SEARCH · Search PubMed

Results for “transcriptome analysis”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

SourceResearch connectionFrom yearThrough year

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,495 records · Page 83Linked to original sources

PubMed2026

Unraveling 'F' factor: towards a genetic-clinical framework for the musculoskeletal-heart crosstalk in metabolic aging.

BACKGROUND: The rising co-occurrence of cardiometabolic diseases and musculoskeletal degeneration poses a critical challenge to healthy aging, yet the shared biological mechanisms underlying this multimorbidity remain poorly defined. This study aimed to establish an integrative clinical-genetic framework to elucidate the common frailty factor, the 'F' factor, that captures the systemic vulnerability linking cardiometabolic multimorbidity (CMM) and musculoskeletal aging. METHODS: Utilizing the prospective China Health and Retirement Longitudinal Study (CHARLS) cohort, we developed and validated novel Frailty-Integrated Indices for CMM risk prediction, evaluated with machine learning models interpreted via SHapley Additive exPlanations (SHAP). Independently, we applied genomic structural equation modeling (Genomic-SEM) to integrate genome-wide association data from six traits-coronary artery disease, type 2 diabetes, hypertension, bone mineral density, frailty, and telomere length-to model a shared latent genetic factor ('F' factor). This was followed by multivariate GWAS, fine-mapping, transcriptome-wide association study (TWAS), gene-based analysis, and functional annotation to prioritize causal genes, pathways, and cell types. RESULTS: Clinically, several Frailty-Integrated Indices significantly improved CMM risk prediction, with the optimal model achieving an AUC of 0.727. Genetically, we modeled a significant shared latent genetic factor ('F' factor), pinpointing novel risk loci and implicating key genes such as APOE and SLC22A3. These genes were enriched in pathways including cellular senescence and cholesterol metabolism and showed specific expression patterns in developmental brain stages and across multi-organ endothelial cells. CONCLUSION: Our findings provide converging evidence for Musculoskeletal‑Heart crosstalk of metabolic aging and inferred the 'F' factor as a genetic correlate of a transdiagnostic state, which links genetic predisposition to metabolic dysregulation, and systemic functional decline. This work provides a multi-level biological characterization of multimorbidity liability, informing early-risk detection and preventive strategies for complex aging-related comorbidities.

Humans↗

PubMed2026

Amino-acids-mTORC1-driven DDA1 phosphorylation promotes DNA repair and glioblastoma progression.

BACKGROUND: DDA1 is a protein involved in protein degradation, cell cycle regulation, and DNA damage repair. Although its expression varies across tumor types, the precise role of DDA1 in gliomagenesis remains unclear. METHODS: We investigated the function of DDA1 in multiple glioblastoma cell models using biochemical assays, phosphorylation analysis, subcellular localization studies, and integrated genomic and transcriptomic profiling to determine its signaling interactions and downstream effects. RESULTS: We identified a physical association between cytoplasmic DDA1 and Raptor, a core component of lysosome-associated mTORC1. Amino acid stimulation triggered phosphorylation of DDA1 at serine 33 promoting its nuclear translocation and involvement in DNA damage repair. Integrated transcriptomic analyses revealed that the mTORC1-DDA1S33-DNA repair axis regulates the expression of a subset of metabolic genes, including ENO2, CA12, and NMRK1. Functional assays further suggested that these genes contribute to the survival capacity of glioblastoma cells, particularly under DDA1-deficient conditions. Consistently, DDA1 deficiency markedly impaired glioblastoma growth and induced compensatory upregulation of metabolic activity. CONCLUSION: Our findings identify DDA1 as a previously unrecognized phosphorylation target downstream of mTORC1 and a critical mediator of the mTORC1 driven DNA damage response. Through its involvement in DNA repair and metabolic gene regulation, DDA1 appears to support glioblastoma progression, providing mechanistic insight into mTORC1 related gliomagenesis and suggesting potential therapeutic relevance.

Glioblastoma↗

PubMed2026

Complement expression profiles in human glomerular mesangial cells, endothelial cells, podocytes and proximal tubular epithelial cells.

