Lix Reunión Anual Sociedad De Biología De Chile X Reunión Anual Sociedad Chilena De Evolución

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Lix Reunión Anual Sociedad De Biología De Chile X Reunión Anual Sociedad Chilena De Evolución LIX REUNIÓN ANUAL SOCIEDAD DE BIOLOGÍA DE CHILE X REUNIÓN ANUAL SOCIEDAD CHILENA DE EVOLUCIÓN XXVII REUNIÓN ANUAL SOCIEDAD DE BOTANICA DE CHILE 8 al 10 de Noviembre 2016 HIPPOCAMPUS RESORT & CLUB-COSTA DE MONTEMAR-CONCÓN 2 AUSPICIADORES BioMed Central (BMC) COMISIÓN NACIONAL DE INVESTIGACIÓN CIENTÍFICA Y TECNOLÓGICA FACULTAD DE CIENCIAS, UNIVERSIDAD DE CHILE FACULTAD DE CIENCIAS BIOLÓGICAS, PONTIFICIA UNIVERSIDAD CATÓLICA DE CHILE FUNDACIÓN CHILENA PARA LA BIOLOGIA CELULAR UNIVERSIDAD AUTÓNOMA DE CHILE 3 CONFERENCIAS 4 CONFERENCIA INAUGURAL HOMEOSTATIC REGULATION OF ARTERIAL PCO2: NEURAL CIRCUITS AND MOLECULAR MECHANISMS OF CO2 SENSING Guyenet, P.G. PhD, Department of Pharmacology, University of Virginia, Charlottesville, VA. Breathing is a rhythmic motor behavior under metabolic, voluntary and emotional control. During quiet rest or sleep, the breathing rhythm is generated by a bilateral cluster of excitatory neurons, the preBötzinger complex which subsequently activates a network of excitatory or inhibitory interneurons (pattern generator) that fire during specific phases of the breathing cycle and eventually trigger the orderly activation of the breathing muscles. The three most powerful stimulatory influences on breathing are exercise, hypercapnia and hypoxia. The effects of hypoxia are mediated primarily via the carotid bodies and those of CO2 via the retrotrapezoid nucleus (RTN). RTN neurons are glutamatergic. Their firing is exquisitely sensitive to arterial pH in vivo (0.5Hz/0.01 pH). Their pH-sensitivity is partly intrinsic (proton sensors: TASK-2 and GPR4) and partly astrocyte–dependent. RTN stimulates every aspect of breathing including active (abdominal) expiration. During quiet rest and non-REM sleep breathing automaticity requires RTN input and the breathing stimulation elicited by RTN is directly proportional to arterial pH. Finally, RTN neurons are silenced by hypobaric hypoxia. RTN development relies on transcription factors egr-2, phox2b and atoh-1. Phox2b mutations cause CCHS, a developmental disease characterized by the absence of chemoreflex and severe night-time hypoventilation. Phox2b mutations in mice abort RTN development selectively and recapitulate the human disease. In brief, RTN are central respiratory chemoreceptors. Except under hypobaric hypoxia, RTN sustains breathing automaticity while maintaining arterial PCO2 constant. This dual function is especially crucial during non-REM sleep. 5 CONFERENCIA DR. HERMAN NIEMEYER MITOCHONDRIAL NON-CODING RNAs: NOVEL TARGETS FOR CANCER THERAPY?. Burzio ,L.O. Andes Biotechnologies Sp.A, Fundación Ciencia & Vida, and Facultad de Ciencias Biológicas, Universidad Andrés Bello, Santiago, Chile ([email protected]). A family of mitochondrial lncRNAs (ncmtRNAs) arising from the mitochondrial 16S rRNA gene will be described. They comprise a Sense (SncmtRNA) and Antisense (ASncmtRNA) members, both of which contain long inverted repeats and therefore dsRNA regions. These transcripts are differentially expressed according to proliferative status; both transcript types are readily detected in normal proliferating cells, but not in resting cells. Tumor cells (human and mouse) express the SncmtRNA but down regulate the ASncmtRNAs. We proposed that the ASncmtRNAs is tumor suppressor and a generalized hallmark of cancer. We showed that knock-down of ASncmtRNA with antisense oligonucleotides (ASK for short) induces selective death of tumor cells, leaving normal cells unaffected. Tumor cell death displays characteristics of apoptosis and is mediated by down-regulation of Survivin and XIAP. Cell death is preceded by a drastic reduction in proliferative index, mediated through a marked decrease only of Cyclin D1 and B1. In addition, ASK induces drastic inhibition of sphere formation together with down regulation of N-cadherin and B-caveolin important factor pre-metastasis. The reduction in survivin, both cyclins, N-cadherin and β-caveolin seem to be mediated by microRNAs arising upon ASncmtRNA knock down. Indeed, ASK induces several described microRNAs several derived from the ASncmtRNAs. Among them, we found strong increase of hsa-miR-1973 and hsa-miR-4485, whose sequence share a perfect match with internal segments of ASncmtRNAs. Mimics assay demonstrate that hsa-miR-4485 expression inhibition of cyclin D1 and B1 plus N-cadherin. Translation studies demonstrate that the ASncmtRNAs are potent target for cancer therapy. This results will include examples of syngeneic (melanoma B16F10 cells and renal carcinoma Renca cells) as well as xenograph assays with human prostate carcinoma (PC3 cells) and breast carcinoma (MDA-MB-231 cells). 