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Apurinic/apyrimidinic endonuclease 1/redox effector factor 1 (APE1/Ref-1) is a multifunctional enzyme that is essential for maintaining cellular homeostasis. APE1 is the major apurinic/apyrimidinic endonuclease in the base excision repair pathway and acts as a redox-dependent regulator of several transcription factors, including NF-κB, AP-1, HIF-1α, and STAT3. These functions render APE1 vital to regulating cell signaling, senescence, and inflammatory pathways. In addition to regulating cytokine and chemokine expression through activation of redox sensitive transcription factors, APE1 participates in other critical processes in the immune response, including production of reactive oxygen species and class switch recombination. Furthermore, through participation in active chromatin demethylation, the repair function of APE1 also regulates transcription of some genes, including cytokines such as TNFα. The multiple functions of APE1 make it an essential regulator of the pathogenesis of several diseases, including cancer and neurological disorders. Therefore, APE1 inhibitors have therapeutic potential. APE1 is highly expressed in the central nervous system (CNS) and participates in tissue homeostasis, and its roles in neurodegenerative and neuroinflammatory diseases have been elucidated. This review discusses known roles of APE1 in innate and adaptive immunity, especially in the CNS, recent evidence of a role in the extracellular environment, and the therapeutic potential of APE1 inhibitors in infectious/immune diseases.

The presence of oxidized DNA lesions, such as 7,8-dihydro-8-oxoguanine (8-oxoG) and apurinic/apyrimidinic sites (AP sites), has been described as epigenetic signals that are involved in gene expression control. In mammals, Apurinic-apyrimidinic endonuclease 1/Redox factor-1 (APE1/Ref-1) is the main AP endonuclease of the base excision repair (BER) pathway and is involved in active demethylation processes. In addition, APE1/Ref-1, through its redox function, regulates several transcriptional factors. However, the transcriptional control targets of each APE1 function are not completely known. In this study, a transcriptomic approach was used to investigate the effects of chemical inhibition of APE1/Ref-1 redox or DNA repair functions by E3330 or methoxyamine (MX) in an inflammatory cellular model. Under lipopolysaccharide (LPS) stimulation, both E3330 and MX reduced the expression of some cytokines and chemokines. Interestingly, E3330 treatment reduced cell viability after 48 h of the treatment. Genes related to inflammatory response and mitochondrial processes were downregulated in both treatments. In the E3330 treatment, RNA processing and ribosome biogenesis genes were downregulated, while they were upregulated in the MX treatment. Furthermore, in the E3330 treatment, the cellular stress response was the main upregulated process, while the cellular macromolecule metabolic process was observed in MX-upregulated genes. Nuclear respiratory factor 1 (NRF1) was predicted to be a master regulator of the downregulated genes in both treatments, while the ETS transcription factor ELK1 (ELK1) was predicted to be a master regulator only for E3330 treatment. Decreased expression of ELK1 and its target genes and a reduced 28S/18S ratio were observed, suggesting impaired rRNA processing. In addition, both redox and repair functions can affect the expression of NRF1 and GABPA target genes. The master regulators predicted for upregulated genes were YY1 and FLI1 for the E3330 and MX treatments, respectively. In summary, the chemical inhibition of APE1/Ref-1 affects gene expression regulated mainly by transcriptional factors of the ETS family, showing partial overlap of APE1 redox and DNA repair functions, suggesting that these activities are not entirely independent. This work provides a new perspective on the interaction between APE1 redox and DNA repair activity in inflammatory response modulation and transcription.

Berardinelli-Seip congenital lipodystrophy (BSCL) is a rare disease characterized by the near total absence of body fat at birth. BSCL etiology involves genetic variations in four different genes: AGPAT2, BSCL2, CAV1, and CAVIN1. The four different biochemical subtypes of the disease are distinguished depending on which gene is mutated. The diagnosis of lipodystrophy can be based on clinical criteria, but the gold standard remains genetic testing. Since many different mutations have already been correlated with the onset of the disease, the most indicative method is DNA sequencing. However, not all laboratories have the resources to perform sequencing. Thus, less expensive techniques that include narrow gene regions may be applied. In such cases, the target mutations to be tested must be carefully determined taking into account the frequency of the description of the mutations in the literature, the nationality of the patient, as well as their phenotype. This review considers the molecular basis of BSCL, including the manual count of the majority of mutations reported in the literature up to the year 2018. Ninety different genetic mutations in 332 cases were reported at different frequencies. Some mutations were distributed homogeneously and others were specific to geographic regions. Type 2 BSCL was mentioned most often in the literature (50.3% of the cases), followed by Type 1 (38.0%), Type 4 (10.2%), and Type 3 (1.5%). The mutations comprised frameshifts (34.4%), nonsense (26.6%), and missense (21.1%). The c.517dupA in the BSCL2 gene was the most frequent (13.3%), followed by c.589-2A>G in the AGPAT2 gene (11.5%), c.507_511delGTATC in the BSCL2 gene (9.7%), c.317-588del in the AGPAT2 gene (7.3%), and c.202C>T in the AGPAT2 gene (4.5%). This information should prove valuable for analysts in making decisions regarding the best therapeutic targets in a population-specific context, which will benefit patients and enable faster and less expensive treatment.

2020-01-01 Oxidative stress generated during inflammation is associated with a wide range of pathologies. Resveratrol (RESV) displays anti-inflammatory and antioxidant activities, being a candidate for the development of adjuvant therapies for several inflammatory diseases. Despite this potential, the cellular responses induced by RESV are not well known. In this work, transcriptomic analysis was performed following lipopolysaccharide (LPS) stimulation of monocyte cultures in the presence of RESV. Induction of an inflammatory response was observed after LPS treatment and the addition of RESV led to decreases in expression of the inflammatory mediators, tumor necrosis factor-alpha (TNF-α), interleukin-8 (IL-8), and monocyte chemoattractant protein-1 (MCP-1), without cytotoxicity. RNA sequencing revealed 823 upregulated and 2098 downregulated genes (cutoff ≥2.0 or ≤−2.0) after RESV treatment. Gene ontology analysis showed that the upregulated genes were associated with metabolic processes and the cell cycle, consistent with normal cell growth and differentiation under an inflammatory stimulus. The downregulated genes were associated with inflammatory responses, gene expression, and protein modification. The prediction of master regulators using the iRegulon tool showed nuclear respiratory factor 1 (NRF1) and GA-binding protein alpha subunit (GABPA) as the main regulators of the downregulated genes. Using immunoprecipitation and protein expression assays, we observed that RESV was able to decrease protein acetylation patterns, such as acetylated apurinic/apyrimidinic endonuclease-1/reduction-oxidation factor 1 (APE1/Ref-1), and increase histone methylation. In addition, reductions in p65 (nuclear factor-kappa B (NF-κB) subunit) and lysine-specific histone demethylase-1 (LSD1) expression were observed. In conclusion, our data indicate that treatment with RESV caused significant changes in protein acetylation and methylation patterns, suggesting the induction of deacetylase and reduction of demethylase activities that mainly affect regulatory cascades mediated by NF-кB and Janus kinase/signal transducers and activators of transcription (JAK/STAT) signaling. NRF1 and GABPA seem to be the main regulators of the transcriptional profile observed after RESV treatment.