BACKGROUND: Local expression of complement components in the kidney has been reported sporadically in both diseased and normal kidneys. This study aimed to comprehensively characterize the expression of complement components in human glomerular mesangial cells (GMCs), glomerular endothelial cells (GECs), podocytes, and proximal tubular epithelial cells (PTECs) in non-diseased renal tissue. METHODS: Complement expression in cultured human renal intrinsic cells was initially evaluated using reverse transcription polymerase chain reaction and immunofluorescence staining. These findings were further examined using publicly available single-cell RNA-sequencing datasets and 10×Genomics single-cell RNA sequencing of non-diseased human kidney tissue. The analyses focused on complement components involved in the initiation of the classical, lectin, and alternative pathways, as well as components shared among these activation pathways, terminal pathway components, complement regulators, and complement receptors. RESULTS: Complement components unique to the initial phase for classical pathway (C1S, C1R, C2, C4), lectin pathway (MBL2, FCN1, MASP1), alternative pathway (CFB, CFD), and the C3 component shared by the three activation pathways were detected in these cells. The components shared by the terminal pathways including C5, C6, C7, C8 and C9 exhibited lower expression, while complement regulators (CFH, CFI, CD55/DAF, CD46/MCP, CD59, C4BPB, PROS1/Protein S) or receptors (CD93/C1QR1, CR1), particularly membrane-bound proteins, such as DAF, MCP and CD59, which inhibit complement activation and the formation of the membrane attack complex, showed relatively high expression. CONCLUSION: These results showed that all four types of intrinsic renal cells expressed multiple complement components associated with the classical, lectin, and alternative pathways. In non-diseased kidney tissue, complement regulatory molecules involved in the control of complement activation showed relatively higher expression, whereas components of the terminal complement pathway were expressed at relatively lower levels, suggesting that renal intrinsic cells maintain a locally poised but tightly regulated complement system.

Humans↗

PubMed2003

[Changes in the gene expression profile of the left heart ventricle during growth in the rat].

Wistar rats of 8, 10 and 12-week-old were chosen for study of the relationship between cardiac growth and its gene expression profile changes during maturation. The ultrasonic parameters of rat hearts were recorded before sacrifice, then total RNA of left ventricle were extracted and gene expression profiles were analyzed by cDNA microarray. During growth from 8 weeks to 12 weeks, the body weight increased by 45.5% (287+/-13 g vs 197+/-10 g), and the increment in the first two-week period was equal to that of the second two-week period. The mass of left ventricle and the posterior wall thickness increased by 27.7% (0.60+/-0.03 g vs 0.47+/-0.02 g) and 23.6% (2.04+/-0.04 mm vs 1.65+/-0.13 mm), respectively, and their increment in the first two-week period was much more than that in the second one. Meanwhile, the gene expression profile of the left ventricle changed significantly, which involved cellular structure, metabolism, oxidative stress, signal transduction, etc. Compared with the 8-week-old rats, these genes were mostly up-regulated in 10-week-old rats, while for 12-week-old rats, the gene expression profile of the left ventricle recovered to the pattern of 8-week-old rats again on the whole. These results suggest that the relationship between the changes in cardiac function and gene expression profile can be analyzed comprehensively with the technique of microarray, and that the changes in gene expression profile of the left ventricle during rat maturation adapt to the physiological growth of heart, which is of benefit for keeping the metabolism balance between materials and energy.

Animals↗

PubMed2005

[Analysis on tumor related gene expression profiles in benzene poisoning using cDNA microarray].

