatively small RAM space.\n\nResultsWe propose a lightweight parallel de Bruijn graph construction approach, de Bruijn Graph Constructor in Scalable Memory (deGSM). The main idea of deGSM is to efficiently construct the Bur-rows-Wheeler Transformation (BWT) of the unipaths of de Bruijn graph in constant RAM space and transform the BWT into the original unitigs. It is mainly implemented by a fast parallel external sorting of k-mers, which allows only a part of k-mers kept in RAM by a novel organization of the k-mers. The experimental results demonstrate that, just with a commonly used machine, deGSM is able to handle very large genome sequence(s), e.g., the contigs (305 Gbp) and scaffolds (1.1 Tbp) recorded in Gen-Bank database and Picea abies HTS dataset (9.7 Tbp). Moreover, deGSM also has faster or comparable construction speed compared with state-of-the-art approaches. With its high scalability and efficiency, deGSM has enormous potentials in many large scale genomics studies.\n\nAvailabilityhttps://github.com/hitbc/deGSM.\n\nContactydwang@hit.edu.cn (YW) and bo.liu@hit.edu.cn (BL)\n\nSupplementary informationSupplementary data are available online.

bioinformatics↗

bioRxiv2018

Urinary protein changes in the early phase of smoking-induced Chronic Obstructive Pulmonary Disease in a rat model

Chronic obstructive pulmonary disease (COPD) is a group of severe respiratory diseases. Identifying COPD through early urinary biomarkers by proteomics technology may help to reduce the mortality rate of the disease, improve the quality of life of patients and reduce the burden on society. Urine samples from a COPD rat model induced by smoking were taken at week 2, week 4 and week 8. By LC-MS/MS, 15 differential proteins with human orthologs were identified. After smoking for 2 weeks when there were no significant pathological changes, 8 differential proteins were identified: 2 proteins had been reported to be markers of COPD, while 4 proteins were associated with COPD. After smoking for 4 weeks, which is when slight pathological changes were observed, 7 differential proteins were identified: 3 of them were reported to be associated with COPD, while 1 protein had been reported to be a marker of COPD. After smoking for 8 weeks, there were significant pathological changes: 5 differential proteins were identified, 3 of which were reported to be associated with COPD. The results of this study suggest that differential urinary proteins may provide important clues for the early diagnosis of COPD.

biochemistry↗

bioRxiv2018

Migration and Differentiation of Osteoclast Precursors under Gradient Fluid Shear Stress

The skeleton is able to adapt to mechanical loading through bone remodeling, i.e. bone resorption followed by bone formation. The osteoclasts close to microdamages are believed to initiate bone resorption, but whether local mechanical loading such as fluid flow regulates recruitment and differentiation of osteoclast precursors at the site of bone resorption has yet to be investigated. In the present study, finite element analysis first revealed that there exists low fluid shear stress (FSS) field inside microdamage. Basing on a custom-made device of cone-and-plate fluid chamber, finite element analysis and particle image velocimetry measurement were performed to verify the formation of gradient FSS flow field. Furthermore, the effects of gradient FSS on the migration, aggregation, and fusion of osteoclast precursors were observed. Results showed that osteoclast precursor RAW264.7 cells migrate along radial direction toward the region with lower FSS during exposure to gradient FSS stimulation for 40 min, obviously deviating from the direction of actual fluid flow indicated by fluorescent particles. When inhibiting calcium signaling pathway with gadolinium and thapsigargin, cell migration toward low-FSS region was significantly reduced. For other cell lines, MC3T3-E1, PDLF, rMSC and MDCK, gradient FSS stimulation did not lead to the low-FSS-inclined migration. After being cultured under gradient FSS stimulation for 6 days, the density of RAW264.7 cells and the ratio of TRAP-positive multinucleated osteoclasts in low-FSS region were significantly higher than those in high-FSS region. Therefore, osteoclast precursor cells may have special ability to sense FSS gradient and tend to actively migrate toward low-FSS region, which is regulated by calcium signaling pathway.

cell biology↗

bioRxiv2018

Multiple roles of the non-structural protein 3 (nsP3) alphavirus unique domain (AUD) during Chikungunya virus genome replication and transcription