The sharp increase of COVID-19 cases in late 2020 has made Brazil the new epicenter of the ongoing SARS-CoV-2 pandemic. The novel viral lineages P.1 (Variant of Concern Gamma) and P.2, respectively identified in the Brazilian states of Amazonas and Rio de Janeiro, have been associated with potentially higher transmission rates and antibody neutralization escape. In this study, we performed the whole-genome sequencing of 185 samples isolated from three out of the five Brazilian regions, including Amazonas (North region), Rio Grande do Norte, Paraíba and Bahia (Northeast region), and Rio de Janeiro (Southeast region) in order to monitor the spread of SARS-CoV-2 lineages in Brazil in the first months of 2021. Here, we showed a widespread dispersal of P.1 and P.2 across Brazilian regions and, except for Amazonas, P.2 was the predominant lineage identified in the sampled states. We estimated the origin of P.2 lineage to have happened in February, 2020 and identified that it has differentiated into new clades. Interstate transmission of P.2 was detected since March, but reached its peak in December, 2020 and January, 2021. Transmission of P.1 was also high in December and its origin was inferred to have happened in August 2020. We also confirmed the presence of lineage P.7, recently described in the southernmost region of Brazil, to have spread across the Northeastern states. P.1, P.2 and P.7 are descended from the ancient B.1.1.28 strain, which co-dominated the first phase of the pandemic in Brazil with the B.1.1.33 strain. We also identified the occurrence of a new lineage descending from B.1.1.33 that convergently carries the E484K mutation, N.9. Indeed, the recurrent report of many novel SARS-CoV-2 genetic variants in Brazil could be due to the absence of effective control measures resulting in high SARS-CoV2 transmission rates. Altogether, our findings provided a landscape of the critical state of SARS-CoV-2 across Brazil and confirm the need to sustain continuous sequencing of the SARS-CoV-2 isolates worldwide in order to identify novel variants of interest and monitor for vaccine effectiveness., Author summary Since its first detection in December 2019, the SARS-CoV-2 has evolved into more than a thousand recognized lineages. Several of these lineages are known to have higher transmissibility or better escape from the immune system. One of them is the P.1 lineage, also known as the variant of concern Gamma. It was first discovered in Brazil in December 2020 and has quickly replaced the previous lineage dominating the country, P.2. We used genomic data from SARS-CoV-2 samples that were collected in the first months of 2021 to analyze how P.1, P.2 and other lineages had spread across Brazil. Our research has identified that P.1 lineage was already present in several states of Brazil almost two months before its first detection in the state of Amazonas. Our work sheds light on the importance of continuous monitoring of SARS-CoV-2 lineages in historically understudied regions to early detect and control the spread of new variants of concern.

Ocular toxoplasmosis (OT) is the most common form of posterior uveitis, and in some countries, it is the most frequent cause of visual impairment. Studies demonstrate that the polymorphism in genes involved with the immune response can be related both to the occurrence and to the recurrence of OT. Thus, the present study aimed to analyze the association between OT and the polymorphism of the APEX1 (rs1130409) and MyD88 (rs7744) genes. The studied sample consisted of 48 volunteers with OT and 96 asymptomatic volunteers, but positive for anti - T. gondii IgG (control group). Blood collection was performed for serological analysis (ELISA) and DNA extraction. Genotyping of the polymorphism was performed using real-time PCR. To analyze the association between gene polymorphism and OT, logistic regression was performed. The results showed no association between the MYD88 gene polymorphism and the development of OT. However, a significant association was found between OT and APEX1 gene polymorphism, indicating that individuals expressing polymorphic (GG) or heterozygous (GT) alleles are more likely to develop the disease (P-value = 0.02 and 0.03 respectively). These results suggest that APEX1 (rs1130409) polymorphism is a risk factor for the occurrence of ocular toxoplasmosis in the studied population.

The diversity of the Penaeus vannamei mitochondrial genome has still been poorly characterized, there are no validated mitochondrial markers available for populational studies, and the heteroplasmy has not yet been investigated in this species. In this study, metagenomic reads extracted from the muscle of a single individual were used to assemble the mitochondrial genome (mtDNA). These data associated with mitochondrial genomes previously described allowed to evaluate the inter-individual variability and heteroplasmy. Comparison among 45 mtDNA control regions led to the detection of conserved and variable segments and the characterization of two hypervariable regions. The analysis of diversity revealed mostly low frequency polymorphisms, and heteroplasmy was found in practically all mitochondrial genes, with a high occurrence of indels. These results indicate that the design of mitochondrial markers for P. vannamei must be done with caution. The mapping of conserved and variable regions and the characterization of heteroplasmy presented here will contribute to increasing the efficiency of mitochondrial markers for population or individual studies.

Lipodystrophy syndromes are a group of rare diseases related to the pathological impairment of adipose tissue and metabolic comorbidities, including dyslipidemia, diabetes, insulin resistance, hypoleptinemia, and hypoadiponectinemia. They can be categorized as partial or generalized according to the degree of fat loss, and inherited or acquired disorders, if they are associated with genetic mutations or are related to autoimmunity, respectively. Some types of lipodystrophies have been associated with changes in both redox and endoplasmic reticulum (ER) homeostasis as well as muscle dysfunction (MD). Although ER stress (ERS) has been related to muscle dysfunction (MD) in many diseases, there is no data concerning its role in lipodystrophies' muscle physiopathology. Here we focused on congenital lipodystrophies associated with ERS and MD. We also described recent advances in our understanding of the relationships among ERS, MD, and genetic lipodystrophies, highlighting the adiponectin-protective roles.