OBJECTIVE: To detect target genes for further study by way of analyzing the gene expression profiles of benzene poisoning by using cDNA microarray. METHODS: Peripheral mononuclear cells were isolated from seven patients with benzene poisoning of different degrees, and sevene age-and sex-matched normal subjects. Total RNA was extracted and purified, followed by revese transcription to cDNAs with concomitant incorporation of fluorescent dCTP (Cy3 or Cy5). The cDNAs were used as probes in microarray of 2780 cloned cDNA. Fluorescent signals were scanned to detect genes differentially expressed in patients and normal subjects. RESULTS: Among 7 pieces of cDNA microarray of 2780 tumour related genes, the expression of 16 genes, such as GRO1, TGFBR3, LYN ctc was upregulated, whereas the expression of 28 genes, such as FOSB, DJ-1, MCT-1 etc was down-regulated. CONCLUSION: Abnormal expression of tumour related genes of patients exposed to benzene suggests that they may be the key genes, which play important role in benzene-induced leucocythemia. cDNA microarray technique is useful to indicate the expression mode of benzene poisoning tumour related genes, and to find rapidly and effectively new research object and the way of gene therapy.

Benzene↗

PubMed2005

The transcriptional response of human endothelial cells to infection with Bartonella henselae is dominated by genes controlling innate immune responses, cell cycle, and vascular remodelling.

The bacterial pathogen Bartonella henselae (Bh) is responsible for a broad range of clinical manifestations, including the formation of vascular tumours as the result of pathogen-triggered vasoproliferation. In vitro, the interaction of Bh with human umbilical vein endothelial cells (Huvec) involves (i) cytoskeletal rearrangements in conjunction with bacterial internalization, (ii) nuclear factor kappaB (NFkappaB)-dependent proinflammatory activation, (iii) the inhibition of apoptosis, and (iv) the modulation of angiogenic properties such as proliferation, migration, and tubular differentiation. To study the transcriptional signature of these pathogen-triggered changes of Huvec, we performed transcriptional profiling with Affymetrix U133 GeneChips. At 6 h or 30 h of infection, a total of 706 genes displayed a clear and statistically significant change of expression (>2.5-fold, t-test p-value<0.05). These included 314 up-regulated genes dominated by the innate immune response. The gene list comprises subsets of tumour necrosis factor alpha (TNFalpha, 99 genes) and interferon alpha (IFNalpha, 30 genes) inducible genes, which encode components of the NF-kappaB-dependent proinflammatory response and the type I IFN-dependent anti-infective response, respectively. The remaining set of 197 up-regulated genes mirrors other cellular changes induced by Bh, in particular proliferation and proangiogenic activation. The set of 362 down-regulated genes includes 41TNFalpha - or IFNalpha-suppressible genes, and 52 genes involved in cell cycle control or progression. This comprehensive analysis of Bh-triggered changes of the Huvec transcriptome identified candidate genes putatively involved in controlling innate immune responses, cell cycle, and vascular remodelling, and may thus provide the basis for functional studies of the molecular mechanisms underlying these pathogen-induced cellular processes.

Bartonella henselae↗

PubMed2005

Marine genomics: a clearing-house for genomic and transcriptomic data of marine organisms.

BACKGROUND: The Marine Genomics project is a functional genomics initiative developed to provide a pipeline for the curation of Expressed Sequence Tags (ESTs) and gene expression microarray data for marine organisms. It provides a unique clearing-house for marine specific EST and microarray data and is currently available at http://www.marinegenomics.org. DESCRIPTION: The Marine Genomics pipeline automates the processing, maintenance, storage and analysis of EST and microarray data for an increasing number of marine species. It currently contains 19 species databases (over 46,000 EST sequences) that are maintained by registered users from local and remote locations in Europe and South America in addition to the USA. A collection of analysis tools are implemented. These include a pipeline upload tool for EST FASTA file, sequence trace file and microarray data, an annotative text search, automated sequence trimming, sequence quality control (QA/QC) editing, sequence BLAST capabilities and a tool for interactive submission to GenBank. Another feature of this resource is the integration with a scientific computing analysis environment implemented by MATLAB. CONCLUSION: The conglomeration of multiple marine organisms with integrated analysis tools enables users to focus on the comprehensive descriptions of transcriptomic responses to typical marine stresses. This cross species data comparison and integration enables users to contain their research within a marine-oriented data management and analysis environment.

Animals↗

PubMedDate not supplied

[Global analysis strategies. Toward the genetic management of neoplasias].

