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PubMed2007

Human bronchial epithelial cell transcriptome: gene expression changes following acute exposure to whole cigarette smoke in vitro.

Cigarette smoke is a complex mixture of more than 4,000 constituents. Its effects on cell biology are poorly understood, partly because whole smoke exposure in vitro is technically challenging. To investigate the effects of smoke on cell signaling and function, a three-dimensional air-liquid interface model of tracheobronchial epithelium, grown from primary human lung epithelial cells, was exposed to air or whole mainstream cigarette smoke for 1 h in a purpose-designed chamber. Gene expression profiles were then determined at 1, 6, and 24 h postexposure using Affymetrix HGU133-2 Plus microarrays. Cells from three different donors were used in the study, and the experiment was performed in triplicate for each donor. Genes significantly regulated by smoke, compared with the air control, in all experiments were determined. Genes exhibiting differential expression were assigned to functional categories and mapped to signaling pathways. Effects were observed on many cellular processes including xenobiotic metabolism, oxidant/antioxidant balance, and DNA damage and repair. Notably, there was marked downregulation of the transforming growth factor-beta pathway, which has not been previously reported. This study provides important data on the acute effects of whole cigarette smoke on mucociliary epithelium and may be used to gain a greater understanding of smoke toxicity.

Bronchi↗

PubMed2005

Genomic technologies and the interrogation of the transcriptome.

Functional genomics refers to the study of whole genomes and the function of its constituent parts to explain biological processes. Though these investigations may involve whole proteome analysis, the primary focus is on the transcriptome and how it is regulated. Recent advances in technologies that can interrogate cellular transcripts on a genome-wide scale seek the complete disclosure of the transcriptome over time-intervals and across many different cellular states. This massively complex data when viewed as a whole can provide surprisingly precise assessment of cellular conditions. Moreover, these data can define hierarchies of importance and have shown us new transcriptional elements. Herein, we describe the technologies and the experimental strategies to study the transcriptome that would be pertinent to cancer and ageing research.

Animals↗

PubMed2006

Analysis of the root-hair morphogenesis transcriptome reveals the molecular identity of six genes with roles in root-hair development in Arabidopsis.

Root-hair morphogenesis is a model for studying the genetic regulation of plant cell development, and double-mutant analyses have revealed a complex genetic network underlying the development of this type of cell. Therefore, to increase knowledge of gene expression in root hairs and to identify new genes involved in root-hair morphogenesis, the transcriptomes of the root-hair differentiation zone of wild-type (WT) plants and a tip-growth defective root-hair mutant, rhd2-1, were compared using Affymetrix ATH1 GeneChips. A set of 606 genes with significantly greater expression in WT plants defines the 'root-hair morphogenesis transcriptome'. Compared with the whole genome, this set is highly enriched in genes known to be involved in root-hair morphogenesis. The additional gene families and functional groups enriched in the root-hair morphogenesis transcriptome are cell wall enzymes, hydroxyproline-rich glycoproteins (extensins) and arabinogalactan proteins, peroxidases, receptor-like kinases and proteins with predicted glycosylphosphatidylinositol (GPI) anchors. To discover new root-hair genes, 159 T-DNA insertion lines identified from the root-hair morphogenesis transcriptome were screened for defects in root-hair morphogenesis. This identified knockout mutations in six genes (RHM1-RHM6) that affected root-hair morphogenesis and that had not previously been identified at the molecular level: At2g03720 (similar to Escherichia coli universal stress protein); At3g54870 (armadillo-repeat containing kinesin-related protein); At4g18640 (leucine-rich repeat receptor-like kinase subfamily VI); At4g26690 (glycerophosphoryl diester phosphodiesterase-like GPI-anchored protein); At5g49270 (COBL9 GPI-anchored protein) and At5g65090 (inositol-1,4,5 triphosphate 5-phosphatase-like protein). The mutants were transcript null, their root-hair phenotypes were characterized and complementation testing with uncloned root-hair genes was performed. The results suggest a role for GPI-anchored proteins and lipid rafts in root-hair tip growth because two of these genes (At4g26690 and At5g49270) encode predicted GPI-anchored proteins likely to be associated with lipid rafts, and several other genes previously shown to be required for root-hair development also encode proteins associated with sterol-rich lipid rafts.