Congenital Generalized Lipodystrophy (CGL) was recently associated with Respiratory Muscle Dysfunction (RMD), as well as changes in redox homeostasis and endoplasmic reticulum stress (ERS). Although ERS has been related to RMD in many diseases, there is no data concerning its role in CGL physiopathology. We hypothesized that CGL-associated RMD may be related to oxidative stress (OS) and ERS. To evaluate the mRNA expression levels of OS and ERS factors, correlating with Maximal Respiratory Pressures in subjects with CGL. A cross-sectional study with 11 CGL subjects was conducted in Northeastern Brazil. NFE2L2, APEX1, OGG1, XBP1 splicing, DDIT3, and HSPA5 RNAm levels from CGL leukocytes were analyzed by qPCR. Gaussian distribution was evaluated by Shapiro Wilk and correlation tests were performed. The significance level was set at 5%. We found that the mean of NFE2L2, APEX1, and OGG1 RNAm levels was higher in CGL subjects compared to the healthy controls. Regarding ERS markers, we found that the mean of XBP1 RNAm levels was increased, while a significant reduction of DDIT3 RNAm was detected. Although no correlation was established between MIP and NFE2L2, APEX1, and OGG1 RNAm, a strong negative correlation was found between MIP and XBP1 RNAm splicing. Further, this ERS marker positively correlated with MEP. The upregulation of OS and ERS markers was observed in CGL subjects compared to the healthy controls. A strong negative correlation was only found between MIP and XBP1 splicing RNAm. These data suggest that CGL is an ERS-related metabolic disease and therapeutic strategies targeted to treat RMD in CGL should include ERS modulators.

The oil drilling process generates large volumes of waste with inadequate treatments. Here, oil drilling waste (ODW) microbial communities demonstrate different hydrocarbon degradative abilities when exposed to distinct nutrient enrichments as revealed by comparative metagenomics. The ODW was enriched in Luria Broth (LBE) and Potato Dextrose (PDE) media to examine the structure and functional variations of microbial consortia. Two metagenomes were sequenced on Ion Torrent platform and analyzed using MG-RAST. The STAMP software was used to analyze statistically significant differences amongst different attributes of metagenomes. The microbial diversity presented in the different enrichments was distinct and heterogeneous. The metabolic pathways and enzymes were mainly related to the aerobic hydrocarbons degradation. Moreover, our results showed efficient biodegradation after 15 days of treatment for aliphatic hydrocarbons (C8-C33) and polycyclic aromatic hydrocarbons (PAHs), with a total of about 50.5% and 46.4% for LBE and 44.6% and 37.9% for PDE, respectively. The results obtained suggest the idea that the enzymatic apparatus have the potential to degrade petroleum compounds.

Seipin is a nonenzymatic protein encoded by the BSCL2 gene. It is involved in lipodystrophy and seipinopathy diseases. Named in 2001, all seipin functions are still far from being understood. Therefore, we reviewed much of the research, trying to find a pattern that could explain commonly observed features of seipin expression disorders. Likewise, this review shows how this protein seems to have tissue-specific functions. In an integrative view, we conclude by proposing a theoretical model to explain how seipin might be involved in the triacylglycerol synthesis pathway.

Drill cuttings leave behind thousands of tons of residues without adequate treatment, generating a large environmental liability. Therefore knowledge about the microbial community of drilling residue may be useful for developing bioremediation strategies. In this work, samples of drilling residue were enriched in different culture media in the presence of petroleum, aiming to select potentially oil-degrading bacteria and biosurfactant producers. Total DNA was extracted directly from the drill cutting samples and from two enriched consortia and sequenced using the Ion Torrent platform. Taxonomic analysis revealed the predominance of Proteobacteria in the metagenome from the drill cuttings, while Firmicutes was enriched in consortia samples. Functional analysis using the Biosurfactants and Biodegradation Database (BioSurfDB) revealed a similar pattern among the three samples regarding hydrocarbon degradation and biosurfactants production pathways. However, some statistical differences were observed between samples. Namely, the pathways related to the degradation of fatty acids, chloroalkanes, and chloroalkanes were enriched in consortia samples. The degradation colorimetric assay using dichlorophenolindophenol as an indicator was positive for several hydrocarbon substrates. The consortia were also able to produce biosurfactants, with biosynthesis of iturin, lichnysin, and surfactin among the more abundant pathways. A microcosms assay followed by gas chromatography analysis showed the efficacy of the consortia in degrading alkanes, as we observed a reduction of around 66% and 30% for each consortium in total alkanes. These data suggest the potential use of these consortia in the bioremediation of drilling residue based on autochthonous bioaugmentation.

Background Berardinelli-Seip Congenital Lipodystrophy (BSCL) is a rare disease characterized by the almost complete absence of adipose tissue. Although a large number of BSCL cases was previously identified in Rio Grande do Norte (RN), a state in Northeast Brazil, its prevalence in RN regions and municipalities remains unknown. The purpose of this study was to better characterize the prevalence of BSCL in RN. Methods A descriptive study was conducted using secondary data obtained from the Association of Parents and People with BSCL of RN to determine its prevalence. The patients’ socio-demographic characteristics and geolocalization were analyzed. Results We estimated a total of 103 BSCL cases in RN, resulting in a prevalence of 3.23 per 100,000 people. The Central Potiguar mesoregion, Seridó territory, Carnaúba dos Dantas and Timbaúba dos Batistas municipalities had a much higher prevalence of BSCL, with 20.56, 20.66, 498.05 and 217.85 per 100,000 people, respectively. Conclusions Together, our results showed that BSCL is highly prevalent in RN and confirmed that our state has one of the highest prevalences of this lipodystrophy worldwide. More studies are still needed to better estimate the prevalence and incidence of BSCL in RN as well as in other states in Brazil. Trial registration Study Number 31809314.0.0000.5568

Xeroderma pigmentosum complementation group A (XPA), is defective in xeroderma pigmentosum patients, causing pre-disposition to skin cancer and neurological abnormalities, which is not well understood. Here, we analyzed the XPA-deficient cells transcriptional profile under oxidative stress. The imbalance in of ubiquitin-proteasome system (UPS) gene expression was observed in XPA-deficient cells and the involvement of nuclear factor erythroid 2-related factor-2 (NFE2L2) was indicated. Co-immunoprecipitation assays showed the interaction between XPA, apurinic-apyrimidinic endonuclease 1 (APE1) and NFE2L2 proteins. Decreased NFE2L2 protein expression and proteasome activity was also observed in XPA-deficient cells. The data suggest the involvement of the growth arrest and DNA-damage-inducible beta (GADD45β) in NFE2L2 functions. Similar results were obtained in xpa-1 (RNAi) Caenorhabditis elegans suggesting the conservation of XPA and NFE2L2 interactions. In conclusion, stress response activation occurs in XPA-deficient cells under oxidative stress; however, these cells fail to activate the UPS cytoprotective response, which may contribute to XPA patient’s phenotypes.

