GCN5 maintains genome stability during development

The histone acetyltransferase, GCN5, is essential for survival of mice during embryogenesis. GCN5 null embryos die early during development due to increased apoptosis. We have demonstrated that the increased apoptosis in associated with increased p53 protein levels. Loss of p53 rescues the embryonic apoptosis in the GCN5 null embryos. These results raised the question of what molecular trigger leads to p53 stabilization and cell death in the absence of GCN5. p53 is generally referred to as the gatekeeper of the cell, monitoring cellular responses to DNA damage, genotoxic stress, and other unfavorable conditions in the cell. Therefore, we examined individual cells in wild type and mutant embryos for gross chromosomal aberrations that might trigger a genome integrity checkpoint. Karyotype analysis indicates that approximately 30% of the cells in an E8.5 GCN5 null embryo display chromosomal aberrations, predominantly chromosomal end adhesions and associations. In wild type E8.5 embryos, only 6% of the cells have chromosomal aberrations. Recent data using telomeric FISH demonstrates that cells from GCN5 null embryos have a decreased telomeric signal. Telomere maintenance is essential for maintaining genome integrity. Telomeric defects are associated with loss of chromosomes and chromosomal rearrangements that can lead to detrimental gene fusions involved in many types of cancers. Little is known about the chromatin structures present near the telomeric ends, or whether any of the telomere-associated proteins are subject to post-translational modification such as acetylation. Our results are the first data to demonstrate the involvement of a histone acetyltransferase, GCN5, in maintaining genome integrity through telomere maintenance and/or capping. ^

The role of deregulated E2F1 expression in brain tumors

Mutations disabling the retinoblastoma (Rb) pathway are among the most common in human cancers, including brain cancer. These mutations promote tumor development through deregulated control of the E2F family of transcription factors. E2F1 belongs to a class of E2F's identified as transcriptional activators and involved in the G1/S phase transition of the cell. However, E2F-1 presents with a paradox as it is considered to have membership in two gene classes, functioning as both an oncogene and a tumor suppressor. This unusual trait generates a degree of uncertainty on the role that E2F1 plays in the development or maintenance of any given tumor. Here we show that E2F1 functions as an oncogene in brain tumors through the generation of mice engineered to overexpress E2F1 specifically within glial cells and neuronal progenitors as directed by the GFAP promoter. Mice carrying the transgene develop with high penetrance a phenotype characterized by neurological deficits including paresia, ataxia, head tilt and seizures. MRI imagining of the tgE2F1 mice reveals a low incidence of mild hydrocephalus, and most notably, histological analysis demonstrates that 25% of tgE2F1 mice present with the spontaneous formation of malignant brain tumors. Overall these neoplasms show histological features from a wide range of aggressive brain cancers including medulloblastoma, choroid plexus carcinoma, primary neuroectodermic tumor and malignant gliomas. Isolation and characterization of astrocytes from the tgE2F1 animal reveals a highly proliferative population of cells with 55% ± 2.5 of the tgE2F1astrocytes, 35% ± 3.4 normal mouse astrocytes in S-phase and the acquired capacity to grow in anchorage independent conditions. Additionally tgE2F1 astrocytes show an aberrant phenotype with random chromosomal fusions and nearly all cells demonstrating polyploidy. Taken together, this model forces a comparison to human brain tumor formation. Mouse age as related to tumoral mimics the human scenario with juvenile tgE2F1 mice presenting embryonal tumors typically identified in children, and older tgE2F1 mice demonstrating gliomas. In this regard, this study suggests a global role for E2F1 in the formation and maintenance of multilineage brain tumors, irrefutably establishing E2F1 as an oncogene in the brain. ^

Role of telomere dysfunction, DNA damage response and p53 mutations in tumorigenesis and aging