Biomedical research in oncological diseases, particularly focused on the study and understanding of the molecular mechanisms involved in cellular transformation, is opening new possibilities for the development of new and more efficient strategies for diagnosis and treatment. The generation and practical application of the results derived from molecular genetic studies in cancer, has evolved in parallel with the development of technological tools that allow us to get a global vision of diverse cellular processes, both in the normal and pathological states. This combination of basic research and technological application, has created methodologies that allow us to analyze the three principal levels of Molecular Genetics, the Genome (DNA, archive of the genetic information), the Transcriptome (RNA, expression of the genetic information), and finally, the Proteome (proteins, functional aspect of the genetic information). The vast amount of information obtained due to these advancements has begun to modify our fundamental vision about oncological diseases, and together with the traditional analytic tools, they hold the promise of changing the ways we classify, detect, diagnose and treat cancer. In this review, we present some of this methods for global genetic analysis, involving the three levels of genetic organization: the genome, with the Human Genome Project, comparative genomic hybridization and chromosome painting; the Transcriptome, with Serial analysis of Gene Expression and DNA microarrays; and the proteome, with bidimensional protein electrophoresis and antibody-microarrays. In each case, together with a brief description of the method, we also present the impact of every one of them on the study and management of neoplastic diseases.

Chromosome Painting↗

PubMed2004

A global approach combining proteome analysis and phenotypic screening with RNA interference yields novel apoptosis regulators.

Global approaches like proteome or transcriptome analyses have been performed extensively to identify candidate genes or proteins involved in biological and pathological processes. Here we describe the identification of proteins implicated in the regulation of apoptosis using proteome analysis and the functional validation of targets by RNA interference. A high-throughput platform for the validation of synthetic small interfering RNAs (siRNAs) by quantitative real-time PCR was established. Genes of the identified factors were silenced by automated siRNA transfection, and their role in apoptotic signaling was investigated. Using this strategy, nine new modulators of apoptosis were identified. A subsequent detailed study demonstrated that hepatoma-derived growth factor (HDGF) is required for TNFalpha-induced release of pro-apoptotic factors from mitochondria. The strategy described here may be used for hypothesis-free, global gene function analysis.

Apoptosis↗

PubMed2005

In silico genome-scale reconstruction and validation of the Staphylococcus aureus metabolic network.

A genome-scale metabolic model of the Gram-positive, facultative anaerobic opportunistic pathogen Staphylococcus aureus N315 was constructed based on current genomic data, literature, and physiological information. The model comprises 774 metabolic processes representing approximately 23% of all protein-coding regions. The model was extensively validated against experimental observations and it correctly predicted main physiological properties of the wild-type strain, such as aerobic and anaerobic respiration and fermentation. Due to the frequent involvement of S. aureus in hospital-acquired bacterial infections combined with its increasing antibiotic resistance, we also investigated the clinically relevant phenotype of small colony variants and found that the model predictions agreed with recent findings of proteome analyses. This indicates that the model is useful in assisting future experiments to elucidate the interrelationship of bacterial metabolism and resistance. To help directing future studies for novel chemotherapeutic targets, we conducted a large-scale in silico gene deletion study that identified 158 essential intracellular reactions. A more detailed analysis showed that the biosynthesis of glycans and lipids is rather rigid with respect to circumventing gene deletions, which should make these areas particularly interesting for antibiotic development. The combination of this stoichiometric model with transcriptomic and proteomic data should allow a new quality in the analysis of clinically relevant organisms and a more rationalized system-level search for novel drug targets.

Computational Biology↗

PubMed2006

Deciphering B-ZIP transcription factor interactions in vitro and in vivo.

