Pharmacological Rac1 inhibitors with selective apoptotic activity in human acute leukemic cell lines

Rac1 GTPase has long been recognized as a critical regulatory protein in different cellular and molecular processes involved in cancer progression, including acute myeloid leukemia. Here we show the antitumoral activity of ZINC69391 and 1A-116, two chemically-related Rac1 pharmacological inhibitors, on a panel of four leukemic cell lines representing different levels of maturation. Importantly, we show that the main mechanism involved in the antitumoral effect triggered by the Rac1 inhibitors comprises the induction of the mitochondrial or intrinsic apoptotic pathway. Interestingly, Rac1 inhibition selectively induced apoptosis on patientderived leukemia cells but not on normal mononuclear cells. These results show the potential therapeutic benefits of targeting Rac1 pathway in hematopoietic malignancies.Fil: Cabrera, Maia Diana Eliana. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Farmacológicas. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Investigaciones Farmacológicas; ArgentinaFil: Echeverría, Emiliana Beatriz. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Farmacológicas. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Investigaciones Farmacológicas; ArgentinaFil: Remes Lenicov, Federico. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; ArgentinaFil: Cardama, Georgina Alexandra. Universidad Nacional de Quilmes. Departamento de Ciencia y Tecnología. Laboratorio de Oncología Molecular; ArgentinaFil: González, Nazareno. Universidad Nacional de Quilmes. Departamento de Ciencia y Tecnología. Laboratorio de Oncología Molecular; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Davio, Carlos Alberto. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Farmacológicas. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Investigaciones Farmacológicas; ArgentinaFil: Fernandez, Natalia Cristina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Farmacológicas. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Investigaciones Farmacológicas; ArgentinaFil: Lorenzano Menna, Pablo. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad Nacional de Quilmes. Departamento de Ciencia y Tecnología. Laboratorio de Oncología Molecular; Argentin

Physiological implications of biased signaling at histamine H2 receptors

Histamine mediates numerous functions acting through its four receptor subtypes all belonging to the large family of seven transmembrane G-protein coupled receptors. In particular, histamine H2 receptor (H2R) is mainly involved in gastric acid production, becoming a classic pharmacological target to treat Zollinger–Ellison disease and gastric and duodenal ulcers. H2 ligands rank among the most widely prescribed and over the counter-sold drugs in the world. Recent evidence indicate that some H2R ligands display biased agonism, selecting and triggering some, but not all, of the signaling pathways associated to the H2R. The aim of the present work is to study whether famotidine, clinically widespread used ligand acting at H2R, exerts biased signaling. Our findings indicate that while famotidine acts as inverse agonist diminishing cAMP basal levels, it mimics the effects of histamine and the agonist amthamine concerning receptor desensitization and internalization. Moreover, the treatment of HEK293T transfected cells with any of the three ligands lead to a concentration dependent pERK increment. Similarly in AGS gastric epithelial cells, famotidine treatment led to both, the reduction in cAMP levels as well as the increment in ERK phosphorylation, suggesting that this behavior could have pharmacological relevant implications. Based on that, histidine decarboxylase expression was studied by quantitative PCR in AGS cells and its levels were increased by famotidine as well as by histamine and amthamine. In all cases, the positive regulation was impeded by the MEK inhibitor PD98059, indicating that biased signaling toward ERK1/2 pathway is the responsible of such enzyme regulation. These results support that ligand bias is not only a pharmacological curiosity but has physiological and pharmacological implications on cell metabolism.Fil: Alonso, Natalia. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental (i); ArgentinaFil: Zappia, Carlos Daniel. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Farmacología. Cátedra de Química Medicinal; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Cabrera, Maia Diana Eliana. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Farmacología. Cátedra de Química Medicinal; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Davio, Carlos Alberto. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Farmacología. Cátedra de Química Medicinal; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Farmacológicas (i); Argentina; ArgentinaFil: Shayo, Carina Claudia. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental (i); ArgentinaFil: Monczor, Federico. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Farmacología. Cátedra de Química Medicinal; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Fernandez, Natalia Cristina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Farmacología. Cátedra de Química Medicinal; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentin

An integrated biochemical system for nitrate assimilation and nitric oxide detoxification in Bradyrhizobium japonicum

Rhizobia are recognized to establish N(2)-fixing symbiotic interactions with legume plants. Bradyrhizobium japonicum, the symbiont of soybeans, can denitrify and grow under free-living conditions with nitrate (NO(3)(−)) or nitrite (NO(2)(−)) as sole nitrogen source. Unlike related bacteria that assimilate NO(3)(−), genes encoding the assimilatory NO(3)(−) reductase (nasC) and NO(2)(−) reductase (nirA) in B. japonicum are located at distinct chromosomal loci. The nasC gene is located with genes encoding an ABC-type NO(3)(−) transporter, a major facilitator family NO(3)(−)/NO(2)(−) transporter (NarK), flavoprotein (Flp) and single-domain haemoglobin (termed Bjgb). However, nirA clusters with genes for a NO(3)(−)/NO(2)(−)-responsive regulator (NasS-NasT). In the present study, we demonstrate NasC and NirA are both key for NO(3)(−) assimilation and that growth with NO(3)(−), but not NO(2)(−) requires flp, implying Flp may function as electron donor to NasC. In addition, bjgb and flp encode a nitric oxide (NO) detoxification system that functions to mitigate cytotoxic NO formed as a by-product of NO(3)(−) assimilation. Additional experiments reveal NasT is required for NO(3)(−)-responsive expression of the narK-bjgb-flp-nasC transcriptional unit and the nirA gene and that NasS is also involved in the regulatory control of this novel bipartite assimilatory NO(3)(−)/NO(2)(−) reductase pathway

Dual role of cAMP in the transcriptional regulation of multidrug resistance-associated protein 4 (MRP4) in pancreatic adenocarcinoma cell lines

Cyclic AMP represents one of the most studied signaling molecules and its role in proliferation and differentiation processes has been well established. Intracellular cAMP levels are tightly regulated where the MRP4 transporter plays a major role. In the present study, we sought to establish whether cAMP modulated MRP4 expression in pancreatic adenocarcinoma cell lines. Quantitative PCR and western blot studies showed that cAMP-increasing agents enhanced MRP4 transcripts and protein levels in PANC-1 cells. Reporter luciferase experiments carried out in pancreatic AR42J cells showed that intracellular cAMP up-regulates MRP4 through an Epac2- and Rap1- mediated mechanism whereas extracellular cAMP reduced MRP4 promoter activity by a MEK/ERK-mediated pathway. Present results show that cAMP regulates MRP4 promoter activity, and further indicate that the balance between intracellular and extracellular cAMP levels determines MRP4 expression.Fil: Carozzo, Alejandro Enrique. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Farmacología. Cátedra de Química Medicinal; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Diez, Federico Ruben. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Farmacología. Cátedra de Química Medicinal; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Gómez, Natalia. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Farmacología. Cátedra de Química Medicinal; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Cabrera, Maia Diana Eliana. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Farmacología. Cátedra de Química Medicinal; ArgentinaFil: Shayo, Carina Claudia. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental (i); Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Farmacología. Cátedra de Química Medicinal; ArgentinaFil: Davio, Carlos Alberto. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Farmacología. Cátedra de Química Medicinal; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Fernández, Natalia Brenda. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Farmacología. Cátedra de Química Medicinal; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental (i); Argentin

The Regulator of G Protein Signaling Homologous Domain of G Protein-Coupled Receptor Kinase 2 Mediates Short-Term Desensitization of β3-Adrenergic Receptor