The ends of eukaryotic chromosomes are protected by specialized ribonucleoprotein structures termed telomeres. Telomeres protect chromosomes from end-to-end fusions, inappropriate repair and degradation. Disruption of this complex activates an ATM/ATR DNA damage response (DDR) pathway. One component of the complex is the Protection Of Telomeres 1 (POT1) protein, an evolutionarily conserved protein which binds single-stranded 3' overhang and is required for both chromosomal end protection and telomere length regulation. The mouse contains two POT1 orthologs, Pot1a and Pot1b. Here we show that both proteins colocalize with telomeres through interaction with the adapter protein TPP1. In addition, compared to Pot1a, the OB-folds of Pot1b possess less sequence specificity for telomeres. Disruption of POT1 proteins result in telomere dysfunction and activation of an ATR-dependent DDR at telomeres, suggesting that this response is normally suppressed by POT1 binding to the single-stranded G-overhang. ^ Telomeres are maintained by telomerase, and its absence in somatic cells results in telomere progressive loss that triggers the activation of p53. Telomere dysfunction initiates genomic instability and induces both p53-dependent replicative senescence and apoptosis to suppress tumorigenesis. In the absence of functional p53, this genomic instability promotes cancer. It was previously not known which aspect of the p53 dependent DNA damage response is important to suppress tumorigenesis initiated by dysfunctional telomeres. The p53R172P knock-in mouse, which is unable to induce apoptosis but retains intact cell cycle arrest/cellular senescence pathways, allowed us to examine whether p53-dependent apoptosis is a major tumor suppression pathway initiated in the setting of telomere dysfunction. Spontaneous tumorigenesis remains potently suppressed in late generation telomerase null mice possessing the p53P/P mutation. These results suggest that suppression of spontaneous tumorigenesis initiated by dysfunctional telomeres requires activation of a p53-dependent senescence pathway. In addition, we used another knock-in mouse model with a p53R172H (p53H) point mutation to test the hypothesis that telomere dysfunction promotes chromosomal instability and accelerates the onset of tumorigenesis in vivo in the setting of this most common gain-of-function mutation in the human Li Fraumeni cancer syndrome. We unexpectedly observed that telomerase null mice possessing dysfunctional telomeres in the setting of the p53H/+ mutation develop significantly fewer tumors, die prematurely and exhibit higher level of cellular senescence, apoptosis and elevated genomic instability compared to telomerase intact p53H/+ and telomerase null p53+/+ mice. These contrasting results thus link cancer and aging to the functional status of telomeres and the integrity of the p53 pathway. ^

Control of the master virulence regulatory gene atxA in Bacillus anthracis

Transcription of the Bacillus anthracis structural genes for the anthrax toxin proteins and biosynthetic operon for capsule are positively regulated by AtxA, a transcription regulator with unique properties. Consistent with the role of atxA in virulence factor expression, a B. anthracis atxA-null mutant is avirulent in a murine model for anthrax. In batch culture, multiple signals impact atxA transcript levels, and the timing and steady state level of atxA expression is critical for optimal toxin and capsule synthesis. Despite the apparent complex control of atxA transcription, only one trans-acting protein, the transition state regulator AbrB, has been demonstrated to directly interact with the atxA promoter. The AbrB-binding site has been described, but additional cis-acting control sequences have not been defined. Using transcriptional lacZ fusions, electrophoretic mobility shift assays, and Western blot analysis, the cis-acting elements and trans-acting factors involved in regulation of atxA in B. anthracis strains containing either both virulence plasmids, pXO1 and pXO2, or only one plasmid, pXO1, were studied. This work demonstrates that atxA transcription from the major start site P1 is dependent upon a consensus sequence for the housekeeping sigma factor SigA, and an A+T-rich upstream element (UP-element) for RNA polymerase (RNAP). In addition, the data show that a trans-acting protein(s) other than AbrB negatively impacts atxA transcription when it binds specifically to a 9-bp palindrome within atxA promoter sequences located downstream of P1. Mutation of the palindrome prevents binding of the trans-acting protein(s) and results in a corresponding increase in AtxA and anthrax toxin production in a strain- and culture-dependent manner. The identity of the trans-acting repressor protein(s) remains elusive; however, phenotypes associated with mutation of the repressor binding site have revealed that the trans-acting repressor protein(s) indirectly controls B. anthracis development. Mutation of the repressor binding site results in misregulation and overexpression of AtxA in conditions conducive for development, leading to a marked sporulation defect that is both atxA- and pXO2-61-dependent. pXO2-61 is homologous to the sensor domain of sporulation sensor histidine kinases and is proposed to titrate an activating signal away from the sporulation phosphorelay when overexpressed by AtxA. These results indicate that AtxA is not only a master virulence regulator, but also a modulator of proper B. anthracis development. Also demonstrated in this work is the impact of the developmental regulators AbrB, Spo0A, and SigH on atxA expression and anthrax toxin production in a genetically incomplete (pXO1+, pXO2-) and genetically complete (pXO1+, pXO2+) strain background. AtxA and anthrax toxin production resulting from deletion of the developmental regulators are strain-dependent suggesting that factors on pXO2 are involved in control of atxA. The only developmental deletion mutant that resulted in a prominent and consistent strain-independent increase in AtxA protein levels was an abrB-null mutant. As a result of increased AtxA levels, there is early and increased production of anthrax toxins in an abrB-null mutant. In addition, the abrB-null mutant exhibited an increase in virulence in a murine model for anthrax. In contrast, virulence of the atxA promoter mutant was unaffected in a murine model for anthrax despite the production of 5-fold more AtxA than the abrB-null mutant. These results imply that AtxA is not the only factor impacting pathogenesis in an abrB-null mutant. Overall, this work highlights the complex regulatory network that governs expression of atxA and provides an additional role for AtxA in B. anthracis development.

