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Moreira, F.

Publications and source records attributed to Moreira, F..

16 recordsLinked to original sources

Escherichia coli-induced gut IL-33 release inhibits lung type 2 allergic responses

BackgroundThe incidence of lung allergies is reduced in countries with higher prevalence of infection and environmental exposure to microbes. However, enteric bacterial infections do not always correlate with lower incidence of allergic disorders and how lung immunity to allergens can be regulated by gut exposure to pathogens and their toxins is not fully understood. ObjectiveWe used mouse models of enterotoxigenic Escherichia coli (ETEC) infection and lung allergy to examine how gut exposure to bacteria, or their related toxins, affects allergic lung inflammation. MethodsNaive C57BL/6 mice were infected with enterotoxigenic Escherichia coli (ETEC) or orally treated with the ETEC LT toxin, to mimic enteric bacterial infections. After two weeks, these mice were treated intranasally with Ovalbumin (OVA) and Papain or IL-33, followed by challenge with OVA, to induce allergic lung inflammation that was assessed using multiple readouts. ResultsGut exposure to ETEC significantly inhibited allergic lung inflammation in a LT-dependent manner, as demonstrated by reduced tissue inflammation, less accumulation of type 2 cytokines, and reduced lung numbers of type 2 immune cells such as type 2 innate lymphoid cells (ILC2) and eosinophils. The anti-allergic capacity of LT was associated with reduced ability of lung ILC2s to recognize IL-33. Counterintuitively, deletion of either IL-33 or ILC2s significantly reverted the LT protective effect, suggesting the LT-mediated protection may occur through gut release and local sensing of IL-33. ConclusionsExposure to ETEC protects hosts against allergic lung inflammation through a negative feedback loop regulated by gut IL-33 release and sensing, suggesting a possible new immunological mechanism for reduced lung allergy incidence observed in areas with enteric bacterial infections. Key Messages- Enteric exposure to enterotoxigenic E. coli (ETEC) bacteria or its toxin LT significantly protects hosts against lung type 2 allergic inflammation. - ETEC and LT downregulate the capacity of lung ILC2s to respond to allergen-induced IL-33. - Deletion of IL-33 or ILC2s significantly impairs the protective effect of ETEC and LT, suggesting the presence of a negative feedback loop driven by toxin-induced gut IL-33 release.

immunology↗

Transcriptional Signatures of Field Cancerization in Gastric Cancer

The high rate of local recurrence in gastric adenocarcinoma (GA) suggests that carcinogenesis is not a focal event but a field-wide process. This phenomenon, known as "field cancerization," posits that histologically normal peritumoral tissue is, in fact, a pre-neoplastic field harboring incipient molecular alterations that confound genomic studies using it as a normal control. To overcome this limitation, we performed a three-way comparative transcriptomic analysis of tumor, peritumoral, and true-normal gastric tissues using a deep learning framework. We identified a stable 138-gene signature established within the peritumoral field and conserved in the tumor, which was absent in healthy controls. Within this signature, three key COSMIC-listed driver genes were highlighted: the Hippo pathway component FAT4 and the p53-inhibitor MDM4 were upregulated, while the EMT-suppressor NDRG1 was repressed. Co-expression analysis revealed a dynamic rewiring of these drivers, with a significant positive correlation between FAT4 and MDM4 emerging exclusively in the peritumoral field. In contrast, a negative correlation between FAT4 and NDRG1 was observed specifically in the tumor context. In public cohorts, high expression of FAT4 and MDM4 was significantly associated with poor patient prognosis, whereas NDRG1 showed no prognostic association. Critically, the prognostic power of MDM4 was validated in our local patient cohort. Our findings demonstrate that the peritumoral field is a molecularly distinct state in gastric carcinogenesis, characterized by a metabolic shift, and identify FAT4 and MDM4 as key drivers of this early transition, with significant potential as prognostic biomarkers.

genetics↗

Cancer-Testis Antigens as Clinical and Prognostic Biomarkers in Gastric Adenocarcinoma: Integration of Differential Expression, Clinical Associations, Survival, and Co-Expression Networks