G protein coupled receptor (GPCR) kinases (GRKs) are key regulators of GPCR signaling. Canonical mechanism of GPCR desensitization involves receptor phosphorylation by GRKs followed by arrestin recruitment and uncoupling from heterotrimeric G protein. Although β3-adrenergic receptor (β3AR) lacks phosphorylation sites by GRKs, agonist treatment proved to induce β3AR desensitization in many cell types. Here we show that GRK2 mediates short-term desensitization of β3AR by a phosphorylation independent mechanism but mediated by its domain homologous to the regulator of G protein signaling (RGS). HEK293T cells overexpressing human β3AR presented a short-term desensitization of cAMP response stimulated by the β3AR agonist, BRL37344, and not by forskolin. We found that β3AR desensitization was higher in cells co-transfected with GRK2. Similarly, overexpression of the RGS homology domain but not kinase domain of GRK2 increased β3AR desensitization. Consistently, stimulation of β3AR increased interaction between GRK2 and Gαs subunit. Furthermore, in rat cardiomyocytes endogenously expressing β3AR, transfection with dominant negative mutant of RH domain of GRK2 (GRK2/D110A) increased cAMP response to BRL37344 and inhibited receptor desensitization. We expect our study to be a starting point for more sophisticated characterization of the consequences of GRK2 mediated desensitization of the β3AR in heart function and disease.Fil: Echeverría, Emiliana Beatriz. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Farmacológicas. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Investigaciones Farmacológicas; ArgentinaFil: Cabrera, Maia Diana Eliana. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Farmacológicas. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Investigaciones Farmacológicas; ArgentinaFil: Burghi, Valeria. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Farmacológicas. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Investigaciones Farmacológicas; ArgentinaFil: Sosa, Máximo Hernán. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Farmacológicas. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Investigaciones Farmacológicas; ArgentinaFil: Ripoll, Sonia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Farmacológicas. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Investigaciones Farmacológicas; ArgentinaFil: Yaneff, Agustín. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Farmacológicas. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Investigaciones Farmacológicas; ArgentinaFil: Monczor, Federico. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Farmacológicas. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Investigaciones Farmacológicas; ArgentinaFil: Davio, Carlos Alberto. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Farmacológicas. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Investigaciones Farmacológicas; ArgentinaFil: Shayo, Carina Claudia. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: Fernandez, Natalia Cristina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Farmacológicas. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Investigaciones Farmacológicas; Argentin

Identification of inhibitors of the RGS homology domain of GRK2 by docking-based virtual screening

Aims: G protein-coupled receptor (GPCR) kinases (GRKs) are mainly involved in the desensitization of GPCRs. Among them, GRK2 has been described to be upregulated in many pathological conditions and its crucial role in cardiac hypertrophy, hypertension, and heart failure promoted the search for pharmacological inhibitors of its activity. There have been several reports of potent and selective inhibitors of GRK2, most of them directed to the kinase domain of the protein. However, the homologous to the regulator of G protein signaling (RH) domain of GRK2 has also been shown to regulate GPCRs signaling. Herein, we searched for potential inhibitors of receptor desensitization mediated by RH domain of GRK2. Materials and methods: We performed a docking-based virtual screening utilizing the crystal structure of GRK2 to search for potential inhibitors of the interaction between GRK2 and Gαq protein. To evaluate the biological activity of compounds we measured, calcium response of histamine H1 receptor (H1R) using Fura-2AM dye and H1R internalization by saturation binding experiments in A549 cells. GRK2(45–178)GFP translocation was determined in HeLa cells through confocal fluorescence imaging. Key findings: We identified inhibitors of GRK2 able to reduce the RH mediated desensitization of the histamine H1 receptor and GRK2 translocation to plasma membrane. Also candidates presented adequate lipophilia and cytotoxicity profile. Significance: We obtained compounds with the ability of reducing RH mediated actions of GRK2 that can be useful as a starting point in the development of novel drug candidates aimed to treat pathologies were GRK2 plays a key role.Fil: Echeverría, Emiliana Beatriz. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Farmacológicas. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Investigaciones Farmacológicas; ArgentinaFil: Velez Rueda, Ana Julia. Universidad Nacional de Quilmes. Departamento de Ciencia y Tecnología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Cabrera, Maia Diana Eliana. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Farmacológicas. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Investigaciones Farmacológicas; Argentina. Universidad Nacional de Quilmes. Departamento de Ciencia y Tecnologia. Laboratorio de Farmacologia Molecular.; ArgentinaFil: Juritz, Ezequiel. Universidad Nacional de Quilmes; Argentina. Universidad Andrés Bello; Chile. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Burghi, Valeria. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Farmacológicas. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Investigaciones Farmacológicas; ArgentinaFil: Fabian, Lucas Emanuel. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Metabolismo del Fármaco. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Metabolismo del Fármaco; ArgentinaFil: Davio, Carlos Alberto. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Farmacológicas. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Investigaciones Farmacológicas; ArgentinaFil: Lorenzano Menna, Pablo. Universidad Nacional de Quilmes. Departamento de Ciencia y Tecnologia. Laboratorio de Farmacologia Molecular.; Argentina. Universidad Nacional de Rosario; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Fernandez, Natalia Cristina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Farmacológicas. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Investigaciones Farmacológicas; Argentin