Regulation of the heat shock response by thiol-reactive compounds in the yeast Saccharomyces cerevisiae

Cells govern their activities and modulate their interactions with the environment to achieve homeostasis. The heat shock response (HSR) is one of the most well studied fundamental cellular responses to environmental and physiological challenges, resulting in rapid synthesis of heat shock proteins (HSPs), which serve to protect cellular constituents from the deleterious effects of stress. In addition to its role in cytoprotection, the HSR also influences lifespan and is associated with a variety of human diseases including cancer, aging and neurodegenerative disorders. In most eukaryotes, the HSR is primarily mediated by the highly conserved transcription factor HSF1, which recognizes target hsp genes by binding to heat shock elements (HSEs) in their promoters. In recent years, significant efforts have been made to identify small molecules as potential pharmacological activators of HSF1 that could be used for therapeutic benefit in the treatment of human diseases relevant to protein conformation. However, the detailed mechanisms through which these molecules drive HSR activation remain unclear. In this work, I utilized the baker's yeast Saccharomyces cerevisiae as a model system to identify a group of thiol-reactive molecules including oxidants, transition metals and metalloids, and electrophiles, as potent activators of yeast Hsf1. Using an artificial HSE-lacZ reporter and the glucocorticoid receptor system (GR), these diverse thiol-reactive compounds are shown to activate Hsf1 and inhibit Hsp90 chaperone complex activity in a reciprocal, dose-dependent manner. To further understand whether cells sense these reactive compounds through accumulation of unfolded proteins, the proline analog azetidine-2-carboxylic acid (AZC) and protein cross-linker dithiobis(succinimidyl propionate) (DSP) were used to force misfolding of nascent polypeptides and existing cytosolic proteins, respectively. Both unfolding reagents display kinetic HSP induction profiles dissimilar to those generated by thiol-reactive compounds. Moreover, AZC treatment leads to significant cytotoxicity, which is not observed in the presence of the thiol-reactive compounds at the concentrations sufficient to induce Hsf1. Additionally, DSP treatment has little to no effect on Hsp90 functions. Together with the ultracentrifugation analysis of cell lysates that detected no insoluble protein aggregates, my data suggest that at concentrations sufficient to induce Hsf1, thiol-reactive compounds do not induce the HSR via a mechanism based on accumulation of unfolded cytosolic proteins. Another possibility is that thiol-reactive compounds may influence aspects of the protein quality control system such as the ubiquitin-proteasome system (UPS). To address this hypothesis, β-galactosidase reporter fusions were used as model substrates to demonstrate that thiol-reactive compounds do not inhibit ubiquitin activating enzymes (E1) or proteasome activity. Therefore, thiol-reactive compounds do not activate the HSR by inhibiting UPS-dependent protein degradation. I therefore hypothesized that these molecules may directly inactivate protein chaperones, known as repressors of Hsf1. To address this possibility, a thiol-reactive biotin probe was used to demonstrate in vitro that the yeast cytosolic Hsp70 Ssa1, which partners with Hsp90 to repress Hsf1, is specifically modified. Strikingly, mutation of conserved cysteine residues in Ssa1 renders cells insensitive to Hsf1 activation by cadmium and celastrol but not by heat shock. Conversely, substitution with the sulfinic acid and steric bulk mimic aspartic acid led to constitutive activation of Hsf1. Cysteine 303, located in the nucleotide-binding/ATPase domain of Ssa1, was shown to be modified in vivo by a model organic electrophile using Click chemistry technology, verifying that Ssa1 is a direct target for thiol-reactive compounds through adduct formation. Consistently, cadmium pretreatment promoted cells thermotolerance, which is abolished in cells carrying SSA1 cysteine mutant alleles. Taken together, these findings demonstrate that Hsp70 acts as a sensor to induce the cytoprotective heat shock response in response to environmental or endogenously produced thiol-reactive molecules and can discriminate between two distinct environmental stressors.