Introduction: Congenital Generalized Lipodystrophy (CGL) is a disease characterized by metabolic, cardiovascular and respiratory disturbances. Although oxidative stress (OS) have been related to decreased Respiratory Muscle Strength (RMS), their contribution in RMS of CGL subjects needs to be investigated. Objective: To evaluate the levels of metabolic parameters and OS markers, correlating with Maximal Respiratory Pressures in CGL subjects. Methods: Eleven CGL subjects participated in this cross-sectional study. Peripheral blood was collected for biochemical dosages of glucose, triglycerides, total cholesterol, HDL, oxidized glutathione:total glutathione (GSSG:GSH) ratio and malondialdehyde (MDA). MIP and MEP were measured by manovacuometry according to the ATS/ERS guidelines. Data normality was assessed by Shapiro Wilk test. Correlations were performed according to data distribution. Significance level was set at 5%. Results: The majority of CGL subjects were genetically diagnosed with type 2 (BSCL2 mutation) and 67% were females. Mean age was 31.45±8.0 years. GSSG:GSH ratio correlation between MIP and MEP were r= -0.70 (p=0.0358) and r= 0.61 (p=0.076), respectively. MDA correlation between MIP and MEP were r= -0.34 (p=0.3) and r= 0.38 (p=0.3), respectively. No correlation was found between metabolic parameters and MIP and MEP. Conclusions: A strong significant correlation was found between MIP and GSSG:GSH ratio. These data suggest that CGL is an oxidative stress-related metabolic disease and the assessment of OS markers, in addition to metabolic parameters, may be essential to reduce pulmonary comorbidities associated with CGL subjects.

CGL type 2 is a rare autosomal recessive syndrome characterized by an almost complete lack of body fat. CGL is caused by loss-of-function mutations in both alleles of the BSCL2 gene that codifies to seipin. Subjects often show hyperglycemia, decreased HDL-c, and hypoadiponectinemia. These laboratory findings are important triggers for changes in redox and ER homeostasis. Therefore, our aim was to investigate whether these intracellular mechanisms are associated with this syndrome. We collected blood from people from Northeastern Brazil with 0, 1, and 2 mutant alleles for the rs786205071 in the BSCL2 gene. Through the qPCR technique, we evaluated the expression of genes responsible for triggering the antioxidant response, DNA repair, and ER stress in leukocytes. Colorimetric tests were applied to quantify lipid peroxidation and to evaluate the redox status of glutathione, as well as to access the panorama of energy metabolism. Long extension PCR was performed to observe leukocyte mitochondrial DNA lesions, and the immunoblot technique to investigate plasma adiponectin concentrations. Subjects with the rs786205071 in both BSCL2 alleles showed increased transcription of NFE2L2, APEX1, and OGG1 in leukocytes, as well as high concentrations of malondialdehyde and the GSSG:GSH ratio in plasma. We also observed increase of mitochondrial DNA lesions and XBP1 splicing, as well as a decrease in adiponectin and HDL-c. Our data suggest the presence of lipid lesions due to changes in redox homeostasis in that group, associated with increased levels of mitochondrial DNA damage and transcriptional activation of genes involved with antioxidant response and DNA repair.

Microorganisms represent the most abundant biomass on the planet; however, because of several cultivation technique limitations, most of this genetic patrimony has been inaccessible. Due to the advent of metagenomic methodologies, such limitations have been overcome. Prevailing over these limitations enabled the genetic pool of non-cultivable microorganisms to be exploited for improvements in the development of biotechnological products. By utilising a metagenomic approach, we identified a new gene related to biosurfactant production and hydrocarbon degradation. Environmental DNA was extracted from soil samples collected on the banks of the Jundiaí River (Natal, Brazil), and a metagenomic library was constructed. Functional screening identified the clone 3C6, which was positive for the biosurfactant protein and revealed an open reading frame (ORF) with high similarity to sequences encoding a hypothetical protein from species of the family Halobacteriaceae. This protein was purified and exhibited biosurfactant activity. Due to these properties, this protein was named metagenomic biosurfactant protein 1 (MBSP1). In addition, E. coli RosettaTM (DE3) strain cells transformed with the MBSP1 clone showed an increase in aliphatic hydrocarbon degradation. In this study, we described a single gene encoding a protein with marked tensoactive properties that can be produced in a host cell, such as Escherichia coli, without substrate dependence. Furthermore, MBSP1 has been demonstrated as the first protein with these characteristics described in the Archaea or Bacteria domains.

Although microorganisms play key roles in mangrove food webs, the global knowledge of their diversity and function in these ecosystems is still scarce. Therefore, this study aimed to describe the microbiomes of pristine (TIM) and anthropized (JAG, PAC and COC) mangroves from a semiarid region of Brazil, and also to compare microbiomes from Southeast (SE) and Northeast (NE) mangroves, aiming to detect patterns related to geographic location. Pyrosequencing of four metagenomes showed that 90% of total classified sequences were assigned to Bacteria with a greater abundance of Proteobacteria (53%–60%), Bacteroidetes (7%–10%), Actinobacteria, Chloroflexi, Firmicutes and Planctomycetes (4%–7%), followed by Acidobacteria, Cyanobacteria and Verrucomicrobia (1.5%–4%) and phyla with relative abundances under 1%. The dominant proteobacterial classes were Deltaproteobacteria, Alphaproteobacteria and Gammaproteobacteria in the pristine (TIM) and in the less anthropized mangroves (JAG and PAC). Interestingly, in COC it was observed a decrease in Gammaproteobacteria with an increase in Betaproteobacteria, possibly related to its eutrophic condition. Our datasets also revealed some previously non-detected phyla in mangroves, comprising rare groups and several candidate divisions, which were previously reported for harsh environments, suggesting the involvement of these groups with the resilience of mangroves in semiarid regions. Comparative in silico analysis of SE and NE microbiomes showed similarities, but it was possible to detect a homogeneous group formed by Northeast mangroves (TIM, JAG and PAC), whereas the eutrophic mangrove (COC) clustered together to the urbanized Southeast mangrove. These results suggest that the semiarid climate might select peculiar bacterial communities and highlight the risk of microbial diversity homogenization due to anthropic actions on mangroves. Despite the detected changes in microbial composition, in general the potential metabolic pathways from these mangroves did not significantly differ. The observed functional redundancy explains the known resilience of these environments.