Over the last 15 years, numerous studies have addressed the structural rules that regulate dimerization stability and dimerization specificity of the leucine zipper, a dimeric parallel coiled-coil domain that can either homodimerize or heterodimerize. Initially, these studies were performed with a limited set of B-ZIP proteins, sequence-specific DNA binding proteins that dimerize using the leucine zipper domain to bind DNA. A global analysis of B-ZIP leucine zipper dimerization properties can be rationalized using a limited number of structural rules [J.R. Newman, A.E. Keating, Comprehensive identification of human bZIP interactions with coiled-coil arrays, Science 300 (2003) 2097-2101]. Today, however, access to the genomic sequences of many different organisms has made possible the annotation of all B-ZIP proteins from several species and has generated a bank of data that can be used to refine, and potentially expand, these rules. Already, a comparative analysis of the B-ZIP proteins from Arabidopsis thaliana and Homo sapiens has revealed that the same amino acids are used in different patterns to generate diverse B-ZIP dimerization patterns [C.D. Deppmann, A. Acharya, V. Rishi, B. Wobbes, S. Smeekens, E.J. Taparowsky, C. Vinson, Dimerization specificity of all 67 B-ZIP motifs in Arabidopsis thaliana: a comparison to Homo sapiens B-ZIP motifs, Nucleic Acids Res. 32 (2004) 3435-3445]. The challenge ahead is to investigate the biological significance of different B-ZIP protein-protein interactions. Gaining insight at this level will rely on ongoing investigations to (a) define the role of target DNA on modulating B-ZIP dimerization partners, (b) characterize the B-ZIP transcriptome in various cells and tissues through mRNA microarray analysis, (c) identify the genomic localization of B-ZIP binding at a genomic level using the chromatin immunoprecipitation assay, and (d) develop more sophisticated imaging technologies to visualize dimer dynamics in single cells and whole organisms. Studies of B-ZIP family leucine zipper dimerization and the regulatory mechanisms that control their biological activities could serve as a paradigm for deciphering the biophysical and biological parameters governing other well-characterized protein-protein interaction motifs. This review will focus on the dimerization specificity of coiled-coil proteins, particularly the human B-ZIP transcription family that consists of 53 proteins that use the leucine zipper coiled-coil as a dimerization motif.

Amino Acid Motifs↗

PubMed2003

Composition and dynamics of the Caenorhabditis elegans early embryonic transcriptome.

Temporal profiles of transcript abundance during embryonic development were obtained by whole-genome expression analysis from precisely staged C. elegans embryos. The result is a highly resolved time course that commences with the zygote and extends into mid-gastrulation, spanning the transition from maternal to embryonic control of development and including the presumptive specification of most major cell fates. Transcripts for nearly half (8890) of the predicted open reading frames are detected and expression levels for the majority of them (>70%) change over time. The transcriptome is stable up to the four-cell stage where it begins rapidly changing until the rate of change plateaus before gastrulation. At gastrulation temporal patterns of maternal degradation and embryonic expression intersect indicating a mid-blastula transition from maternal to embryonic control of development. In addition, we find that embryonic genes tend to be expressed transiently on a time scale consistent with developmental decisions being made with each cell cycle. Furthermore, overall rates of synthesis and degradation are matched such that the transcriptome maintains a steady-state frequency distribution. Finally, a versatile analytical platform based on cluster analysis and developmental classification of genes is provided.

Animals↗

PubMed2026

Chronic ethanol exposure alters the expression of genes associated with GPCR-related signaling in the olfactory bulb of male mice.

Chronic ethanol exposure, a key feature of alcohol use disorder (AUD), can affect the nervous system, but its molecular impact on the olfactory bulb remains unclear. In this study, an intermittent two-bottle voluntary drinking model was established in male mice, and transcriptome sequencing was performed on olfactory bulb tissues. DESeq2 analysis identified 188 differentially expressed genes, including 68 upregulated and 120 downregulated genes. Kyoto Encyclopedia of Genes and Genomes (KEGG) and Reactome pathway database (Reactome) analyses indicated that ethanol-responsive genes were predominantly enriched in receptor-mediated signaling pathways, particularly those linked to G protein-coupled receptor (GPCR) signaling. Protein-protein interaction analysis further identified eight core GPCR-related genes. Quantitative real-time PCR (qRT-PCR) validation revealed that Cxcl10, Grp, Pcp2, and Pdyn were markedly downregulated in the ethanol group. These results suggest that chronic ethanol exposure is associated with transcriptional alterations in the male mouse olfactory bulb and may selectively affect several GPCR-related signaling components. This study provides candidate molecular evidence for further investigation of ethanol-associated olfactory dysfunction.