Gastric adenocarcinoma (GAC) remains one of the leading causes of cancer-related mortality, characterized by marked molecular and clinical heterogeneity, which underscores the need for robust biomarkers. In this study, we aimed to evaluate the role of cancer-testis antigens (CTAs) in GAC through integrated analyses of differential expression, clinical associations, survival impact, and gene co-expression networks. The cohort included 156 patients with complete clinical data, comprising a total of 362 tissue samples (tumor, peritumoral, and metaplastic). We identified 541 differentially expressed genes, of which 49 corresponded to previously described CTAs. Between GAC and peritumoral tissues, 14 CTAs exhibited significant differential expression, with MAGEA3, MAGEA6, GOLGA6L1, and MAGEA2 among the most highly expressed in tumors. Relevant associations were observed between the expression of MAGEA3, MAGEA6, POTEF, and CTCFL with TNM staging, as well as IGF2BP1, DAZ1/3/4, YBX2, and PCDHA4 in relation to variables such as tumor depth, metastasis, and TCGA subtypes. Survival analysis demonstrated that high expression of IGF2BP1, CTCFL, CT45A5, and LIN28B was strongly associated with worse prognosis (HR > 2.7), whereas SYCE1L, PIK3R3, and ZNF683 showed a protective effect. The co-expression network revealed five main clusters, highlighting germline-related modules (MAGEA, DAZ, CSAG), adhesion and transcriptional regulation (YBX2, POTEF, PCDHA, TAF1L), and immune-related genes (IRAK3, CXCR1, PIK3R3), evidencing functional integration between proliferation, adhesion, and immune microenvironment modulation. Collectively, these findings reinforce CTAs as potential clinical and prognostic biomarkers in GAC, with direct implications for risk stratification and the development of personalized therapeutic strategies.

cancer biology↗

Transcriptomic Mutational Profiling of Gastric Adenocarcinoma in Northern Brazil

Gastric cancer (GC) remains among the neoplasms with the worst prognosis, partly due to its biological heterogeneity and the scarcity of robust biomarkers. The characterization of mutational profiles from transcripts can reveal specific tumor signatures and point to therapeutic targets. This study investigated the landscape of mutations expressed in 102 samples of gastric adenocarcinoma from northern Brazil, which were sequenced using NGS. Readings were aligned to the reference genome using STAR (two-pass mode), and variants were called with GATK and VarDict. Annotations and impact predictions were generated using VEP, SIFT, and PolyPhen. We identified >90,000 variants; among the most frequently mutated genes, FTH1 stood out. The mutational profile was described using maftools, and signatures were inferred with MutationalPatterns. We observed a predominant distribution of SNVs, with C>T transitions as the most common event, in addition to patterns compatible with signatures related to replication damage and DNA repair. To mitigate biases inherent to RNA-seq, we applied filters for coverage, strand bias, and RNA editing hotspots. Together, the data outline a regional landscape of mutations expressed in GC and reinforce the usefulness of the transcriptome for prioritizing biomarkers and functional hypotheses that may guide genomic validations and subsequent clinical studies.

bioinformatics↗

Integrated Expression Analysis of C-MYC Oncogene-Associated Pathways in Gastric Adenocarcinoma and its Correlation with Clinicopathological Factors

BackgroundThe C-MYC oncogene is a well-established driver of gastric carcinogenesis, yet the integrated expression pattern of its complex regulatory network and its clinical implications in gastric adenocarcinoma (GAC) remain to be fully elucidated. This study aimed to perform an integrated bioinformatic analysis of C-MYC and its associated pathways in a cohort of GAC patients to delineate its expression profile, assess its potential as a biomarker, and correlate its patterns with clinicopathological factors such as Lauren classification and neoadjuvant treatment status. MethodsThe study included transcriptome data from 74 GAC tumor samples and 68 normal gastric tissue samples. Following RNA sequencing, a comprehensive bioinformatic analysis was conducted on a curated list of 21 C-MYC-associated genes. The methodology included differential expression analysis (DESeq2), unsupervised hierarchical clustering, Principal Component Analysis (PCA), and Receiver Operating Characteristic (ROC) curve analysis to evaluate diagnostic performance. Gene expression levels were also statistically correlated with Lauren histological subtypes and neoadjuvant therapy status using the Wilcoxon rank-sum test. ResultsThe analysis revealed a profound dysregulation of the C-MYC network in GAC. While MYC itself was significantly upregulated, its transcriptional antagonists, particularly MXD4 and MXD3, were the most significantly downregulated genes. This gene signature robustly separated tumor from normal tissues in both hierarchical clustering and PCA. ROC analysis demonstrated the outstanding diagnostic potential of several genes, with MXD4 achieving a perfect Area Under the Curve (AUC) of 1.00, surpassing the diagnostic value of MYC (AUC=0.86). Stratification by Lauren classification showed that MYC and its stability regulator PTBP1 were significantly more expressed in the intestinal subtype, whereas the repressors MXD3 and MXI1 were higher in the diffuse subtype. No significant expression differences were observed based on neoadjuvant treatment status. ConclusionGastric adenocarcinoma is characterized by a coordinated dysregulation of the C-MYC network, marked by both oncogene activation and a concurrent loss of its key transcriptional repressors. The profound downregulation of antagonists like MXD4 serves as an exceptionally accurate molecular signature for GAC, suggesting its potential as a diagnostic biomarker superior to MYC alone. The divergent expression patterns between Lauren subtypes highlight distinct molecular pathobiology and may have implications for targeted therapies

