Esta tesis, que integra los estudios de la Sociología del Arte, se centra en la vinculación de la poética del artista Edgardo Antonio Vigo (1928 - 1997) con la política y lo político, así como con los procesos sociales más generales entre 1968 y 1975. Vigo ocupó una posición emergente en el desarrollo del arte platense y desplegó producciones que emprendieron una poética rupturista con lo establecido por algunos de los cánones tradicionales del arte y sus instituciones, y elaboró propuestas estéticas innovadoras que abarcaban las artes visuales en sus diversas formas. Se analizan en esta tesis los modos por los que Vigo al mismo tiempo que apunta a cuestionar las estructuras y manifestaciones de las Bellas Artes, lo hace con las formas dominantes de la cultura a través de obras y textos que tendían a desestabilizar los roles de autor, espectador y obra, así como a involucrarse de distintos modos en los acontecimientos políticos de la época. Se estudian, además, las producción de acciones artísticas en el espacio público, que Vigo llamó señalamientos, la utilización y apropiación del discurso y aspectos materiales de lo judicial-administrativo y la edición de la revista ensamblada Hexágono ’71 (1971 -1975). En estas zonas de la poética de Vigo se consideran las diversas relaciones entre arte y política, las cuales no han sido lineales ni unidireccionales, sino modos de distorsionar y disentir con las jerarquías, lugares y funciones de los sujetos y objetos del entramado social. Para la realización de la tesis se produjo un diseño metodológico cualitativo, se utilizaron fuentes documentales y entrevistas. Se desarrolla un análisis de las obras del artista, más que remitiéndolas a una corriente artística particular, haciendo foco en su relación con la situación social y política, especialmente en sus vinculaciones con el particular proceso de subjetivación política de la época. Se procuró para ello realizar una investigación que se detenga de manera pormenorizada en el trabajo artístico y sus particularidades (materiales, técnicas, formas, estrategias de intervención), así como en sus discursos escritos, plasmados en ensayos, artículos y otros textos, para avanzar desde allí hacia un análisis interpretativo y comprensivo de las conexiones y de los efectos que perseguía tal trabajo con los procesos políticos. Se presentan en los Anexos matrices de datos de los señalamientos y de Hexágono ’71, así como un índice razonado de la misma. / This dissertation is part of the field of Sociology of Arts and focuses on the relationship between the poetics of the artist Edgardo Antonio Vigo (1928-1997) and politics and the political, as well as the general social processes between 1968 and 1975. Vigo occupied an emerging position in the development of local art and carried out productions that undertook a poetics which broke with some traditional canons of art and their institutions, and he also made innovative aesthetic proposals in visual arts. We analyze the ways in which Vigo, while questioning structures and manifestations of Beaux Arts, did it with the dominant culture forms through works and texts that tended to destabilize the roles of author, spectator and work, as well as to be involved in political events. We also study the production of artistic actions in the public space, which Vigo called señalamientos [signalings], the use and appropriation of the judicial-administrative discourse and materials, and the publication of the assembling magazine Hexágono ’71 (1971-1975). In these zones of Vigo’s poetics we consider diverse relationships between art and politics, which were not linear or one-way, but means of distorting and dissenting from hierarchies, places and roles of subjects and objects in society. To prepare this dissertation we produced a qualitative research design and used documental sources and interviews. We developed an analysis of Vigo’s works, focusing on the relationship with the social and political situation and the process of political subjectivation of that time, rather than following a specific artistic movement. The research discusses in detail the artistic work and its distinctive features (materials, techniques, forms, strategies of intervention), as well as Vigo’s written discourses expressed in essays, articles and other texts, to progress from there to an interpretative and comprehensive analysis of the connections and effects pursued by those works with regard to the political process. In the Appendix we include data matrices of señalamientos and Hexágono ’71, and an index of this magazine.