Analysis of VirB4, a membrane-associated ATPase subunit essential for T -complex transport in Agrobacterium tumefaciens

Agrobacterium tumefaciens is a plant pathogen with the unique ability to export oncogenic DNA-protein complexes (T-complexes) to susceptible plant cells and cause crown gall tumors. Delivery of the T-complexes across the bacterial membranes requires eleven VirB proteins and VirD4, which are postulated to form a transmembrane transporter. This thesis examines the subcellular localization and oligomeric structure of the 87-kDa VirB4 protein, which is one of three essential ATPases proposed to energize T-complex transport and/or assembly. Results of subcellular localization studies showed that VirB4 is tightly associated with the cytoplasmic membrane, suggesting that it is a membrane-spanning protein. The membrane topology of VirB4 was determined by using a nested deletion strategy to generate random fusions between virB4 and the periplasmically-active alkaline phosphatase, $\sp\prime phoA$. Analysis of PhoA and complementary $\beta$-galactosidase reporter fusions identified two putative periplasmically-exposed regions in VirB4. A periplasmic exposure of one of these regions was further confirmed by protease susceptibility assays using A. tumefaciens spheroplasts. To gain insight into the structure of the transporter, the topological configurations of other VirB proteins were also examined. Results from hydropathy analyses, subcellular localization, protease susceptibility, and PhoA reporter fusion studies support a model that all of the VirB proteins localize at one or both of the bacterial membranes. Immunoprecipitation and Co$\sp{2+}$ affinity chromatography studies demonstrated that native VirB4 (87-kDa) and a functional N-terminally tagged HIS-VirB4 derivative (89-kDa) interact and that the interaction is independent of other VirB proteins. A $\lambda$ cI repressor fusion assay supplied further evidence for VirB4 dimer formation. A VirB4 dimerization domain was localized to the N-terminal third of the protein, as judged by: (i) transdominance of an allele that codes for this region of VirB4; (ii) co-retention of a His-tagged N-terminal truncation derivative and native VirB4 on Co$\sp{2+}$ affinity columns; and (iii) dimer formation of the N-terminal third of VirB4 fused to the cI repressor protein. Taken together, these findings are consistent with a model that VirB4 is topologically configured as an integral cytoplasmic membrane protein with two periplasmic domains and that VirB4 assembles as homodimers via an N-terminal dimerization domain. Dimer formation is postulated to be essential for stabilization of VirB4 monomers during T-complex transporter assembly. ^