genetics↗

GASTRIC CANCER BASED ON TRANSCRIPTION FACTORS

IntroductionGastric adenocarcinoma (GA) is responsible for thousands of deaths annually and significantly affects patients quality of life. To increase knowledge about this disease, several studies have focused on the transcriptional control mechanism by analyzing the role of transcription factors (TFs) in GA. MethodsThis study identified differential expression (DE) of TFs in GA samples from 74 patients using NGS, biostatistical analysis in R, and comparison with 68 normal tissue samples in the genetic databases of the National Center for Biotechnology Information (NCBI). Results1,564 human transcription factors were DE. Of these, 87 were selected using the established cutoff value of AUC [≥] 0.95, and 25 were analyzed for their influence on GA carcinogenesis. Based on their role in biological processes, nine TFs were found to be underexpressed due to their growth suppression and cell differentiation properties, notably the TFs IRF3 and CXXC1. Sixteen TFs were overexpressed, associated with drug resistance, disease promotion, metastasis, and poor prognosis in GA, such as AHR, NCOA3, RRB1, and STAT3, respectively. ConclusionThis study integrated systematic bioinformatics and NGS, which revealed novel TFs with important oncogenic and suppressive functions in GA. Therefore, it provides new insights into genes with potential biomarkers for prognostic prediction in GA, which may offer important implications for clinical practice and may effectively target treatment, monitoring, or disease recurrence.

cancer biology↗

Treasure: A Sensitive Pipeline for Species-Level and Functional Microbiome Profiling

Next Generation Sequencing (NGS) methods, such as 16S rRNA amplicon sequencing and Whole Genome Sequencing (WGS), enable taxonomic analyses but have limitations. This project proposes the development of a computational tool capable of performing functional analysis of the most abundant microorganisms within a microbiome based on taxonomic analysis. The proposed method integrates the tools Kraken, Gffread, and Salmon. Compared to Samsa 2, a commonly used pipeline for RNA-Seq Total samples, the new approach demonstrated superior performance across all evaluated scenarios (p < 0.01). The tool aims to functionally characterize the microbiome of regions affected by Gastric Cancer (GC) and adjacent areas, assess associations between survival, expression/abundance, and identify potential microbial biomarkers for GC.

bioinformatics↗

Molecular Insights into ANPEP in Gastric Adenocarcinoma

Alanyl aminopeptidase (ANPEP) has been implicated in various cancers, but its specific role in gastric adenocarcinoma (GC) remains incompletely understood. This study analyzed ANPEP gene expression in gastric cancer (GC), peritumoral tissue (PTT), metaplasia (M), and normal tissue (N). Total RNA was extracted, libraries were prepared and sequenced on the Illumina NextSeq 500. Data was processed using the nf-core/rnaseq pipeline. Transcript quantifications were imported with tximport and normalized using DESeq2. Differential expression (|log2FC| >2; adj. p < 0.05) and Kruskal-Wallis tests identified key genes. ANPEP was significantly upregulated in GC, PTT, and M compared to normal tissue (p < 0.01), suggesting its involvement in early mucosal transformation and malignant progression. Heatmap analysis revealed upregulation of genes related to immune function and oxidative stress, indicating an immunosuppressive and apoptosis-resistant tumor microenvironment. Correlation analyses identified strong positive associations between ANPEP and genes involved in cytoskeletal remodeling, immune modulation, and metabolic regulation, suggesting that ANPEP supports both the invasive potential of tumor cells and the establishment of an immunosuppressive niche. These findings position ANPEP as a promising biomarker for early detection and a candidate for targeted therapies.