Arabidopsis↗

PubMed2026

Convergent methodologies in prosthetic joint infection research: integrating transdisciplinary approaches to understand and prevent biofilm-driven failure of orthopaedic prostheses.

Prosthetic joint infections (PJIs) remain among the most devastating complications of arthroplasty, imposing substantial clinical, economic and patient burdens. Although culture-based diagnostics underpin current clinical practice, PJIs are biofilm-driven infections shaped by taxonomic diversity, spatial organization, host responses and surface interactions, meaning conventional approaches provide only a partial and often decontextualized view of the infection process. We examine how convergent methodologies can transform PJI research by integrating approaches that have traditionally been studied in isolation, including sequencing, transcriptomics, metabolomics, advanced imaging and culture-based characterization. We discuss how whole-genome sequencing, shotgun metagenomics, transcriptomic and metabolomic approaches resolve pathogen identity, functional activity and adaptive persistence and how cross-scale imaging and spatial biology techniques reveal where microbes colonize, interact and survive across implant surfaces. We highlight emerging opportunities to unify these datasets into coherent frameworks that capture both the molecular and physical dimensions of PJIs. Integrating these complementary approaches will enable a multi-layered understanding of PJIs that link composition, function and spatial organization. Ultimately, this provides a foundation for predictive diagnostics, precision antimicrobial strategies and improved implant design and supports a shift towards more effective, mechanism-informed management of implant-associated infection.

Prosthesis-Related Infections↗

PubMed2025

Genomic and Transcriptomic Landscape of Epstein-Barr Virus-Positive Inflammatory Follicular Dendritic Cell Sarcoma: A Multicenter Study.

Epstein-Barr virus (EBV)-positive inflammatory follicular dendritic cell sarcoma (EBV+ IFDCS) is a rare indolent malignant neoplasm, which occurs almost exclusively in the liver or spleen and may arise from a common EBV-infected mesenchymal cell that differentiates along the follicular or fibroblastic dendritic cell pathway. Despite its rarity, it presents a pressing need for an improved understanding of its genetic underpinnings and potential treatment strategies for recurrent or disseminated cases. To address this, we conducted comprehensive whole-exome sequencing and transcriptome sequencing (mRNA-seq) analyses on 31 and 6 cases of EBV+ IFDCS, respectively, collected from multiple centers in China. We also compared the genetic features of EBV+ IFDCS with those of other EBV-associated malignancies. Our analyses revealed a relatively high somatic mutation rate and widespread copy number variations affecting the major histocompatibility complex-I/II in EBV+ IFDCS. Integrated mutational profiling identified key signaling pathways involved in epigenetic regulation, NF-κB signaling, RTK/RAS/PI(3)K, and the Hippo pathway. Furthermore, we identified several frequently altered genes that could serve as potential therapeutic targets in EBV+ IFDCS. Transcriptomic analysis unveiled significant upregulation of pathways related to virus infection, immune responses, and multiple immune checkpoint genes in EBV+ IFDCS. Comparative analysis demonstrated clear genetic distinctions between EBV+ IFDCS and other EBV-associated tumors. In conclusion, our study provides comprehensive insights into the unique genomic and transcriptomic landscape of EBV+ IFDCS. We have identified multiple genetic alterations that likely contribute to the development and progression of this malignancy. Our results suggest that targeted therapy and immune checkpoint inhibitors may hold promise as potential therapeutic approaches for patients with recurrent or disseminated EBV+ IFDCS.

Humans↗

PubMed2026

Dietary Titanium Dioxide (E171) Alters the Colon Transcriptome-Evidence From a Human Dietary Intervention Study.