ATXA -dependent gene expression in Bacillus anthracis

The Bacillus anthracis toxin genes, cya, lef , and pag, can be viewed as a regulon, in which transcription of all three genes is activated in trans by the same regulatory gene, atxA, in response to the same signal, CO2. I determined that several phenotypes are associated with the atxA gene. In addition to being toxin-deficient, an atxA -null mutant grows poorly on minimal media and sporulates early compared to the parent strain. Furthermore, an atxA-null mutant has an altered 2-D gel protein profile. I used a genetic approach to find additional atxA-regulated genes. Random transcriptional lacZ fusions were generated in B. anthracis using transposon Tn 917-LTV3. Transposon-insertion libraries were screened for mutants expressing increased β-galactosidase activity in 5% CO2. Introduction of an atxA-null mutation in these mutants revealed that 79% of the CO2-regulated fusions were also atxA-dependent. DNA sequence analysis of transposon insertion sites in mutants carrying CO 2/atxA-regulated fusions revealed ten mutants harboring transposon insertions in loci distinct from the toxin genes. The majority of the tcr (toxin co-regulated) loci mapped within the pXO1 pathogenicity island. These results indicate a clear association of atxA with CO2-enhanced gene expression in B. anthracis and provide evidence that atxA regulates genes other than the structural genes for the anthrax toxin proteins. ^ Characterization of one tcr locus revealed a new regulatory gene, pagR. The pagR gene (300 nt) is located downstream of pag. pagR is cotranscribed with pag and is responsible for autogenous control of the operon. pagR also represses expression of cya and lef. Repression of toxin gene expression by pagR may be mediated by atxA. The steady state level of atxA mRNA is increased in a pagR mutant. Recombinant PagR protein purified from Escherichia coli did not specifically bind the promoter regions of pagA or atxA. An unidentified factor in B. anthracis crude extracts, however, was able to bind the atxA promoter in the absence of PagR or AtxA. These investigations increase our knowledge of virulence regulation in B. anthracis and ultimately will lead to a better understanding of anthrax disease. ^

¿Desarrollo local o enclave turístico? El caso paradigmático de Santa Ana, Misiones, Argentina. 16H298

a) Se ha relevando la oferta turística tradicional y nueva del municipio. b) Se han realizado encuestas a visitantes (encuesta personal y online) para analizar su opinión sobre el parque temático y propuestas de mejoras y cambios. c) Se hicieron encuestas a residentes de Santa Ana (encuesta personal) para analizar su opinión del parque temático y los posibles impactos positivos y negativos que el mismo podría producir en el municipio. d) Se han efectuado entrevistas a los funcionarios municipales y provinciales vinculados a la actividad turística del área en estudio. e) Se realizaron entrevistas a empresarios locales vinculados directa e indirectamente al turismo.

Territorialidad, economía de la ciudad y estructuración social: El Proyecto Yacyretá y los cambios en el espacio urbano de Posadas. 16H261