cancer biology↗

TOWARDS CLIMATE-SMART REWILDING: AN INTEGRATED FRAMEWORK FOR BIODIVERSITY, CLIMATE CHANGE, AND SOCIETY

The UN Decade on Ecosystem Restoration and the Kunming-Montreal Global Biodiversity Framework aim to restore 30% of degraded ecosystems. Both the IPCC and IPBES highlight the crucial role of ecosystem restoration in addressing the interconnected crises of climate change and biodiversity loss. One key restoration strategy is rewilding, which enhances ecosystem complexity with minimal human intervention. While traditional rewilding strategies often focus on benefits for biodiversity, we propose a climate-smart rewilding framework as a new approach designed to deliver climate benefits alongside biodiversity restoration. This framework seeks to integrate biodiversity, climate change adaptation and mitigation, as well as socio-economic benefits and trade-offs. We illustrate how this framework can be utilized to identify areas across Europe where rewilding could increase carbon sequestration, enhance species abilities to adapt to the velocity of climate change, and maximize wildlife-watching benefits while minimizing the costs associated with livestock-wildlife conflict. Finally, we acknowledge some limitations of climate-smart rewilding, but we argue that its adaptability and low cost render it a promising solution to the challenges facing Europe and beyond.

ecology↗

Unmasking Epstein-Barr Role in Gastric Carcinogenesis: A Gene Expression Approach to Virus-Positive Tumors

Human gammaherpesvirus 4 or Epstein-Barr virus (EBV) is an oncogenic virus linked to malignancies like gastric adenocarcinoma. Notably, EBV infection induces genetic and epigenetic modifications that play a crucial role in oncogenesis and tumor progression, underscoring the importance of analyzing viral gene expression in the context of gastric cancer (GC) to elucidate its unique characteristics. This study aimed to perform a molecular characterization of EBV gene expression using next-generation sequencing (NGS). The analysis included human gene expression patterns in EBV-positive and EBV-negative samples and the expression of viral genes in EBV-positive samples. The study received approval from the Ethics and Research Committee of Joao de Barros Barreto University Hospital under reference number 47580121.9.0000.5634. It utilized 76 tumor tissue samples from patients with gastric cancer who had undergone surgical resection, and both fresh and paraffin-embedded samples were gathered for total RNA sequencing (RNA-seq) and in situ hybridization (ISH). The RNA-seq was conducted in a pair-end manner on the NextSeq(R) platform (Illumina(R), US). The NextSeq(R) 500 MID Output V2 kit - 150 cycles (Illumina(R)) were utilized following the manufacturers instructions. ISH targeting RNA-1 of EBER1 (Y5200, DAKO, Carpinteria) was performed using the automated Dako system. Molecular characterization was conducted using the Kraken2 software. Subsequently, to elucidate the mechanisms through which EBV may influence gastric cancer, we analyzed the patterns of human gene expression in EBV-positive and EBV-negative samples. Of the 76 samples, 8 were classified as EBV-positive according to the applied methodology. Our analysis identified approximately 834 differentially expressed genes, 92 of which exhibited an AUC > 0.85. These genes are implicated in tumor progression, cellular metabolism, and both innate and adaptive immune responses. Additionally, viral genes expressed in the positive samples were evaluated, and we found manifestations of both lytic phase and latent phase genes. Finally, our study presents an efficient strategy for molecular classification of EBV-positive gastric cancer based on NGS and shows the effects of EBV on human gene expression. Author summaryIn our study, we explored how EBV influences the development of stomach cancer. EBV is a virus known to be linked to various cancers, including gastric cancer, and it can alter the behavior of both human and viral genes within infected cells. To investigate this, we analyzed tissue samples from 76 patients with stomach cancer, focusing on differences between samples with and without EBV. Using advanced sequencing technology, we identified over 800 genes that behave differently in EBV-positive cancers. These genes are involved in critical processes like how cells grow, how the immune system responds, and how energy is produced within cells. We also examined which EBV genes were active in the cancer samples and found evidence of both dormant and active phases of the virus. Our work demonstrated how EBV may contribute to stomach cancer and suggests new ways to classify and understand this disease. By uncovering these details, we hope to pave the way for more targeted treatments in the future.