Food-grade titanium dioxide (E171) has been removed from the European food market due to concerns about its potential genotoxicity, yet human evidence remains limited. Given its continuous use outside the European Union, clarifying its potential hazard is essential for human risk assessment. In a randomized crossover study, 31 adults consumed 2 mg/kg body weight/day of E171 for 2 weeks, with biospecimens collected after both control and exposure periods. Oral intake resulted in elevated titanium concentrations in feces (CTRL: 6.3 mg/kg; E171: 377 mg/kg). Particle characterization showed a median size of 228 nm, with 9% <100 nm. Systemic oxidative stress increased, evidenced by increased superoxide radical levels in whole blood (p = 0.057). Transcriptomic profiling of colon biopsies revealed activation of 73 pathways linked to oxidative stress, cellular metabolism, and colorectal cancer-associated processes. The observed transcriptional changes were consistent with findings of its proposed mode of action. This human intervention study characterizes the effects of dietary E171 following human gastrointestinal digestion and provides evidence that exposure to dietary E171 induces systemic oxidative stress and transcriptional changes in the colon. These findings strengthen regulatory concerns about E171 as a food additive and its potentially harmful effects on human gastrointestinal health.

Humans↗

PubMed2026

Functional characterization of lncIMF_17214 in regulating intramuscular fat deposition of yellow-feathered broilers.

Intramuscular fat (IMF) content and lipid composition are key determinants of both the nutritional value and sensory attributes of poultry meat, yet the underlying regulatory mechanisms remain insufficiently elucidated. In this study, triglyceride (TG) content was employed as a quantitative phenotypic proxy to dissect the molecular basis of IMF deposition in yellow-feathered broilers. By integrating TG phenotypic data from 315 individuals with transcriptomic profiles and whole-genome resequencing datasets, a TG-associated long noncoding RNA (lncRNA), lncIMF_17214, was identified. Functional characterization revealed that lncIMF_17214 functions as a negative regulator of lipid deposition. Specifically, its knockdown led to significant increases in TG and total cholesterol concentrations, promoted lipid droplet accumulation, and decreased shear force in breast muscle, whereas its overexpression elicited the opposite effects. Mechanistically, lncIMF_17214 interacts with the RNA-binding protein CNBP, forming a regulatory complex that inhibits lipid accumulation. Furthermore, liver-directed overexpression increased the abundance of lncIMF_17214 in plasma exosomes, while liver-directed manipulation was associated with changes in hepatic and breast-muscle lipid deposition; direct exosome-mediated transfer to intramuscular adipocytes remains to be established. Transcriptomic profiling coupled with pathway enrichment analyses demonstrated that lncIMF_17214 predominantly influences steroid biosynthesis, unsaturated fatty acid metabolism, and peroxisome proliferator-activated receptor (PPAR) signaling pathways. This suggests that it may be involved in the regulation of these pathways, although the underlying molecular mechanisms remain to be further elucidated. Collectively, these findings define a lncIMF_17214-centered regulatory axis linking intracellular and systemic lipid metabolism and provide a robust molecular framework for the targeted improvement of meat quality traits in yellow-feathered broilers.

Breast muscle↗

PubMed2005

Whole-genome transcriptional analysis of heavy metal stresses in Caulobacter crescentus.

The bacterium Caulobacter crescentus and related stalk bacterial species are known for their distinctive ability to live in low-nutrient environments, a characteristic of most heavy metal-contaminated sites. Caulobacter crescentus is a model organism for studying cell cycle regulation with well-developed genetics. We have identified the pathways responding to heavy-metal toxicity in C. crescentus to provide insights for the possible application of Caulobacter to environmental restoration. We exposed C. crescentus cells to four heavy metals (chromium, cadmium, selenium, and uranium) and analyzed genome-wide transcriptional activities postexposure using an Affymetrix GeneChip microarray. C. crescentus showed surprisingly high tolerance to uranium, a possible mechanism for which may be the formation of extracellular calcium-uranium-phosphate precipitates. The principal response to these metals was protection against oxidative stress (up-regulation of manganese-dependent superoxide dismutase sodA). Glutathione S-transferase, thioredoxin, glutaredoxins, and DNA repair enzymes responded most strongly to cadmium and chromate. The cadmium and chromium stress response also focused on reducing the intracellular metal concentration, with multiple efflux pumps employed to remove cadmium, while a sulfate transporter was down-regulated to reduce nonspecific uptake of chromium. Membrane proteins were also up-regulated in response to most of the metals tested. A two-component signal transduction system involved in the uranium response was identified. Several differentially regulated transcripts from regions previously not known to encode proteins were identified, demonstrating the advantage of evaluating the transcriptome by using whole-genome microarrays.