En el primer punto de este informe final se realizó un estado del arte y un análisis monográfico del problema que abordamos al que denominamos La Ciudad como Objeto de Estudio, es decir un marco conceptual que nos permita situar el problema abordado además de señalar los avances en cuanto a la gestión de la ciudad. Al tratarse de un análisis teórico abordamos largamente diversos aspectos que se vinculan a la construcción epistemológica del tema. Algunos de los temas tratados son: el futuro de las ciudades en el proceso globalizador, la relación entre campo-ciudad, ciudad y estado nacional, Nación y fronteras nacionales, las teorías del desarrollo y la exclusión social, entre otras cuestiones. En el segundo punto tratamos y profundizamos la descripción de el Proyecto Yacyretá y las Obras Civiles en la Ciudad teniendo en cuenta que este proyecto modifico sustancialmente la urbanización de Posadas, la gestión municipal y la estructura social local. En este sentido se hace referencia a los proyectos del ente público que directamente se desarrollan en el área urbana, denominado en el proyecto como Obras Complementarias, se describe y evalúa ahí las diferentes proyecciones elaboradas por los diferentes momentos de los diferentes gerenciamientos que se sucedieron en el tiempo, a la vez se trata de explicitar las condiciones históricas en que se proyectaron y realizaron las obras. En el tercer punto "El entorno regional y los involucrados" se describe el entorno social del emplazamiento de las obras de análisis a la vez de los actores directa e indirectamente involucrados. Entre otras cuestiones se analizan los indicadores económicos, las características y cambios de la pobreza urbana y rural, el mercado inmobiliario, la infraestructura y los servicios, los sistemas de transporte: terrestre, fluvial y ferroviario, Actores Sociales, entre otros temas. En el punto cuarto se pone el foco de trabajo en la Ciudad de Posadas. Se vincula esta con la dinámica de frontera con su "gemela" ciudad de Encarnación, República del Paraguay que también es modificada por el mismo proyecto y en análogas dimensiones, tanto por su vinculación histórico-geográfico como por sus transformaciones a la luz de las obras del Proyecto Yacyretá. Se realiza una historización de la división y uso del suelo en Posadas, el proyecto Yacyretá y sus efectos en la dinamización del mercado inmobiliario, las políticas municipales y el problema de la vivienda. El punto quinto hace referencia a cual es la percepción de los actores y ciudadanos de Posadas con respecto a la ciudad, la gestión local, lo servicios públicos, etc. Se han adoptado diferentes técnicas en un diseño técnico metodológico que permita triangular técnicas cualitativas y cuantitativas. En tal sentido se ha trabajado diferentes técnicas que a la vez nos permita muestrear y elaborar tipos actores y condiciones de la población en relación al asentamiento en el que se sitúan. Primero exponemos los resultados de una encuesta realizada en la ciudad de Posadas sobre la visión de los ciudadanos respecto a los problemas de la ciudad y las responsabilidades institucionales. Segundo se hace referencia a información cualitativa recogida en lo que denominamos el primer cordón o conglomerado urbano, conformado por una heterogeneidad de barrios de NES medio y bajo. Las técnicas utilizadas en este punto fueron tres grupos focalizados. Tercero, se trata del procesamiento de una encuesta realizada en barrios de construcción pública en Posadas y Garupá, ambos conforman el gran conglomerado metropolitano de Posadas aunque se trate de dos municipios diferentes. Cuarto se analizar allí talleres realizados con población vulnerable de barrios de construcción pública. En las conclusiones se realiza una interpretación de los datos construidos. Durante todo el proceso de investigación el equipo de trabajo colaboró en todos los momentos y fases de investigación, desde el diseño y elaboración del proyecto, la construcción del objeto (problemas, estado del arte y elaboración de hipótesis), el diseño técnico metodológico en el que se fijaron a las estrategias o combinación de técnicas de recolección de información, (información secundaria, encuestas, entrevistas, grupos focales y talleres) procesamiento e interpretación. En las conclusiones se elaboran interpretaciones mediante técnicas del planeamiento estratégico como matriz DAFO, análisis de Juego de Actores, Árbol de Problemas y análisis prospectivo. Pero fundamentalmente se realiza una evaluación territorial de clases sociales. Se incluyen ilustraciones fotográficas y mapas temáticos en algunos puntos del informe.

Desarrollo local y políticas rurales en elMunicipio del Pilar. En: Avá, nº 16

Analizamos el rol del municipio y las políticas municipales en las problemáticas de los productores hortícolas, considerando que las nuevas funciones de los gobiernos locales implican un nuevo perfil del Estado. En Pilar se reformularon estrategias de intervención en la gestión de los espacios hortícolas. Repasamos ejes del concepto de desarrollo local, el perfil del territorio y el rol de la sociedad civil y desafíos de la gestión municipal, mediante avances de una investigación que aplica metodología cualitativa con trabajo de campo etnográfico en distintos ámbitos municipales del partido. La capacidad de respuesta de las estructuras burocráticas gubernamentales locales es, por el momento, adecuada a las demandas de los productores. Se visualiza cierta coordinación y articulación entre y dentro de los organismos públicos del municipio.

Políticas Sociales y Contexto. Sobre escenarios y capacidades en y para la gestión. En: Revista Perspectivas. Nº 9, Año 9

En este artículo interesa compartir las ideas relacionadas con la realidad del escenario de la Provincia de Misiones – Argentina – en cuanto a la posibilidad de articulación entre agenda pública y actores responsables de las mismas al momento de gestionar y/o administrar políticas sociales – puntualmente las de familia – teniendo en cuenta para ello las particularidades del enclave regional específico. Tomando las décadas 1995 / 2005 donde la vida ciudadana se desarrollaba en proyectos políticos de corte netamente democráticos pero al mismo tiempo con un hiato significativo ante la reforma del Estado, se intenta compartir las líneas rectoras que guiaron el accionar de los actores protagónicos vinculados al diseño y ejecución de políticas sociales de familia en un contexto regional particular. En esta oportunidad, tomando lo realizado por los responsables de los ejecutivos municipales y sus gabinetes en cuanto a posicionamientos, realidades, posibilidades, en relación con la gestión.