Chikungunya virus (CHIKV) is a re-emerging Alphavirus causing fever, joint pain, skin rash, arthralgia, and occasionally death. Antiviral therapies and/or effective vaccines are urgently required. CHIKV biology is poorly understood, in particular the functions of the non-structural protein 3 (nsP3). Here we present the results of a mutagenic analysis of the alphavirus unique domain (AUD) of nsP3. Informed by the structure of the Sindbis virus AUD and an alignment of amino acid sequences of multiple alphaviruses, a series of mutations in the AUD were generated in a CHIKV sub-genomic replicon. This analysis revealed an essential role for the AUD in CHIKV RNA replication, with mutants exhibiting species- and cell-type specific phenotypes. To test if the AUD played a role in other stages of the virus lifecycle, the mutant panel was also analysed in the context of infectious CHIKV. Results indicated that, in addition to a role in RNA replication, the AUD was also required for virus assembly. Further analysis revealed that one mutant (P247A/V248A) specifically blocked transcription of the subgenomic RNA leading to a dramatic reduction in synthesis of the structural proteins and concomitant reduction in virus production. This phenotype could be explained by both a reduction in the binding of the P247A/V248A mutant nsP3 to viral genomic RNA in vivo, and the reduced affinity of the mutant AUD for the subgenomic promoter RNA in vitro. We propose that the AUD is a pleiotropic protein domain, with multiple functions during CHIKV RNA synthesis.\n\nAuthor summaryChikungunya virus (CHIKV) is an emerging threat to world health. It is transmitted by Aedes species mosquitos, and has caused massive epidemics across the globe. The virus causes fever, rash, arthritis and can sometimes be fatal. The biology of CHIKV is poorly understood, to address this deficiency we aimed to identify functions of one of the viral proteins, nsP3. We focussed on the central part of this protein, termed the alphavirus unique domain (AUD) because it is unique to the genus of viruses to which CHIKV belongs - the Alphaviruses - and not present in other related viruses. By making changes (mutations) in the AUD and analysing the effects of these changes we show that it is involved in multiple stages of the virus lifecycle. These observations identify nsP3 and the AUD in particular as a potential target for antiviral therapy or rational vaccine design.

microbiology↗

bioRxiv2018

Kinase Driver Mutations in Protein-protein Structure may associate to Disease by Effecting Kinase Stability

Activating mutations are significant drug targets of diseases. Statistical analysis on the mutated amino acids, the mutation characteristic and the related disease information of activating mutations is of great significance for the diagnosis and treatment of diseases. Study on the protein stability by predicting Gibbs free energy ({Delta}{Delta}G) change after mutation is very helpful for understanding the relationship between protein structure and function. By combining mCSM and disease datasets, this paper studies the effect of mutation on the protein stability and disease. The results show that the mutations in protein may be the cause of disease for PPI structures, which statistically afford significant information for disease related research and medical diagnosis and treatment.

biochemistry↗

bioRxiv2018

Changes in the urinary proteome in a Patient-Derived Xenograft model

In this report, the urinary proteome from a patient-derived xenograft (PDX) model was compared at the peptide level to study the origins of urinary proteins in tumor-bearing nude mice. Urine was collected from the PDX mice before and after tumor implantation. A total of 515 mouse proteins were identified, of which 8 were differential proteins. Seventy-eight unambiguous human peptides from 42 human proteins were identified in the tumor-bearing group. Compared with the differential urinary proteins from the tumor-bearing immuno-competent rats, the differential proteins in the urine from the PDX model had no host immune response proteins in the very early stage urine in the tumor-bearing immuno-competent rat model.

biochemistry↗

bioRxiv2018

MicroRNA miR-7 and miR-17-92 in POMC neurons are associated with sex-specific regulation of diet-induced obesity

Proopiomelanocortin (POMC) neurons in the arcuate nucleus (ARC) in mammalian hypothalamus play important roles in regulating appetite, energy expenditure, and glucose and fat metabolisms. Diet-induced obesity often show sex-specific difference. But the underlying mechanisms remain unclear. Here we show that microRNA (miRNA) miR-7 and miR-17-92 are expressed in the mouse ARC, and mostly in POMC neurons. Knockdown of miR-7 and knockout of miR-17-92 specifically in POMC neurons aggravate diet-induced obesity only in females and males, respectively. Moreover, gene expression profile analysis identifies sex-differential genes in male and female ARCs in wildtype adult mice. Interestingly, these genes that normally show low-expression in the female and male ARCs display upregulated expression in female miR-7 knockdown and male miR-17-92 knockout mice, respectively. Our results demonstrate an important role of miRNAs in regulating sex-specific diet-induced obesity, likely through modulating expression of target genes that show sex-differential expression in the ARC of hypothalamus.

neuroscience↗

bioRxiv2018

Impact of acetolactate synthase inactivation on 1,3-propanediol fermentation by Klebsiella pneumoniae

1,3-Propanediol (1,3-PDO) is an important compound that is mainly used in industry for polymer production. Fermentation of 1,3-PDO from glycerol by marine Klebsiella pneumoniae is accompanied by formation of 2,3-butanediol (2,3-BDO) as one of the main byproduct. The first step in the formation of 2,3-BDO from pyruvate is catalyzed by acetolactate synthase (ALS), an enzyme that competes with 1,3-PDO oxidoreductase for the cofactor NADH. This study aimed to analyze the impact of engineering the 2,3-BDO formation pathway via inactivation of ALS on 1,3-PDO fermentation by marine K. pneumoniae HSL4. An ALS mutant was generated using Red recombinase assisted gene replacement. The ALS specific activities of K. pneumoniae {Delta}ALS were notably lower than that of the wild-type strain. Fed-batch fermentation of the mutant strain resulted in a 1,3-PDO concentration, productivity and conversion of 72.04 g L-1, 2.25 g L-1 h-1, and 0.41 g g-1, a slightly increase compared with the parent strain. Moreover, inactivation of ALS decreased meso-2,3-BDO formation to trace amounts, significantly increased 2S,3S-BDO and lactate production, and a pronounced redistribution of intracellular metabolic flux was apparent.