cancer biology↗

Narratives for positive nature futures in Europe

O_LIThe Nature Futures Framework (NFF) is a novel tool for the development of positive scenarios centred on the relationship of nature and people, emphasising biodiversity as part of the solution to environmental challenges across various spatial and temporal scales, explicitly addressing a plurality of values for nature. C_LIO_LIIn this work, we describe the process that has led to the formulation of continental-scale positive narratives for conservation in Europe based on the NFF and its value perspectives (Nature for Nature; Nature for Society; Nature as Culture), through a stakeholder group elicitation. We focused on 6 topics in the narratives: Nature Protection and Restoration; Forestry; Freshwater Ecosystems; Urban Systems; Agriculture, and Energy. We analyse differences and similarities among the narratives across these topics. C_LIO_LIWe develop three novel Nature Futures narratives for Europe with contrasting perspectives and priorities for the six topics. Within the EU socioeconomic trends and policy framework, common solutions that simultaneously tackle biodiversity conservation and instrumental and cultural Natures Contributions to People (NCP) provision emerged. C_LIO_LIThis set of narratives may integrate preferences concerning EU-level conservation targets and plausible socio-ecological development pathways, supporting the modelling of positive scenarios for nature that can be crucial in guiding policy decisions towards recovery of nature. C_LI

ecology↗

Mechanisms underlying the loss of migratory behaviour in a long-lived bird

Human-induced environmental changes are shifting the migration patterns of birds worldwide. Species are adjusting migration timings, shortening and diversifying migratory routes, or even completely disrupting migration and transitioning towards residency. Whilst the ultimate causes driving changes in migratory patterns are well established, the underlying mechanisms by which migratory species adapt to environmental change remain unclear. Here, we studied the mechanisms driving the recent and rapid loss of migratory behaviour in Iberian white storks Ciconia ciconia, a long-lived and previously fully migratory species through the African-Eurasian flyway. We combined 25 years of census data, GPS-tracking data from 213 individuals (80 adults and 133 first-year juveniles) followed for multiple years, and whole-genome sequencing, to disentangle whether within- (phenotypic flexibility) or between- (developmental plasticity or microevolution, through selection) individual shifts in migratory behaviour over time can explain the observed population-level changes towards residency. Between 1995 and 2020, the proportion of individuals no longer migrating and remaining in Southern Europe year-round increased dramatically, from 18% to 68-83%. We demonstrate that this behavioural shift is likely explained by developmental plasticity. Within first-year birds, 98% crossed the Strait of Gibraltar towards their African wintering grounds, in Morocco or Sub-Saharan Africa. However, the majority shifted towards a non-migratory strategy as they aged - the proportion of migrants decreased to 67% and 33%, on their second and third year of life, respectively - suggesting that migratory behaviour is determined during ontogeny. Supporting these findings, only 19% of GPS-tracked adults migrated. Moreover, we did not find evidence of phenotypic flexibility, as adults were highly consistent in migratory behaviour over multiple years (only 3 individuals changed strategy between years, out of 113 yearly transitions), nor of selection acting on genetic variation, since genomes of migrants and residents are essentially undifferentiated. Our results suggest that through developmental plasticity, traits that are plastic during specific windows of development, become fixed during adulthood. Thus, inter-generational shifts in the frequency of migratory and non-migratory young individuals could drive population changes in migratory behaviour. This can provide a fast mechanism for long-lived migratory birds to respond to rapid human-driven environmental changes.

evolutionary biology↗

Biodiversity monitoring in Europe: user and policy needs

To implement the goals of the 2030 Global Biodiversity Framework, the European Biodiversity Strategy and the EU Green Deal, biodiversity monitoring is a pivotal instrument to achieve accountability and progress in conservation. Monitoring efforts in Europe, however, suffer from gaps and biases in taxonomy, spatial coverage, and temporal resolution, resulting in fragmented and disconnected data which does not provide sufficient evidence for policy making. To assess user and policy needs in biodiversity monitoring, we employed with EuropaBON a four-step user-centred stakeholder engagement process, including an international public stakeholder workshop, a standardised online survey, semi-structured interviews, and an expert meeting with representatives of EU member states, the European Commission and the European Environment Agency. The resulting insights into national and European biodiversity monitoring schemes identify policy needs, current challenges and potential solutions. Based on this in-depth policy and science stakeholder assessment, we recommend the establishment of a European Biodiversity Observation Network through a permanent Biodiversity Monitoring and Coordinating Centre to optimise existing observation efforts, harmonise data, and enhance our ability to predict and respond to key challenges related to biodiversity loss in a changing climate in Europe.