Chronic ethanol exposure↗

PubMed2003

Integration of proteomics and genomics in platelets: a profile of platelet proteins and platelet-specific genes.

Platelets, while anucleate, contain RNA, some of which is translated into protein upon activation. Hypothesising that the platelet proteome is reflected in the transcriptome, we identified 82 proteins secreted from activated platelets and compared these, as well as published proteomic data, to the transcriptional profile. We also compared the transcriptome of platelets to other tissues to identify platelet-specific genes and used ontology to determine gene categories over-represented in platelets. RNA was isolated from highly pure platelet preparations for hybridization to Affymetrix oligonucleotide arrays. We identified 2,928 distinct messages as being present in platelets. The platelet transcriptome was compared with the proteome by relating both to UniGene clusters. Platelet proteomic data correlated well with the transcriptome, with 69% of secreted proteins detectable at the mRNA level, and similar concordance was obtained using two published datasets. While many of the most abundant mRNAs are for known platelet proteins, messages were detected for proteins not previously reported in platelets. Some of these may represent residual megakaryocyte messages; however, proteomic analysis confirmed the expression of many previously unreported genes in platelets. Transcripts for well-described platelet proteins are among the most platelet-specific messages. Ontological categories related to signal transduction, receptors, ion channels, and membranes are over-represented in platelets, while categories involved in protein synthesis are depleted. Despite the absence of gene transcription, the platelet proteome is mirrored in the transcriptome. Conversely, transcriptional analysis predicts the presence of novel proteins in the platelet. Transcriptional analysis is relevant to platelet biology, providing insights into platelet function and the mechanisms of platelet disorders.

Blood Platelets↗

PubMed2026

CpG hypermethylation and WNT/AP-1 cooperativity define the epigenetic landscape and a clinical subgroup of high-risk pediatric adrenocortical carcinoma.

Pediatric adrenocortical tumors are rare, clinically heterogeneous neoplasms with unpredictable outcomes and limited treatment options. Through integrated multi-omic analysis of 214 pediatric adrenocortical tumors combining DNA methylation profiling, transcriptomics, chromatin accessibility, and spatial deconvolution, we identify four distinct risk groups. A high-risk subgroup is characterized by CpG island hypermethylation, chromosomal instability, and dismal survival. These tumors exhibit transcriptional co-activation of WNT signalling and activator protein-1 transcriptional programs and display balanced admixture of zona glomerulosa and zona fasciculata/reticularis-like cells. Spatial analysis reveals zona glomerulosa cells as WNT signaling hubs driving intercellular crosstalk. Mechanistically, the histone deacetylase inhibitor entinostat reverses promoter methylation, silences activator protein-1 activity, and induces apoptotic reprogramming in tumor models. These findings establish a molecular framework for risk stratification and identify actionable therapeutic vulnerabilities, providing an essential resource for studying this molecularly uncharted pediatric malignancy.

Humans↗

PubMed2026

Integrative Cross-platform Analysis of Kinase Inhibitor Effects on Statin-relevant Cardioprotective Pathways in Human Cardiomyocytes.