Comparative analysis of arterial stiffness non invasively evaluated in hemodialyzed patients

pacientes hemodializados se producen en vasos elásticos y musculares pero sólo la Velocidad de la Onda del Pulso (VOP) aórtica ha demostrado ser un índice de alto valor pronóstico. Lo cual deja de lado a las arterias musculares. Los objetivos del estudio fueron: a) medir la VOP aórtica y la carotido-radial de pacientes hemodializados, y b) repetir el análisis anterior en la misma cohorte 5 años después, comparando cuatro índices diferentes de rigidez arterial. Material y métodos: a 23 pacientes hemodializados se les evaluó la VOP aórtica (VOPcf), la carotido-radial (VOPcr) y se calculó: la VOP centro-periférica (VOPcp), la diferencia (ΔVOP), el desacople de VOP y su cambio porcentual (%VOP). Las evaluaciones se hicieron en 2007 (Tiempo 1) y en 2012 (Tiempo 2). Resultados: La VOPcp mostró un aumento significativo entre la evaluación realizada entre el Tiempo 1 y el 2 (de 1.1±0.3 a 1.4±0.4; p<0.01). En los mismos tiempos ΔVOP mostró que los valores se incrementaban en términos negativos (de -0.9±3.0 a -2.7±2.9; p<0.05). El desacople de la rigidez centro-periférica mostró un significativo aumento (valores negativos) entre el Tiempo 1 y 2 (de 0.0±0.1 a -0.1±0.1; p<0.02). El %VOP ANÁLISIS COMPARATIVO DE LA RIGIDEZ ARTERIAL EVALUADA EN FORMA NO INVASIVA EN PACIENTES HEMODIALIZADOS COMPARATIVE ANALYSIS OF ARTERIAL STIFFNESS NON INVASIVELY EVALUATED IN HEMODIALYZED PATIENTS Cinthia Galli (1,2), Rodolfo Valtuille (3), Maia Daniela Percunte (2), Nahuel Hernán Carrizo (2), Daniel Bia (4), Ricardo Armentano (1,2), Edmundo Cabrera Fischer (1,2) 1) Área de Investigación y Desarrollo Universidad de Favaloro (AIDUF), Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Buenos Aires 2) Facultad Regional Buenos Aires, Universidad Tecnológica Nacional, Buenos Aires 3) Fresenius FME Burzaco, Buenos Aires 4) Departamento de Fisiología, Facultad de Medicina, Universidad de la República, Montevideo, Uruguay Nefrología, Diálisis y Trasplante 2016; 36 (1) Pág. 26-33 entre ambas mediciones (valores negativos) mostró un significativo aumento (de -4.8±22.0 a -21.5±24.2; p<0.05). Conclusiones: en la presente investigación los índices de rigidez obtenidos en pacientes hemodializados, incluyendo arterias tanto elásticas y musculares, mostraron diferencias estadísticamente significativas cuando se compararon dos mediciones separadas por cinco años. Sin embargo los niveles de significación no fueron similares.Objectives: Changes in arterial stiffness in hemodialysis patients occur both, in elastic and muscular vessels but only the aortic Pulse Wave Velocity (PWV) has demonstrated to be a high prognostic value index, however, muscular arteries are not involved in the aortic PWV measurement. The purpose of this research was: a) to evaluate the aortic and carotid-radial PWV of hemodialysis patients, b) to repeat these measurements in the same cohort after 5 years comparing four different arterial stiffness indexes. Methods: 23 hemodialyzed patients carotid-femoral PWV (PWVcf) and carotidradial (PWVcr) were evaluated and calculations were as follows: PWV ratio, PWV difference (/ PWV), PWV mismatch and PWV percentage change (%PWV). These evaluations were performed using data obtained in 2007 (Time 1) and 2012 (Time 2). Results: PWV ratio showed a significant increase between measurements performed in Time 1 and 2 (from 1.1±0.3 to 1.4±0.4; p≤0.01). Similar increases in negative terms were found when /PWV was calculated from -0.9±3.0 to -2.7±2.9; p≤0.05) Calculated values of PWV mismatch increased significantly (negative values) between Time 1 and 2 (from 0.0±0.1 to -0.1±0.1; p≤0.02) Percent changes of PWV between Time 1 and 2 (negative values) showed a significant increase (from -4.8±22.0 to -21.5±24.2; p≤0.05). Conclusions: Stiffness indexes, obtained in hemodialyzed patients including both elastic and muscular arteries used in this research showed statistically significant differences when two measures with 5 years interval were compared. However significance levels were not similar.Fil: Galli, Cintia Nora. Universidad Tecnológica Nacional. Facultad Regional Buenos Aires; Argentina. Universidad Favaloro. Área de Investigación y Desarrollo; ArgentinaFil: Valtuille, Rodolfo. Fresenius Medical Care Burzaco; ArgentinaFil: Percunte, Maia Daniela. Universidad Tecnológica Nacional. Facultad Regional Buenos Aires; ArgentinaFil: Carrizo, Nahuel Hernán. Universidad Tecnológica Nacional. Facultad Regional Buenos Aires; ArgentinaFil: Bia, Daniel. Universidad de la República; UruguayFil: Armentano, Ricardo Luis. Universidad Tecnológica Nacional. Facultad Regional Buenos Aires; Argentina. Universidad Favaloro. Área de Investigación y Desarrollo; ArgentinaFil: Cabrera Fischer, Edmundo Ignacio. Universidad Favaloro. Área de Investigación y Desarrollo; Argentina. Universidad Tecnológica Nacional. Facultad Regional Buenos Aires; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentin

Anthropogenic Effects on the Fouling Community: Impacts of Biological Invasions and Anthropogenic Structures on Community Structure

Coastal anthropogenic infrastructure has significantly modified nearshore environments. Because these structures often have a strong association with shipping as would be found in ports and harbors, they have been identified as invasion hotspots. Due to propagule pressure from shipping and recreational boating and suitable uncolonized substrate that provides a refuge from native predators, a greater number of non-native species have been found on these structures compared to nearby natural substrate. The mechanisms that limit the spread of non-native species from anthropogenic structures to natural substrate have been explored for several taxa at a species-specific level, but less so from an overall community perspective. Predation has been identified as one of the biotic interactions limiting invasion success. In addition to predation, dispersal ability may also prevent the spread of non-native species from anthropogenic structures to natural substrate. This thesis addresses how these two mechanisms interact to limit the spread of non-native species from anthropogenic structures to natural substrate and how that alters overall community composition. I aimed to explore differences between communities inside and outside of a marina and determine the extent to which predator and dispersal limitation were structuring these communities. I used a three-factor design, deploying seven unglazed ceramic tiles per each treatment combination of 1) inside versus outside a marina in Yaquina Bay, Oregon; 2) cage keeping out predators greater than the mesh size, no cage, or partial cage; 3) fixed near the substrata (benthic) versus suspended 1 meter below the surface. I also transplanted caged, suspended tiles of either adults or recruits from inside the marina to benthic and suspended caging treatments outside of the marina. These tiles allowed me to examine predation when dispersal limitation was not a factor for the community inside the marina, i.e. what happens to both recruits and adults if they can get outside of the marina. I found that the communities inside and outside of the marina were different and the data suggest that both predation and dispersal limitation interact to limit the spread of non-native species. Additionally, I found that mesopredators that could fit through the caging may be influencing predation results and community structure. This research addresses gaps in scientific knowledge regarding the mechanisms that prevent or facilitate the spread of non-native species. Future work could include the further exploration of mesopredation as an important factor in limiting the spread of non-native species and exploring dispersal limitation more in depth as well as broadening the geographic scope to see if the same trends hold true across bays and bioregions