ecology↗

Efficacy of the oral nucleoside prodrug GS-5245 (Obeldesivir) against SARS-CoV-2 and coronaviruses with pandemic potential

Despite the wide availability of several safe and effective vaccines that can prevent severe COVID-19 disease, the emergence of SARS-CoV-2 variants of concern (VOC) that can partially evade vaccine immunity remains a global health concern. In addition, the emergence of highly mutated and neutralization-resistant SARS-CoV-2 VOCs such as BA.1 and BA.5 that can partially or fully evade (1) many therapeutic monoclonal antibodies in clinical use underlines the need for additional effective treatment strategies. Here, we characterize the antiviral activity of GS-5245, Obeldesivir (ODV), an oral prodrug of the parent nucleoside GS-441524, which targets the highly conserved RNA-dependent viral RNA polymerase (RdRp). Importantly, we show that GS-5245 is broadly potent in vitro against alphacoronavirus HCoV-NL63, severe acute respiratory syndrome coronavirus (SARS-CoV), SARS-CoV-related Bat-CoV RsSHC014, Middle East Respiratory Syndrome coronavirus (MERS-CoV), SARS-CoV-2 WA/1, and the highly transmissible SARS-CoV-2 BA.1 Omicron variant in vitro and highly effective as antiviral therapy in mouse models of SARS-CoV, SARS-CoV-2 (WA/1), MERS-CoV and Bat-CoV RsSHC014 pathogenesis. In all these models of divergent coronaviruses, we observed protection and/or significant reduction of disease metrics such as weight loss, lung viral replication, acute lung injury, and degradation in pulmonary function in GS-5245-treated mice compared to vehicle controls. Finally, we demonstrate that GS-5245 in combination with the main protease (Mpro) inhibitor nirmatrelvir had increased efficacy in vivo against SARS-CoV-2 compared to each single agent. Altogether, our data supports the continuing clinical evaluation of GS-5245 in humans infected with COVID-19, including as part of a combination antiviral therapy, especially in populations with the most urgent need for more efficacious and durable interventions.

microbiology↗

Host genetic variation guides hepacivirus clearance, chronicity, and liver fibrosis in mice

Background & AimsHuman genetic variation is thought to guide the outcome of hepatitis C virus (HCV) infection but model systems within which to dissect these host genetic mechanisms are limited. Norway rat hepacivirus (NrHV), closely related to HCV, causes chronic liver infection in rats but causes acute self-limiting hepatitis in typical strains of laboratory mice, which resolves in two weeks. The Collaborative Cross (CC) is a robust mouse genetics resource comprised of a panel of recombinant inbred strains, which model the complexity of the human genome and provide a system within which to understand diseases driven by complex allelic variation. Approach & ResultsWe infected a panel of CC strains with NrHV and identified several that failed to clear virus after 4 weeks. Strains displayed an array of virologic phenotypes ranging from delayed clearance (CC046) to chronicity (CC071, CC080) with viremia for at least 10 months. Body weight loss, hepatocyte infection frequency, viral evolution, T-cell recruitment to the liver, liver inflammation and the capacity to develop liver fibrosis varied among infected CC strains. ConclusionsThese models recapitulate many aspects of HCV infection in humans and demonstrate that host genetic variation affects a multitude of virus and host phenotypes. These models can be used to better understand the molecular mechanisms that drive hepacivirus clearance and chronicity, the virus and host interactions that promote chronic disease manifestations like liver fibrosis, therapeutic and vaccine performance, and how these factors are affected by host genetic variation.

microbiology↗

Genomic approach for conservation and the sustainable management of endangered species of the Amazon

A broad panel of potentially amplifiable microsatellite loci and a multiplex system were developed for the Amazonian symbol fish species Arapaima gigas, which is currently in high danger of extinction due to the disorderly fishing exploitation. Several factors have contributed to the increase of this threat, among which we highlight the lack of genetic information about the structure and taxonomic status of the species, as well as the lack of accurate tools for evaluation of the effectivity of current management programs. Based on Arapaima gigas whole genome, available at the NCBI database (ID: 12404), a total of 95,098 unique perfect microsatellites were identified, including their proposed primers. From this panel, a multiplex system containing 12 tetranucleotide microsatellite markers was validated. These tools are valuable for research in as many areas as bioinformatics, ecology, genetics, evolution and comparative studies, since they are able to provide more accurate information for fishing management, conservation of wild populations and genetic management of aquaculture.

genomics↗