Adaptation, Physiological↗

PubMed2026

Single-cell and spatial transcriptomics define a progenitor subpopulation and fibroinflammatory niche at the leading edge of parathyroid carcinoma.

Parathyroid carcinoma (PC) is a rare but clinically aggressive endocrine malignancy with limited treatment options and a poorly defined tumor microenvironment (TME). To elucidate its cellular heterogeneity and spatial architecture, we integrated single-cell and spatial transcriptomic profiling with whole-exome sequencing and multiplex immunohistochemistry on eight parathyroid neoplasm specimens, including PC, parathyroid adenoma, and atypical parathyroid tumor. We identified a distinct progenitor-like endocrine subpopulation (Ca-1) enriched in CDC73-mutant PC, exhibiting stem-like properties, elevated cell cycle activity, and pronounced genomic instability. Spatial mapping revealed that Ca-1 cells preferentially localize at the leading edge, forming a fibroinflammatory niche characterized by the enrichment of inflammatory cancer-associated fibroblasts (iCAFs) and SPP1+ macrophages. Within this niche, the dipeptidyl peptidase 4 (DPP4) is selectively expressed in Ca-1 cells and iCAFs, implicating a potential paracrine axis driving stromal remodeling and immunosuppression. These findings suggest that a spatially organized ecosystem may promote PC progression through TME remodeling and highlight the DPP4-CXCL2 axis as a candidate pathway for future investigation in aggressive parathyroid neoplasms.

Humans↗

PubMed2026

Identification and characterization of non-canonical azole antifungal resistance pathways in Aspergillus fumigatus.

UNLABELLED: Human fungal infections, especially those caused by Aspergillus fumigatus, pose a significant global health threat, particularly in immunocompromised individuals. Azole antifungals are the primary treatment for this pathogen; however, the prevalence of azole-resistant A. fumigatus strains is steadily increasing. Mutations in cyp51A, which encodes an enzyme involved in ergosterol biosynthesis and the molecular target of the azoles, are well established to confer resistance in this fungal species. However, additional mechanisms governing resistance to this antifungal class remain understudied and poorly characterized, despite growing recognition of their importance in clinical resistance. In this study, we investigated the genetic basis of azole resistance in A. fumigatus isolates from clinical settings worldwide, with a particular focus on mechanisms independent of cyp51A (non-canonical). Using a combination of genomic and functional approaches, including whole-genome sequencing and transcriptomic analysis, we identified novel genetic variants and characterized population structure, advancing our understanding of the genetic diversity and evolutionary dynamics of resistance in A. fumigatus. By expanding our understanding of the complex genetic and molecular factors underlying azole resistance in this important human fungal pathogen, this research is poised to inform the development of novel antifungal strategies and contribute to global efforts to combat fungal infections. IMPORTANCE: Azole antifungals are the frontline therapy for infections caused by the opportunistic mold Aspergillus fumigatus, yet resistance to these drugs is rapidly increasing worldwide. Most studies have focused on mutations in cyp51A, the canonical target of azoles; however, a growing proportion of resistant clinical isolates lack these mutations, indicating that alternative resistance mechanisms are emerging. Here, we integrate population genomics, transcriptomics, and functional analyses across a global collection of isolates to define the architecture of cyp51-independent (non-canonical) azole resistance. We show that this resistance phenotype is strongly associated with a distinct population lineage and is driven by a highly polygenic network of metabolic, mitochondrial, and regulatory adaptations rather than single target site mutations. These isolates exhibit extensive transcriptional rewiring and metabolic remodeling under azole stress, suggesting distinct survival strategies beyond canonical resistance. Our findings reveal that azole resistance in A. fumigatus can evolve through diverse evolutionary routes and emphasize the need to monitor and therapeutically target non-canonical pathways that may increasingly contribute to antifungal treatment failure.