microbiology↗

bioRxiv2018

NudCL2 is an Hsp90 cochaperone to regulate sister chromatid cohesion by stabilizing cohesin subunits

Sister chromatid cohesion plays a key role in ensuring precise chromosome segregation during mitosis, which is mediated by the multisubunit complex cohesin. However, the molecular regulation of cohesin subunits stability remains unclear. Here, we show that NudCL2 (NudC-like protein 2) is essential for the stability of cohesin subunits by regulating Hsp90 ATPase activity in mammalian cells. Depletion of NudCL2 induces mitotic defects and premature sister chromatid separation and destabilizes cohesin subunits that interact with NudCL2. Similar defects are also observed upon inhibition of Hsp90 ATPase activity. Interestingly, ectopic expression of Hsp90 efficiently rescues the protein instability and functional deficiency of cohesin induced by NudCL2 depletion, but not vice versa. Moreover, NudCL2 not only binds to Hsp90, but also significantly modulates Hsp90 ATPase activity and promotes the chaperone function of Hsp90. Taken together, these data suggest that NudCL2 is a previously undescribed Hsp90 cochaperone to modulate sister chromatid cohesion by stabilizing cohesin subunits, providing a hitherto unrecognized mechanism that is crucial for faithful chromosome segregation during mitosis.

cell biology↗

bioRxiv2018

TP53 mutations promote immunogenic activity in breast cancer

BackgroundAlthough immunotherapy has recently achieved clinical successes in a variety of cancers, thus far there is no any immunotherapeutic strategy for breast cancer (BC). Thus, it is important to discover biomarkers for identifying the BC patients responsive to immunotherapy. TP53 mutations were often associated with worse clinical outcome in BC, of which the triple-negative BC (TNBC) has a high TP53 mutation rate (approximately 80%). TNBC is high-risk due to its high invasiveness, and lack of targeted therapy. To explore a potentially promising therapeutic option for the TP53-mutated BC subtype, we studied the associations between TP53 mutations and immunogenic activity in BC.\n\nMethodsWe compared enrichment levels of 26 immune gene-sets that indicated activities of diverse immune cells, functions, and pathways between TP53-mutated and TP53-wildtype BCs based on two large-scale BC multi-omics data. Moreover, we explored the molecular cues that were associated with the differences in immunogenic activity between TP53-mutated and TP53-wildtype BCs. Furthermore, we performed experimental validation of the findings from bioinformatics analysis.\n\nResultsWe found that almost all analyzed immune gene-sets had significantly higher enrichment levels in TP53-mutated BCs compared to TP53-wildtype BCs. Moreover, our experiments confirmed that mutant p53 could increase BC immunogenicity. Furthermore, our computational and experimental results showed that TP53 mutations could promote BC immunogenicity via regulation of the p53-mediated pathways including cell cycle, apoptosis, Wnt, Jak-STAT, NOD-like receptor, and glycolysis. Interestingly, we found that elevated immune activities were likely to be associated with better survival prognosis in TP53-mutated BCs, but not necessarily in TP53-wildtype BCs.\n\nConclusionsTP53 mutations promote immunogenic activity in breast cancer. This finding demonstrates a different effect of p53 dysfunction on tumor immunogenicity from that of previous studies, suggesting that the TP53 mutation status could be a useful biomarker for stratifying BC patients responsive to immunotherapy.

cancer biology↗

bioRxiv2018

Free-living Bacterial Communities Are Mostly Dominated by Oligotrophs

In response to resource availability, bacteria have evolved two distinct ecological strategies. Copiotrophic bacteria grow fast and are heavily favored by selection where the resource is abundant. In contrast, oligotrophic bacteria grow slowly but more efficiently and are highly adaptive in nutrient-poor environments (Koch, 2001). Although oligotrophs and copiotrophs are ubiquitous, except for a few well-characterized environments like the open ocean and animal gut, the relative abundance of oligotrophic and copiotrophic bacteria and their importance in the global ecosystem are still unclear. In addition, although several studies have demonstrated the impact of nutrient availability on the bacterial community structure under experimental conditions (Klappenbach et al., 2000, Nemergut et al., 2016), the role of nutrients in shaping the structures of bacterial communities in their natural habitats remains largely unknown. Using the ribosomal RNA operon (rrn) copy number to capture the bacterial ecological strategy, we analyzed 44,045 samples from two large bacterial community repositories that cover 78 environmental types. Here we show that animal-associated microbiota are dominated by copiotrophs while plant-associated and free-living bacterial communities are mostly dominated by oligotrophs. Our results suggest that nutrient availability plays an important role in determining the structure and ecological strategy of bacterial communities in nature. We demonstrate that the average and distribution of rrn copy number are simple yet robust predictors of the ecological strategy of bacterial communities that can be applied to all sequence-based microbial surveys to link the community structure and function.

microbiology↗