<p dir="ltr">Embryonic development relies on the complex interplay of epigenetic regulation, timely expression of genes, signal transduction pathways, and diverse morphological changes. The heart is the first organ to form during mammalian embryonic development. The proper development of the heart is critical to supply nutrients and oxygen to other cell types of the organism. Most cells that comprise the heart originate from the mesoderm post-gastrulation. Cardiomyocytes are the predominant cell type and confer function to the heart via contractile activity. The development and proliferation of cardiomyocytes ceases shortly after birth, where cardiomyocytes only nucleate and increase in size. Consequently, cardiomyocyte insufficiency underlies most cardiovascular diseases, a leading cause of death globally.</p><p dir="ltr">Vascular endothelial zinc finger 1 (VEZF1) is a transcription factor expressed predominantly in mesoderm during development. Previous studies from our lab show that the loss of VEZF1 impairs the differentiation of embryonic stem cells into endothelial cells, a cell type derived from mesoderm. Other published studies also show that Vezf1 loss impairs cardiomyocyte growth in Zebrafish and hematopoietic cell differentiation. Our work here describes a detailed investigation of the role of Vezf1 in the differentiation of mesoderm and cardiomyocytes using mouse embryonic stem cell (ESC) differentiation as a mammalian model system. We initially developed an efficient method, known as the Wnt Switch method, to differentiate ESCs into cardiomyocytes. Our technique relies on the treatment of differentiating ESCs with small molecule inhibitors: i) CHIR99021, which induces mesoderm development via the activation of Wnt signaling in the first 48 hours of differentiation, followed by ii) XAV939, which inhibits Wnt signaling and drives mesoderm cells toward cardiomyocyte differentiation pathway. The Wnt Switch method significantly increases the efficiency of cardiomyocyte derivation (86%) from ESC compared to published methods (56%).</p><p dir="ltr">Interestingly, the Wnt Switch method showed that despite the external stimulation of Wnt signaling, Vezf1 KO cells are unable to differentiate into cardiomyocytes and show reduced expression of mesodermal genes 48 hrs post-differentiation. To better understand the stage-specific role of Vezf1 in cardiomyocyte development, we generated doxycycline-inducible Vezf1 knockdown clones that significantly reduce Vezf1 protein levels upon treatment with doxycycline. We found that the knockdown of Vezf1 prior to mesoderm induction significantly impaired ESC differentiation but had no significant effect on cardiomyocyte development after mesoderm induction. These data indicate that Vezf1 expression is crucial for proper mesoderm and, thus, mesodermal lineage development. Further, FACS analysis showed reduced mesoderm cell populations derived from Vezf1 null post-differentiation. We used high throughput sequencing methods to determine genome-wide Vezf1 binding by ChIP-SEQ and compared gene expression in WT and Vezf1 null cells using RNA-SEQ. The data indicated that VEZF1 binds near the promoters of numerous Wnt signaling genes after differentiation and that the expression of Wnt pathway genes decreases when Vezf1 is lost. Interestingly, supplementing WNT3A protein in culture media of Vezf1 null cells rescues the expression of Wnt target genes necessary for mesoderm formation.</p><p dir="ltr">Differentiating Vezf1 KO cells to endothelial or cardiomyocyte lineages also resulted in massive cell death. The surviving cells interestingly stained positive for alkaline phosphatase (AP) staining, indicating retention of the pluripotency in Vezf1 KO cells. Whereas, re-culturing of WT ESC in LIF media, after differentiating them for five days in the absence of LIF, results in cell death, Vezf1 KO cells proliferate and form AP-positive and SSEA-positive colonies. We further show the retention of pluripotency gene expression post-differentiation using RNA sequencing and RT-qPCR. Moreover, we show that the continued expression of pluripotency genes post-differentiation was not a consequence of reduced global DNA methylation in Vezf1 KO cells.</p><p dir="ltr">Interestingly, our data show that Vezf1 is a transcriptional activator and binds to key pro-differentiation pathways like the MAPK signaling and WNT signaling pathways. The loss of Vezf1 correlates with reduced expression of genes in the pro-differentiation pathways. We show that CTCF, an insulator-binding protein, opportunistically binds to VEZF1 sites on genes in the pro-differentiation signaling pathways in VEZF1 KO cells. Therefore, we hypothesized that this opportunistic CTCF binding is the mechanism that drives the repression of pro-differentiation signaling genes or compensates for the loss of Vezf1 binding to support basal gene expression in the absence of VEZF1. Given the dire consequences of pluripotency in cancer stem cells, we investigated the expression of Vezf1 in cancers. We found that Vezf1 expression is reduced in many cancers and is correlated with poor prognosis. We also show that MAPK3, a prominent member of the MAPK signaling pathway, is reduced in these cancers, highlighting a strong correlation between Vezf1 expression and Mapk3 gene expression in cancers. The data extend our observation of pluripotency in ESCs to cancers. To gain further insights into the role of Vezf1 in cancer, we utilized F9 embryonic carcinoma cells. F9 cells have been reported to retain pluripotency expression post-differentiation. Interestingly, the ectopic and transient expression of Vezf1 in F9 cells significantly reduced the expression of pluripotency genes, suggesting that Vezf1 is sufficient to repress pluripotency gene expression in F9 carcinoma cells. These data highlight the significant role of Vezf1 in pluripotency gene repression and provide an excellent avenue for treating cancer relapse caused by the occurrence of cancer stem cells.</p><p dir="ltr">In conclusion, our research elucidates the critical role of Vezf1 in cardiomyocyte formation and pluripotency regulation during embryonic development. Understanding the molecular mechanisms underlying Vezf1-mediated pathways provides insights into developmental processes and holds promise for therapeutic interventions for cardiomyocyte regeneration and against cancers.</p>