Aspergillus fumigatus↗

PubMed2026

A Cooperative Release of Mitochondrial DNA From Platelets and Neutrophils Drives an Interferon Signature in Systemic Sclerosis.

OBJECTIVE: Mitochondria are organelles with a hypomethylated circular genome. Mitochondrial DNA (mtDNA) in the systemic circulation has been implicated in inflammation. This study investigates the role of circulating DNA in systemic sclerosis (SSc) and the cellular mechanisms governing its release. METHODS: Total DNA was isolated from the plasma of healthy controls (HCs) and patients with SSc. Copy numbers were analyzed for mtDNA (ATP-6) and GAPDH abundance by quantitative real-time polymerase chain reaction. mtDNA was isolated from HCs and patients with SSc. Neutrophils and platelets were incubated with the plasma and mtDNA of patients with SSc, and neutrophil extracellular trap (NET) formation was assessed by SytoxGreen and immunostainings. Platelets were tested for mtDNA release propensity. DNA oxidation was evaluated by MitoSOX Red staining in vitro and 8-OHdG enzyme-linked immunosorbent assay (ELISA) of patient plasma. Plasma interferon (IFN) type 1 and chemokine (C-X-C motif) ligand 4 (CXCL4) were measured by ELISA. IFN signaling activation capacity was evaluated using THP-1 reporter cells and confirmed by a whole blood bulk RNA transcriptomic analysis. RESULTS: Median plasma mtDNA levels were 152-fold higher in patients with SSc compared with HCs, whereas nuclear DNA levels were similar. mtDNA from SSc plasma was highly oxidized. SSc-derived mtDNA efficiently promoted its own release by NETosis, most potently in the neutrophils of patients with SSc and by platelet activation. Oxidized mtDNA from SSc platelets in complex with CXCL4 further stimulated mtDNA release in both neutrophils and platelets. mtDNA plasma concentrations correlated with type I IFN concentrations in the blood of patients with SSc, and SSc blood exhibited elevated IFN-stimulated gene expression. SSc plasma-derived mtDNA-induced IFN signaling and NET formation via endosomal Toll-like receptors, cyclic GMP-AMP synthase/stimulator of IFN genes, and the JAK/STAT pathway. The type I IFN pathway further promoted NETosis and mtDNA release because IFN receptor and JAK inhibition antagonized the proNETotic effects of IFN. CONCLUSION: SSc plasma is characterized by highly abundant mtDNA, which drives feedback loops amplifying its own release from both neutrophils and platelets. Thus, mtDNA contributes to inflammation and tissue damage in SSc.

Humans↗

PubMed2006

Gene expression changes in human cells after exposure to mobile phone microwaves.

Possible biological effects of mobile phone microwaves were investigated in vitro. In this study, which was part of the 5FP EU project REFLEX (Risk Evaluation of Potential Environmental Hazards From Low-Energy Electromagnetic Field Exposure Using Sensitive in vitro Methods), six human cell types, immortalized cell lines and primary cells, were exposed to 900 and 1800 MHz. RNA was isolated from exposed and sham-exposed cells and labeled for transcriptome analysis on whole-genome cDNA arrays. The results were evaluated statistically using bioinformatics techniques and examined for biological relevance with the help of different databases. NB69 neuroblastoma cells, T lymphocytes, and CHME5 microglial cells did not show significant changes in gene expression. In EA.hy926 endothelial cells, U937 lymphoblastoma cells, and HL-60 leukemia cells we found between 12 and 34 up- or down-regulated genes. Analysis of the affected gene families does not point towards a stress response. However, following microwave exposure, some but not all human cells might react with an increase in expression of genes encoding ribosomal proteins and therefore up-regulating the cellular metabolism.