In recent years, the understanding of how DNA repair contributes to the development of innate and acquired immunity has emerged. The DNA damage incurred during the inflammatory response triggers the activation of DNA repair pathways, which are required for host-cell survival. Here, we reviewed current understanding of the mechanism by which DNA repair contributes to protection against the oxidized DNA damage generated during infectious and inflammatory diseases and its involvement in innate and adaptive immunity. We discussed the functional role of DNA repair enzymes in the immune activation and the relevance of these processes to: transcriptional regulation of cytokines and other genes involved in the inflammatory response; V(D)J recombination; class-switch recombination (CSR); and somatic hypermutation (SHM). These three last processes of DNA damage repair are required for effective humoral adaptive immunity, creating genetic diversity in developing T and B cells. Furthermore, viral replication is also dependent on host DNA repair mechanisms. Therefore, the elucidation of the pathways of DNA damage and its repair that activate innate and adaptive immunity will be important for a better understanding of the immune and inflammatory disorders and developing new therapeutic interventions for treatment of these diseases and for improving their outcome.

White spot syndrome virus (WSSV) has been the cause of great economic losses in world shrimp farming. In this work the genome of a Brazilian WSSV isolate was determined from direct sequencing of total DNA extracted from an infected whiteleg shrimp, and assembled based on a chimera template approach. Comparisons between WSSV-BR and other isolates revealed that the Brazilian virus has a relatively small genome, and is very similar to isolates from Thailand and Mexico. A phylogenetic relationship using different approaches has demonstrated that these isolates share a common evolutionary history. An analysis of conflicting phylogenetic signals also considering genomes of other isolates revealed that the evolutionary history of WSSV may be related to recombination events. We observed that these events can also be traced at some level by analyzing the homologous regions in the WSSV genome. The existence of recombination events introduces a new point of view that must be considered in the evolutionary history of WSSV.

Background Bacterial and Archaeal communities have a complex, symbiotic role in crude oil bioremediation. Their biosurfactants and degradation enzymes have been in the spotlight, mainly due to the awareness of ecosystem pollution caused by crude oil accidents and their use. Initially, the scientific community studied the role of individual microbial species by characterizing and optimizing their biosurfactant and oil degradation genes, studying their individual distribution. However, with the advances in genomics, in particular with the use of New-Generation-Sequencing and Metagenomics, it is now possible to have a macro view of the complex pathways related to the symbiotic degradation of hydrocarbons and surfactant production. It is now possible, although more challenging, to obtain the DNA information of an entire microbial community before automatically characterizing it. By characterizing and understanding the interconnected role of microorganisms and the role of degradation and biosurfactant genes in an ecosystem, it becomes possible to develop new biotechnological approaches for bioremediation use. This paper analyzes 46 different metagenome samples, spanning 20 biomes from different geographies obtained from different research projects. Results A metagenomics bioinformatics pipeline, focused on the biodegradation and biosurfactant-production pathways, genes and organisms, was applied. Our main results show that: (1) surfactation and degradation are correlated events, and therefore should be studied together; (2) terrestrial biomes present more degradation genes, especially cyclic compounds, and less surfactation genes, when compared to water biomes; and (3) latitude has a significant influence on the diversity of genes involved in biodegradation and biosurfactant production. This suggests that microbiomes found near the equator are richer in genes that have a role in these processes and thus have a higher biotechnological potential. Conclusion In this work we have focused on the biogeographical distribution of hydrocarbon degrading and biosurfactant producing genes. Our principle results can be seen as an important step forward in the application of bioremediation techniques, by considering the biostimulation, optimization or manipulation of a starting microbial consortia from the areas with higher degradation and biosurfactant producing genetic diversity. Electronic supplementary material The online version of this article (doi:10.1186/s12866-017-1077-4) contains supplementary material, which is available to authorized users.

MutY is a glycosylase known for its role in DNA base excision repair (BER). It is critically important in the prevention of DNA mutations derived from 7,8-dihydro-8-oxoguanine (8-oxoG), which are the major lesions resulting from guanine oxidation. MutY has been described as a DNA repair enzyme in the GO system responsible for removing adenine residues misincorporated in 8-oxoG:A mispairs, avoiding G:C to T:A mutations. Further studies have shown that this enzyme binds to other mispairs, interacts with several enzymes, avoids different transversions/transitions in DNA, and is involved in different repair pathways. Additional activities have been reported for MutY, such as the repair of replication errors in newly synthesized DNA strands through its glycosylase activity. Moreover, MutY is a highly conserved enzyme present in several prokaryotic and eukaryotic organisms. MutY defects are associated with a hereditary colorectal cancer syndrome termed MUTYH-associated polyposis (MAP). Here, we have reviewed the roles of MutY in the repair of mispaired bases in DNA as well as its activities beyond the GO system.

Although microorganisms play crucial roles in ecosystems, metagenomic analyses of soil samples are quite scarce, especially in the Southern Hemisphere. In this work, the microbial diversity of soil samples from an Atlantic Forest and Caatinga was analyzed using a metagenomic approach. Proteobacteria and Actinobacteria were the dominant phyla in both samples. Among which, a significant proportion of stress-resistant bacteria associated to organic matter degradation was found. Sequences related to metabolism of amino acids, nitrogen, and DNA and stress resistance were more frequent in Caatinga soil, while the forest sample showed the highest occurrence of hits annotated in phosphorous metabolism, defense mechanisms, and aromatic compound degradation subsystems. The principal component analysis (PCA) showed that our samples are close to the desert metagenomes in relation to taxonomy, but are more similar to rhizosphere microbiota in relation to the functional profiles. The data indicate that soil characteristics affect the taxonomic and functional distribution; these characteristics include low nutrient content, high drainage (both are sandy soils), vegetation, and exposure to stress. In both samples, a rapid turnover of organic matter with low greenhouse gas emission was suggested by the functional profiles obtained, reinforcing the importance of preserving natural areas.