Re.Sa.Ma.Ja.V- Patrimonio, Historia y Turismo: Plan Estratégico Situacional (PES) del Territorio de las Misiones del Uruguay. (Disp. / Res.). 16H282

Actividades desarrolladas durante el período: actividades con financiamiento del ministerio de Educación de la Nación y Universidad Nacional de Misiones (UNaM.):durante 2010 se realizaron las tareas previstas en los proyectos cuyo financiamiento fue obtenido en 2009 Planificación interpretativa de circuitos turísticos locales. Misiones. 2009. Programa de Voluntariado universitario. Secretaría de Políticas Universitarias. SPU. Ministerio de Educación de la Nación. Nº de resolución de rectorado: 1553/09. Articulaciones para el Plan de manejo integrado de las misiones jesuíticas Santa María y Santos Mártires en Misiones Argentina. UNaM. Programa de fortalecimiento a la extensión universitaria. PROFAE 2009. Nº de Resolución del CD: 1790/09. Planificación interpretativa del centro de visitantes de Santa María la Mayor. Misiones. UNaM. Programa de fortalecimiento a la extensión universitaria. PROFAE 2009. Nº de Resolución: Nº de Resolución del CD: 1790/09. AECID: Actividades con Financiamiento de la Agencia Española de Cooperación Internacional para el desarrollo: Durante 2009 el equipo ha presentado a la Agencia Española de Cooperación Internacional para el Desarrollo (AECID)2 una propuesta denominada: Proyecto de activación patrimonial: Santos Mártires del Japón, Santa María La Mayor y Nuestra Señora de la Concepción del Ibitiracuá, por considerar conveniente y sumamente positivo trabajar en conjunto con AECID ya que permitiría articular los esfuerzos de las instituciones implicadas: Gobiernos municipales y provincial, UNaM y actores locales. Por ello se han combinado los recursos de la Universidad con los del financiamiento otorgado por AECID para llevar adelante los proyectos; Formación y capacitación: el equipo desarrolla permanentemente acciones de formación y perfeccionamiento durante 2010; Diagnóstico situacional referido al área del proyecto: durante esta etapa nos propusimos ampliar el equipo de profesionales a los efectos de elaborar lineamientos que contribuyan al diagnostico para el ordenamiento territorial del área proyecto. En principio nos habíamos propuesto obtener los servicios profesionales de un economista y un, ingeniero agrónomo o forestal a los efectos de que colaboren desde de sus respectivas áreas temáticas en la elaboración de la agenda de proyectos sociales básicos.

¿Desarrollo local o enclave turístico? El caso paradigmático de Santa Ana, Misiones, Argentina. 16H298

Actividades desarrolladas durante el período: se han relevado y estudiado estadísticas sociales, económicas y turísticas del Municipio y su zona de influencia, desde los organismos oficiales de estadísticas (IPEC, INDEC, Programa Misiones Jesuíticas, Ministerio de Turismo de la Provincia de Misiones), además de analizar otros estudios inéditos de la Universidad vinculados al área de estudio. Además se relevaron las noticias vinculadas al tema de investigación en los diarios de circulación provincial; se realizó un relevamiento de la existencia y estado actual de la escasa oferta complementaria (alojamiento, alimentación, actividades conexas, servicio de agencias de turismo) del área de estudio;se han efectuado las primeras entrevistas a los funcionarios municipales y provinciales vinculados a la actividad económica y turística tradicional del área en estudio; se realizaron entrevistas a empresarios y responsables turísticos y productivos del área de estudio para conocer su opinión antes de la inauguración del parque temático y su posible impacto económico productivo y turístico en el municipio y zona de influencia, se efectuaron las primeras observaciones en el Parque Temático en relación a sus consideraciones ambientales y socio productivas, aspectos críticos y mejoras necesarias.