Cell Line↗

PubMed2026

Selenium nanoparticle synthesis in Stenotrophomonas maltophilia: Mutagenesis and molecular mechanisms.

Biosynthetic selenium nanoparticles (SeNPs) exhibit superior bioavailability and detoxification potential compared to inorganic selenium forms. In this study, the strain Stenotrophomonas maltophilia SE5, isolated from the feces of piglets (Duroc × Large White × Landrace), was utilized as the wild-type strain and subjected to atmospheric and room temperature plasma (ARTP) mutagenesis. A high-yielding mutant, Mu537, was successfully obtained, which exhibited an enhanced tolerance to sodium selenite, with its maximum tolerable concentration increasing from 1.0 g/L to 1.5 g/L. After 48 h of cultivation, Mu537 achieved an approximate 35% increase in SeNPs conversion rate and a 40% increase in SeNPs concentration relative to the parental strain. Integrated whole-genome sequencing and transcriptomic analysis revealed that pivotal genes associated with efficient SeNPs biosynthesis, including cysB, trxA, and sufE, were significantly up-regulated. These findings provide a systematic understanding of the potential molecular mechanisms driving enhanced SeNPs biosynthesis, offering both high-quality microbial resources and theoretical support for the industrial production of SeNPs.

Stenotrophomonas maltophilia↗

PubMed2024

Implications of noncoding regulatory functions in the development of insulinomas.

Insulinomas are rare neuroendocrine tumors arising from pancreatic β cells, characterized by aberrant proliferation and altered insulin secretion, leading to glucose homeostasis failure. With the aim of uncovering the role of noncoding regulatory regions and their aberrations in the development of these tumors, we coupled epigenetic and transcriptome profiling with whole-genome sequencing. As a result, we unraveled somatic mutations associated with changes in regulatory functions. Critically, these regions impact insulin secretion, tumor development, and epigenetic modifying genes, including polycomb complex components. Chromatin remodeling is apparent in insulinoma-selective domains shared across patients, containing a specific set of regulatory sequences dominated by the SOX17 binding motif. Moreover, many of these regions are H3K27me3 repressed in β cells, suggesting that tumoral transition involves derepression of polycomb-targeted domains. Our work provides a compendium of aberrant cis-regulatory elements affecting the function and fate of β cells in their progression to insulinomas and a framework to identify coding and noncoding driver mutations.

Humans↗

PubMed2002

Functional characterization of the antagonistic flagellar late regulators FliA and FlgM of Helicobacter pylori and their effects on the H. pylori transcriptome.

Helicobacter pylori is thought to regulate gene expression with a very small set of regulatory genes. We identified a previously unannotated open reading frame (ORF) in the H. pylori 26695 genome (HP1122) as a putative H. pylori flgM gene (sigma28 factor antagonist) by a motif-based bioinformatic approach. Deletion of HP1122 resulted in a fourfold increase in transcription of the sigma28-dependent major flagellin gene flaA, supporting the function of HP1122 as H. pylori FlgM. Helicobacter pylori FlgM lacks a conserved 20-amino-acid N-terminal domain of enterobacterial FlgM proteins, but was able to interact with the Salmonella typhimurium sigma28 (FliA) and inhibit the expression of FliA-dependent genes in Salmonella. Helicobacter pylori FlgM inhibited FliA to the same extent in a Salmonella strain with an intact flagellar export system and in an export-deficient strain. Helicobacter pylori FliA was able to drive transcription of FliA-dependent genes in Salmonella. The effects of mutations in the H. pylori flgM and fliA genes on the H. pylori transcriptome were analysed using whole genome DNA microarrays. The antagonistic roles of FlgM and FliA in controlling the transcription of the major flagellin gene flaA were confirmed, and two additional FliA/FlgM dependent operons (HP472 and HP1051/HP1052) were identified. None of the three genes contained in these operons has a known function in flagellar biogenesis in other bacteria. Like other motile bacteria, H. pylori has a FliA/FlgM pair of sigma and anti-sigma factors, but the genes controlled by these differ markedly from the Salmonella/Escherichia coli paradigm.