A dramatização teatral “O Julgamento da Mutação” discute se a Mutação é vilã, fonte de patologias ou se é a mocinha, indispensável para a evolução das espécies, tendo como advogada de defesa a Seleção Natural e o promotor, o gene TP53. A partir dos depoimentos das testemunhas, vários conceitos de Genética são abordados contribuindo para a compreensão do que é mutação e principalmente de seu papel para os seres vivos. Entre as testemunhas estão: Célula-Mãe, Célula-Filha, Enzimas de Reparo, Mutantes, tataraneto de Mendel, Evolução e uma Cientista renomada da área. A decisão final caberá à plateia. [...]

Aesculus hippocastanum L. (Sapindaceae), vulgarly known as horse chestnut, is a native European plant, but widely distributed all over the world. The parts used in medicine are the seeds and the bark of young branches. The seed extract has been marketed as a phytotherapeutic product and it is extensively recommended for treatment of chronic venous insufficiency, traumatic edema, hemorrhoid and postoperative edema. Most of the beneficial effects of horse chestnut are attributed to its principal component aescin. The present study aims to evaluate the citotoxic, genotoxic, mutagenic, and antioxidant activity of this seed extract by performing a set of bacterial and cell-free tests. Phytochemical screening and thin layer chromatography confirmed the presence of aescin as well as others chemical constituents in the studied extract. Negative results were obtained for the occurrence of double-strand breaks in pBCKS plasmid DNA. Two different effects were detected in Escherichia coli strains CC104 and CC104mutMmutY: mutagenic (non-oxidative lesions) and antioxidant. The mutagenic effect was confirmed by Kado assay, where the extract was considered weakly mutagenic towards frameshift mutations. Moreover, the extract demonstrated to protect bacterial cells from lesions induced by mitomycin C, suggesting an antioxidative potential. A. hippocastanum seed extract demonstrated to be genotoxic and weakly mutagenic, as well as antioxidative.

The drawbacks related to the use of viral vectors in gene therapy have been stimulated the research in non-viral strategies such as cationic nanoemulsions. The aim of this work was to develop a stearylamine-containing nanoemulsion for gene therapy purpose. The formulation was chosen from a Pseudo-Ternary Phase Diagram and had its long-term stability assessed by Dynamic Light Scattering and Phase Analysis Light Scattering during 180 days at 4 degrees C, 25 degrees C and 40 degrees C. Besides, studies of sterilization and scale up of the product were conducted. It was demonstrated that the proposed system was stable up to 180 days when stored at 4 degrees C and could be sterilized by a 0.22 microm filter pore without changes on its characteristics. The scale up was possible by adjusting the volume to the sonication time. Because the nanoemulsion presented a droplet size smaller than 200 nm and a zeta potential higher than 30 mV, this system was able to correctly complex the plasmid model PIRES2-EGFP, as confirmed by the agarosis gel electrophoresis assay. The nanoemulsion toxicity evaluated over lung fetus human cells (MRC-5) was dose-dependent. However, it does not appear to be a limiting factor for further experiments aiming gene transfection. As a conclusion, stearylamine-containing cationic nanoemulsions can be used for gene therapy, since it presents suitable characteristics, stability and possibility of sterilization.

Maritime ports are anthropogenic interventions capable of causing serious alterations in coastal ecosystems. In this study, we examined the benthic microbial diversity and community structure under the influence of two maritime ports, Mucuripe (MUC) and Pecém (PEC), at Equatorial Atlantic Ocean in Northeast Brazil. Those seaports differ in architecture, time of functioning, cargo handling and contamination. The microbiomes from MUC and PEC were also compared in silico to 11 other globally distributed marine microbiomes. The comparative analysis of operational taxonomic units (OTUs) retrieved by PCR-DGGE showed that MUC presents greater richness and β diversity of Bacteria and Archaea than PEC. In line with these results, metagenomic analysis showed that MUC and PEC benthic microbial communities share the main common bacterial phyla found in coastal environments, although can be distinguish by greater abundance of Cyanobacteria in MUC and Deltaproteobacteria in PEC. Both ports differed in Archaea composition, being PEC port sediments dominated by Thaumarchaeota. The microbiomes showed little divergence in their potential metabolic pathways, although shifts on the microbial taxonomic signatures involved in nitrogen and sulphur metabolic pathways were observed. The comparative analysis of different benthic marine metagenomes from Brazil, Australia and Mexico grouped them by the geographic location rather than by the type of ecosystem, although at phylum level seaport sediments share a core microbiome constituted by Proteobacteria, Cyanobacteria, Actinobacteria, Tenericuteres, Firmicutes, Bacteriodetes and Euryarchaeota. Our results suggest that multiple physical and chemical factors acting on sediments as a result of at least 60 years of port operation play a role in shaping the benthic microbial communities at taxonomic level, but not at functional level.

DNA repair mechanisms are responsible for maintaining the integrity of DNA and are essential to life. However, our knowledge of DNA repair mechanisms is based on model organisms such as Escherichia coli, and little is known about free living and uncultured microorganisms. In this study, a functional screening was applied in a metagenomic library with the goal of discovering new genes involved in the maintenance of genomic integrity. One clone was identified and the sequence analysis showed an open reading frame homolog to a hypothetical protein annotated as a member of the Exo_Endo_Phos superfamily. This novel enzyme shows 3′-5′ exonuclease activity on single and double strand DNA substrates and it is divalent metal-dependent, EDTA-sensitive and salt resistant. The clone carrying the hypothetical ORF was able to complement strains deficient in recombination or base excision repair, suggesting that the new enzyme may be acting on the repair of single strand breaks with 3′ blockers, which are substrates for these repair pathways. Because this is the first report of an enzyme obtained from a metagenomic approach showing exonuclease activity, it was named ExoMeg1. The metagenomic approach has proved to be a useful tool for identifying new genes of uncultured microorganisms.