BACKGROUND/AIM: Kinase inhibitors (KIs) can cause cardiotoxicity through mechanisms overlapping with statin cardioprotective pathways, yet their effects on these pathways in cardiomyocytes remain uncertain. We evaluated six literature-defined statin-relevant gene sets using transcriptomic and proteomic data. MATERIALS AND METHODS: Pre-ranked gene set enrichment analysis was performed for 23 KIs in primary cardiac cells (GSE146096; n=319) and iPSC-derived cardiomyocytes (GSE217421; n=541), with cross-platform analysis of 21 KIs by shotgun proteomics (PXD014791; n=300). Pathway-specific concordance was assessed by Spearman correlation with Benjamini-Hochberg correction; protein scores were estimated after adjustment for cell line. RESULTS: KI effects were heterogeneous. The anti-fibrotic pathway showed nominal concordance across the two transcriptomic datasets (ρ=0.495, p=0.016, q=0.098; 91% direction concordance) and significant cell-line-adjusted transcriptomic-proteomic concordance (ρ=0.644, p=0.0016, q=0.0081). Nilotinib reproducibly upregulated NF-κB pathway genes [normalized enrichment score (NES)=+2.29 and +2.18 in discovery and validation], with targeted inter-gene-correlation-adjusted testing supporting higher NF-κB expression than under rosuvastatin (CAMERA p=3.54×10-8). No global cross-omics summary remained significant after harmonizing pathway universes and accounting for repeated pathways. CONCLUSION: KI effects on statin-relevant pathways were pathway-specific. Anti-fibrotic concordance and nilotinib-associated NF-κB upregulation are hypothesis-generating candidates for experimental validation.

Humans↗

PubMed2005

Protein encoding genes in an ancient plant: analysis of codon usage, retained genes and splice sites in a moss, Physcomitrella patens.

BACKGROUND: The moss Physcomitrella patens is an emerging plant model system due to its high rate of homologous recombination, haploidy, simple body plan, physiological properties as well as phylogenetic position. Available EST data was clustered and assembled, and provided the basis for a genome-wide analysis of protein encoding genes. RESULTS: We have clustered and assembled Physcomitrella patens EST and CDS data in order to represent the transcriptome of this non-seed plant. Clustering of the publicly available data and subsequent prediction resulted in a total of 19,081 non-redundant ORF. Of these putative transcripts, approximately 30% have a homolog in both rice and Arabidopsis transcriptome. More than 130 transcripts are not present in seed plants but can be found in other kingdoms. These potential "retained genes" might have been lost during seed plant evolution. Functional annotation of these genes reveals unequal distribution among taxonomic groups and intriguing putative functions such as cytotoxicity and nucleic acid repair. Whereas introns in the moss are larger on average than in the seed plant Arabidopsis thaliana, position and amount of introns are approximately the same. Contrary to Arabidopsis, where CDS contain on average 44% G/C, in Physcomitrella the average G/C content is 50%. Interestingly, moss orthologs of Arabidopsis genes show a significant drift of codon fraction usage, towards the seed plant. While averaged codon bias is the same in Physcomitrella and Arabidopsis, the distribution pattern is different, with 15% of moss genes being unbiased. Species-specific, sensitive and selective splice site prediction for Physcomitrella has been developed using a dataset of 368 donor and acceptor sites, utilizing a support vector machine. The prediction accuracy is better than those achieved with tools trained on Arabidopsis data. CONCLUSION: Analysis of the moss transcriptome displays differences in gene structure, codon and splice site usage in comparison with the seed plant Arabidopsis. Putative retained genes exhibit possible functions that might explain the peculiar physiological properties of mosses. Both the transcriptome representation (including a BLAST and retrieval service) and splice site prediction have been made available on http://www.cosmoss.org, setting the basis for assembly and annotation of the Physcomitrella genome, of which draft shotgun sequences will become available in 2005.

Alternative Splicing↗

PubMed2005

SuperSAGE.

The application of transcriptomics to study host-pathogen interactions has already brought important insights into the mechanisms of pathogenesis, and is expanding further keeping pace with the accumulation of genomic sequences of host organisms (human and economically important organisms such as food crops) and their pathogens (viruses, bacteria, fungi and protozoa). In this review, we introduce SuperSAGE, a substantially improved variant of serial analysis of gene expression (SAGE), as a potent tool for the transcriptomics of host-pathogen interactions. Notably, the generation of 26 bp tags in the SuperSAGE procedure allows to decipher the 'interaction transcriptome', i.e. the simultaneous monitoring of quantitative gene expression, of both a host and one of its eukaryotic pathogens. The potential of SuperSAGE tags for a rapid functional analysis of target genes is also discussed.

Animals↗