Amino Acid Sequence↗

PubMed2026

Changes of DNA methylation and gene expression profile in placental villi and chorioamniotic membranes under preeclampsia.

BACKGROUND: Preeclampsia (PE) is a serious pregnancy complication with elusive pathogenesis. Although epigenetic dysregulation is implicated, its layer-specific placental roles are poorly defined. This study aimed to identify shared and layer-specific epigenetic alterations in PE by profiling DNA methylation and gene expression in placental villi (PV) and chorioamniotic membranes (CAM). RESEARCH DESIGN AND METHODS: PV and CAM samples were collected from 7 normal and 8 PE pregnancies, and three public DNA methylation datasets (GSE98224, GSE44667, GSE75196) were integrated. Differentially methylated genes (DMGs) and differentially expressed genes (DEGs) were identified based on whole-genome methylation and transcriptome sequencing. Layer-specific and shared gene sets were identified by cross-analysis, with functional annotation using Gene Ontology (GO). RESULTS: EM-seq revealed a hypermethylation-dominant, tissue-specific methylation landscape in PE placentas. Cross-tissue comparison identified shared DMGs between the two layers, including nine key genes consistently altered in public datasets. Integrated analysis in PV further identified 22 co-dysregulated genes, enriched in thermoregulation, maternal-fetal immunity, signal transduction, and cell differentiation. CONCLUSIONS: This study elucidates the shared and layer-specific dysregulation of gene networks at methylomic and transcriptomic levels in PE placenta. Comparing PV and CAM highlights placental epigenetic heterogeneity and dysfunction, offering novel clues for mechanistic research and layer-targeted therapies.

Humans↗

PubMed2006

Taking the first steps towards a standard for reporting on phylogenies: Minimum Information About a Phylogenetic Analysis (MIAPA).

In the eight years since phylogenomics was introduced as the intersection of genomics and phylogenetics, the field has provided fundamental insights into gene function, genome history and organismal relationships. The utility of phylogenomics is growing with the increase in the number and diversity of taxa for which whole genome and large transcriptome sequence sets are being generated. We assert that the synergy between genomic and phylogenetic perspectives in comparative biology would be enhanced by the development and refinement of minimal reporting standards for phylogenetic analyses. Encouraged by the development of the Minimum Information About a Microarray Experiment (MIAME) standard, we propose a similar roadmap for the development of a Minimal Information About a Phylogenetic Analysis (MIAPA) standard. Key in the successful development and implementation of such a standard will be broad participation by developers of phylogenetic analysis software, phylogenetic database developers, practitioners of phylogenomics, and journal editors.

Genomics↗

PubMed2005

Role of the regulatory gene rirA in the transcriptional response of Sinorhizobium meliloti to iron limitation.

A regulatory network of Sinorhizobium meliloti genes involved in adaptation to iron-limiting conditions and the involvement of the rhizobial iron regulator gene (rirA) were analyzed by mutation and microarray analyses. A constructed S. meliloti rirA mutant exhibited growth defects and enhanced H2O2 sensitivity in the presence of iron, but symbiotic nitrogen fixation was not affected. To identify iron-responsive and RirA-regulated S. meliloti genes, a transcriptome approach using whole-genome microarrays was used. Altogether, 45 genes were found to be jointly derepressed by mutation of rirA and under different iron-limited conditions. As expected, a number of genes involved in iron transport (e.g., hmuPSTU, shmR, rhbABCDEF, rhtX, and rhtA) and also genes with predicted functions in energy metabolism (e.g., fixN3, fixP3, and qxtAB) and exopolysaccharide production (e.g., exoY and exoN) were found in this group of genes. In addition, the iron deficiency response of S. meliloti also involved rirA-independent expression changes, including repression of the S. meliloti flagellar regulon. Finally, the RirA modulon also includes genes that are not iron responsive, including a gene cluster putatively involved in Fe-S cluster formation (sufA, sufS, sufD, sufC, and sufB).

Bacterial Proteins↗