Submitted by Vitor Silverio Rodrigues (vitorsrodrigues@reitoria.unesp.br) on 2014-05-27T11:26:50Z No. of bitstreams: 0Bitstream added on 2014-05-27T14:36:47Z : No. of bitstreams: 1 2-s2.0-84863632967.pdf: 452523 bytes, checksum: 1468b79190780eca3a32d7671b90322c (MD5) Made available in DSpace on 2014-05-27T11:26:50Z (GMT). No. of bitstreams: 0 Previous issue date: 2012-06-13 Cationic lipids have been used in the development of non-viral gene delivery systems as lipoplexes. Stearylamine, a cationic lipid that presents a primary amine group when in solution, is able to compact genetic material by electrostatic interactions. In dispersed systems such as nanoemulsions this lipid anchors on the oil/water interface confering a positive charge to them. The aim of this work was to evaluate factors that influence DNA compaction in cationic nanoemulsions containing stearylamine. The influence of the stearylamine incorporation phase (water or oil), time of complexation, and different incubation temperatures were studied. The complexation rate was assessed by electrophoresis migration on agarose gel 0.7%, and nanoemulsion and lipoplex characterization was done by Dynamic Light Scattering (DLS). The results demonstrate that the best DNA compaction process occurs after 120 min of complexation, at low temperature (4 ± 1 °C), and after incorporation of the cationic lipid into the aqueous phase. Although the zeta potential of lipoplexes was lower than the results found for basic nanoemulsions, the granulometry did not change. Moreover, it was demonstrated that lipoplexes are suitable vehicles for gene delivery. © 2012 by the authors; licensee MDPI, Basel, Switzerland. Laboratório de Sistemas Dispersos (LASID) Universidade Federal do Rio Grande do Norte (UFRN), Natal/RN Laboratório de Biologia Molecular e Genômica (LBMG) Departamento de Biologia Celular e Genética Centro de Biociências, Universidade Federal do Rio Grande do Norte (UFRN), Natal/RN Laboratório de Analises Extratograficas Centro de Ciências Exatas e Tecnológicas Universidade Federal do Rio Grande do Norte (UFRN), Natal/RN Departamento de Fármacos e Medicamentos Faculdade de Ciências Farmacêuticas Universidade Estadual Paulista-Unesp, Rodovia Araraquara-Jaú, 14801-902, Araraquara, SP Departamento de Fármacos e Medicamentos Faculdade de Ciências Farmacêuticas Universidade Estadual Paulista-Unesp, Rodovia Araraquara-Jaú, 14801-902, Araraquara, SP

Background and Objectives One of the mechanisms proposed by which H. pylori causes gastric cancer (GC) is through DNA damage due to chronic inflammation. Genomic integrity is guaranteed by repair enzymes such as APE-1, OGG-1, and PARP-1. Host genetic polymorphisms associated with the bacterial strain may influence the ability to repair the damage, contributing to the development of H. pylori-associated GC. The aim of this study was to determine the association of the polymorphisms APE-1 (T2197G), OGG-1 (C1245G), and PARP-1 (A40676G) with H. pylori-genotype in 109 patients with GC. Methods Polymorphism was assessed by polymerase chain reaction (PCR)-restriction fragment length polymorphism (RFLP) and H. pylori detection/genotyping by PCR. Results In the intestinal subtype, PARP-1 wild-type was more frequent (P = 0.001) in patients >50 years old. The repair enzymes genotypes analyzed in combination showed that the less pathogenic strains are associated with the APE-1 polymorphic allele and, unexpectedly, with PARP-1 wild-type, but this last one associated with APE-1 polymorphic allele or in older patients. Conclusions Our results indicate the importance of H. pylori and APE-1 genotypes in the gastric carcinogenesis. Also, support the hypothesis of a decrease of PARP-1 wild-type activity in older individuals. Taken together these data may be an important clue to understand the role of low-virulence strains of H. pylori in gastric carcinogenesis and point the importance to analyze the polymorphisms as a group. J. Surg. Oncol. 2012; 106:448–455. © 2012 Wiley Periodicals, Inc.

Several pharmacological properties are attributed to polysaccharides and glucans derived from fungi such as tumor, anti-inflammatory, and immunomodulatory activity. In this work, the anti-inflammatory potential of polysaccharides from the fungus Scleroderma nitidum and their possible action mechanism were studied. The effect of these polymers on the inflammatory process was tested using the carrageenan and histamine-induced paw edema model and the sodium thioglycolate and zymosan-induced model. The polysaccharides from S. nitidum were effective in reducing edema (73% at 50 mg/kg) and cell infiltrate (37% at 10 mg/kg) in both inflammation models tested. Nitric oxide, a mediator in the inflammatory process, showed a reduction of around 26% at 10 mg/kg of body weight. Analysis of pro-and anti-inflammatory cytokines showed that in the groups treated with polysaccharides from S. nitidum there was an increase in cytokines such as IL-1ra, IL-10, and MIP-1β concomitant with the decrease in INF-γ (75%) and IL-2 (22%). We observed the influence of polysaccharides on the modulation of the expression of nuclear factor κB. This compound reduced the expression of NF-κB by up to 64%. The results obtained suggest that NF-κB modulation an mechanisms that explain the anti-inflammatory effect of polysaccharides from the fungus S. nitidum.

article i nfo The aim of this work was to analyze the genotoxicity in surface water from the Pitimbu River (Natal, Brazil) using a neotropical species Crenicichla menezesi as bioindicator for in situ evaluation. The genotoxicity was analyzed using the micronucleus (MN) and comet assays in erythrocytes. The animals were collected from five sites of the river. A significant increase of MN frequency and comet class L1 to L4 were observed only in specimens collected from three sampling sites (SS3, SS4 and SS5) located into urban areas. These same sites also presented high metals concentration. Correlation of DNA damage and concentrations of Cu (Spearman r=0.8080), Cr (Spearman r=0.9772), and Ni (Spearman r=0.9909) were observed. These data indicate the presence of genotoxic agents. Moreover the C. menezesi species showed to be a good indicator for prompt analyses since this species presents sedentary and carnivore habits.

Several therapeutic properties have been described for Eugenia caryophyllata (clove). In the present study the infusion of E. caryophyllata was evaluated in a series of bacterial and cell-free assays in order to determine genotoxic potential. Negative results were obtained in the SOS chromotest and in the Salmonella reversion assay using strains TA97a, TA98, TA100, and TA102. However, in a forward mutagenesis assay an increase in mutagenesis and high cytotoxicity was observed with the CC104 mutMmutY strain, suggesting that oxidative DNA damage occurred. The treatment of plasmid with clove infusion showed that DNA strand breaks and sites recognized by formamidopyrimidine-DNA-glycosylase (FPG/MutM) were generated. Data suggest that the occurrence of oxidative DNA damage, with low mutagenic potential, may also be involved in the cytotoxicity attributed to clove infusion.

Plant genomic projects, such as Arabidopsis thaliana, rice, and maize, have provided excellent tools for comparative genome analysis on Base Excision DNA Repair (BER). A data-mining study associated with the SUCEST Genome project identified two EST clusters that shared homology to the bacteria MutM/Fpg protein. Comparative analyses presented here show a duplication of the MutM/Fpg gene in sugarcane, wheat and rice. The complementation assays show that both cDNAs from sugarcane are able to complement the Fpg and MutY-glycosylase deficiency in a double mutant Escherichia coli strain (CC104mutMmutY), reducing the spontaneous mutation frequency by 10-fold. The expression analyses by semi-quantitative RT-PCR show that these two mRNAs have different expression levels.