6 CONFERENCIA SOCIEDAD DE BIOLOGÍA DE CHILE- GRUPO BIOS AL CIENTIFICO JOVEN MAS DESTACADO 2015 INFECCIONES CAUSADAS POR CLOSTRIDIUM DIFFICILE: AVANCES EN LA BIOLOGÍA DE LAS ESPORAS DE C. DIFFICILE Y LOS MECANISMOS DE INTERACCIÓN CON EL HOSPEDERO. Paredes-Sabja, D. Microbiota-Host Interactions and Clostridia Research Group; Universidad Andrés Bello, Santiago Chile. Clostridium difficile es un patógeno anaerobio, formador de esporas y el agente etiológico más importante de las diarreas asociadas a antibióticos tanto nosocomiales como adquiridas en la comunidad. A pesar que las esporas de C. difficile son el principal vehículo de infección, de persistencia en el hospedero y de transmisión, pocos estudios se han enfocado sobre este clave aspecto. En este sentido, nuestro grupo se ha enfocado en estudiar como las esporas de C. difficile interactúan con la mucosa intestinal del hospedero. Nuestros estudios han revelado características únicas de las esporas que las hacen ser altamente transmisibles relacionadas con las propiedades de resistencia intrínsecas de las esporas de C. difficile. Hemos desarrollado métodos para identificar la composición de la superficie de las esporas C.de difficile, y caracterizado la variabilidad ultraestructural de las capas más externas de la esporas de cepas epidémicas. Recientemente, mediante la inactivación de genes del exosporium, hemos comenzado a elucidar los mecanismos asociados al ensamblaje de las capas externas de esporas de C. difficile, e identificado varios factores morfogenéticos esenciales para su ensamblaje. Otras líneas de investigación incluyen el desarrollo de nuevas estrategias terapéuticas para el tratamiento de las infecciones recurrentes deC. difficile. 7 CONFERENCIA SOCIEDAD CHILENA DE EVOLUCIÓN VERTEBRATE MACROEVOLUTION AND THE IMPORTANCE OF MUSEUMS, FOSSILS AND DATA-SCIENCE Price, S. Department of Evolution & Ecology, University of California Davis, 1 Shields Avenue, Davis, CA 95618, USA. Understanding how patterns of ecomorphological and lineage diversity are influenced by biotic and abiotic factors and the interaction between them is of fundamental importance. Only by understanding the regulators of biodiversity in the past can we begin to predict future responses to global change. The successful synthesis of phylogenetic and paleontological information has the potential to vastly improve our understanding of macroevolution as separate analyses of the fossil record and extant phylogenies frequently infer different factors as important drivers of diversification. To identify macroevolutionary patterns of biodiversity and their drivers requires an integrative approach, tapping the vast reserves of scientific data in museum collections and the published scientific literature data and thus combining traditional ecomorphology and phylogenetics with data-science techniques. I illustrate how this approach can identify repeating themes and general principles governing the evolution of vertebrate diversity using my recent work on dietary evolution and its impact on mammalian diversification and the ecological drivers of fish body shape diversity. 8 CONFERENCIA SOCIEDAD CHILENA DE EVOLUCIÓN LA ESPECIALIZACIÓN HA MUERTO...¡VIVA LA ESPECIALIZACIÓN! (Specialization is dead...¡long live to specialization!) Medel R1, 1Departamento de Ecología, Facultad de Ciencias, Universidad de Chile. La especialización como estrategia evolutiva ha sido un concepto central en estudios de ecología y evolución, en parte debido a su íntima conexión con fenómenos de adaptación biológica. En consecuencia, gran parte de nuestra interpretación de la naturaleza se ha sustentado en teorías construidas bajo ese paradigma. Sin embargo, en las últimas décadas ha ocurrido un reemplazo desde un paradigma de especialización a uno de generalización, donde interacciones múltiples y a menudo reticulares parecieran caracterizar de mejor manera los sistemas naturales. Así, la idea de especialización ha dado paso a una visión más generalista donde lo que predomina son las interacciones entre conjuntos de poblaciones y especies por sobre relaciones más estrechas. No obstante lo anterior, la especialización puede ser: a) un resultado directo de la evolución de los linajes o, b) un producto colateral impuesto por restricciones históricas. En esta charla desarrollaré ambos conceptos, poniendo especial énfasis en la segunda definición. Para ello, usando ejemplos de interacciones mutualistas y antagonistas de la biota chilena, ilustro la manera en que restricciones históricas han generado un ambiente Mediterráneo que, a diferencia de lo observado en otras latitudes, contiene una alta prevalencia de interacciones especializadas. Este fenómeno, propio de biotas insulares, resulta de un pool inicial limitado de especies de flora y fauna mas que de estrategias de especialización evolutiva en los linajes. En consecuencia, y de acuerdo a estas consideraciones,
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