Cell-free and bacterial assays indicate that flavonoid-enriched fractions and the flavonoids of pepper tree stem bark from Schinus terebinthifolius Raddi have genotoxic rather than antigenotoxic properties. In the present report, we have examined the ability of flavonoid-enriched fractions to damage plasmid DNA and the repair pathways involved in the recognition of these DNA lesions. High concentrations of two flavonoid-enriched fractions were able to break phosphodiester bonds in DNA. In addition, studies using bacterial strains deficient in nucleotide excision repair and base excision repair (BER) enzymes indicated that the flavonoid-enriched fractions generated lesions that were substrates for enzymes belonging to the BER pathway. In addition, in vitro studies indicated that the DNA damage produced by the flavonoid-enriched fractions was also a substrate for exonuclease III and that the phosphodiester breakage was amplified by copper ions. These results indicate that flavonoids from the pepper tree (Schinus terebinthifolius, Raddi) generate lesions on DNA that are potential targets of FPG and MutY glycosylase from the BER pathway. Chromatographic and spectral analyses helped to support the hypothesis that the flavonoids of the Brazilian pepper tree bark are the main factors involved in the fraction's damage potential. The isolated flavonoids from Fraction II were also tested in vitro and support the oxidative damage potential of these flavonoids.

Cockayne syndrome (CS) is a rare genetic disorder in which 80% of cases are caused by mutations in the Excision Repair Cross-Complementation group 6 gene (ERCC6). The encoded ERCC6 protein is more commonly referred to as Cockayne Syndrome B protein (CSB). Classical symptoms of CS patients include failure to thrive and a severe neuropathology characterized by microcephaly, hypomyelination, calcification and neuronal loss. Modeling the neurological aspect of this disease has proven difficult since murine models fail to mirror classical neurological symptoms. Therefore, a robust human in vitro cellular model would advance our fundamental understanding of the disease and reveal potential therapeutic targets. Herein, we successfully derived functional CS neural networks from human CS induced pluripotent stem cells (iPSCs) providing a new tool to facilitate studying this devastating disease. We identified dysregulation of the Growth Hormone/Insulin-like Growth Factor-1 (GH/IGF-1) pathway as well as pathways related to synapse formation, maintenance and neuronal differentiation in CSB neurons using unbiased RNA-seq gene expression analyses. Moreover, when compared to unaffected controls, CSB-deficient neural networks displayed altered electrophysiological activity, including decreased synchrony, and reduced synapse density. Collectively, our work reveals that CSB is required for normal neuronal function and we have established an alternative to previously available models to further study neural-specific aspects of CS.

Oxidative DNA damage is considered to be a major cause of neurodegeneration and internal tumors observed in syndromes that result from nucleotide excision repair (NER) deficiencies, such as Xeroderma Pigmentosum (XP) and Cockayne Syndrome (CS). Recent evidence has shown that NER aids in removing oxidized DNA damage and may interact with base excision repair (BER) enzymes. Here, we investigated APE1 and OGG1 expression, localization and activity after oxidative stress in XPC-deficient cells. The endogenous APE1 and OGG1 mRNA levels were lower in XPC-deficient fibroblasts. However, XPC-deficient cells did not show hypersensitivity to oxidative stress compared with NER-proficient cells. To confirm the impact of an XPC deficiency in regulating APE1 and OGG1 expression and activity, we established an XPC-complemented cell line. Although the XPC complementation was only partial and transient, the transfected cells exhibited greater OGG1 expression and activity compared with XPC-deficient cells. However, the APE1 expression and activity did not significantly change. Furthermore, we observed a physical interaction between the XPC and APE1 proteins. Together, the results indicate that the responses of XPC-deficient cells under oxidative stress may not only be associated with NER deficiency per se but may also include new XPC functions in regulating BER proteins.

Background Violacein is a purple pigment from Chromobacterium violaceum that possesses diverse biological and pharmacological properties. Among these, pro-oxidant and antioxidant activities have been suggested. However, the cytotoxic mechanisms induced by violacein are poorly understood and the improvement in knowledge regarding these cell death mechanisms will be useful to develop new therapeutic approaches. Considering this, in our work, we investigated the pro-oxidant effects of violacein in non-tumor (CHO-K1 and MRC-5) and tumor (HeLa) cell lines, searching for a better understanding of reactive oxygen species (ROS) production and cell death induction. Results Cytotoxicity induced by violacein was observed in the three cell lines; however, MRC-5 and HeLa cells were shown to be more sensitive to violacein treatment. Although punctual alterations in the antioxidant apparatus and increase in oxidative stress biomarkers was observed in some violacein concentrations, no association was found between increased oxidative stress and induction of cell death. However, the increase of mitochondrial membrane potential was observed. Conclusions In fact, the increase of mitochondrial membrane potential in MRC-5 and HeLa cells suggests that mitochondrial membrane hyperpolarization might be the main cause of cell death triggered by violacein.

Crude oil extraction, transportation and use provoke the contamination of countless ecosystems. Therefore, bioremediation through surfactants mobilization or biodegradation is an important subject, both economically and environmentally. Bioremediation research had a great boost with the recent advances in Metagenomics, as it enabled the sequencing of uncultured microorganisms providing new insights on surfactant-producing and/or oil-degrading bacteria. Many research studies are making available genomic data from unknown organisms obtained from metagenomics analysis of oil-contaminated environmental samples. These new datasets are presently demanding the development of new tools and data repositories tailored for the biological analysis in a context of bioremediation data analysis. This work presents BioSurfDB, www.biosurfdb.org, a curated relational information system integrating data from: (i) metagenomes; (ii) organisms; (iii) biodegradation relevant genes; proteins and their metabolic pathways; (iv) bioremediation experiments results, with specific pollutants treatment efficiencies by surfactant producing organisms; and (v) a biosurfactant-curated list, grouped by producing organism, surfactant name, class and reference. The main goal of this repository is to gather information on the characterization of biological compounds and mechanisms involved in biosurfactant production and/or biodegradation and make it available in a curated way and associated with a number of computational tools to support studies of genomic and metagenomic data. Database URL: www.biosurfdb.org