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NICHD - Eunice Kennedy Shriver National Institute of Child Health and Human Development

PROJECT SUMMARY / ABSTRACT This proposal is for the graduate training program at Vanderbilt University that is structured to support the early phases of neuroscience predoctoral education and training. In support of the overall NIH mission, the overarching objective of the program is to provide an exceptional training environment for the next generation of neuroscientists, and is built on the foundation of a strong training faculty with exceptional records of scholarship, research support and graduate mentoring. The heart of this mission is expressed in the academic and research goals of the program, which are to provide our students with a strong didactic foundation in the neurosciences through our core curriculum offerings, and to provide them with the opportunity to carry out state-of-the-art neuroscience research in the laboratories of a group of highly successful and committed mentors. In addition, the program has strong emphases on professional development, quantitative literacy and rigorous science, with the objective of building the requisite skills needed for success in graduate school and beyond, and of training an inclusive cadre of future independent investigators in neuroscience research. The Neuroscience Graduate Program at Vanderbilt is an interdisciplinary program that encompasses 5 different colleges and schools and 23 departments. Traditional and emerging areas of research strength in the program include: addiction, attention, brain evolution, cell signaling, cognitive neuroscience, circadian rhythms and sleep, CNS drug development, development, developmental disabilities, molecular genetics, neurodegeneration and neurotoxicity, neuroimaging, plasticity, psychiatric illness, sensory and multisensory systems, synaptic transmission, and vision. The program is currently home to 67 trainees and 73 training faculty. The proposal requests support 5 slots and provides the rationale and justification for this request.

National Park Service

1. Create a science and technology showcase for art conservators to expose more conservators to scientific methods. The showcase will lead to better conservation of cultural heritage. 2. Create a research opportunity for youth, students, and new professional conservators to be exposed to and undertake research in an art conservation science laboratory. Research opportunities will lead to a new generation of conservators with an understanding of research within the art conservation practice. 3. Disseminate preservation technology information.

National Park Service

The intern will be part of the Cultural Landscape Inventory team for the National Park Service and based at the Olmsted Center for Landscape Preservation in Boston, Massachusetts. Responsibilities and learning opportunities include: creating field maps to document cultural landscape characteristics and features, field measurements and photography, meetings and interviews with park staff, archival research for historic photographs and maps, writing landscape descriptions, preparing landscape management and maintenance recommendations, and formatting reports for distribution. These responsibilities will be carried out with the guidance of Olmsted Center staff, including landscape architects and horticulturists. The intern will also collaborate with other interns and the Olmsted Center's youth education program. The intern should have skills and enthusiasm for reading and writing; skills in communicating and working as a member of a team; an interest in landscape architecture, horticulture, history, and historic preservation; and an interest in learning graphics programs, including Adobe Illustrator and Photoshop. No previous experience working in digital graphics is necessary, but an interest in art and drawing is helpful. This position is NOT eligible for AmeriCorps.

Patrons of the Trumbull Nature and Arts

FY25-ARPA-Sub Recipient

Bridgeport Arts & Cultural Council

FY25-ARPA-Sub Recipient

NCI - National Cancer Institute

PROJECT ABSTRACT/SUMMARY Neoplasms of the central nervous system (CNS) are the most frequently encountered solid tumors of childhood and remain one of the top causes of death in children. Pediatric high-grade gliomas (pHGGs) and atypical teratoid rhabdoid tumor (ATRT) are particularly aggressive pediatric CNS (pedCNS) tumors associated with poor outcome. Therapy consists of extremely burdensome multi-modal treatment protocols with toxic profiles that cause patients to suffer from detrimental effects, which significantly impact the quality of life during their already limited lifespan. New therapeutic strategies are badly needed to increase the survival benefit and quality of life of patients with pHGG and ATRT. To address this need, we performed initial studies that demonstrated that primary CNS cancers display dysregulated iron homeostasis and that gallium maltolate (GaM), an iron mimetic metallocompound, inhibits the growth of pHGG and ATRT cells in vitro and in an orthotopic rat model, extending overall survival. Cancer iron metabolism is an attractive target for therapeutical intervention. Iron plays a vital role in the pathobiology of many cancers, including brain cancer. Gallium acts as an iron mimetic, enabling it to hijack common iron trafficking pathways to enter cancer cells. However, unlike iron, gallium cannot take part in cellular redox reactions, thus disrupting critical iron-dependent processes and resulting in cell death. Our group has demonstrated the effectiveness of gallium maltolate (GaM), a newer generation compound with high oral bioavailability and therapeutic index, both in vitro and in vivo. In animal studies of adult glioblastoma, the most aggressive type of primary brain tumors, we demonstrated a slower tumor growth rate, a doubling of survival, and an improved quality of life with treatment. Preliminary studies in pHGGs and ATRTs suggest similar benefits. Despite this promising initial step, questions regarding the efficacy of GaM remain. Specifically, we intend to address the knowledge gap as to what drives response to GaM therapy. Therefore, our overall goal is to be able to offer a new treatment strategy to brain tumor patients with few therapeutic options. In Specific Aim 1, we propose a sophisticated multi-pronged approach leveraging behavioral assessments, state-of-the-art MRI-guided biopsy, cellular bioenergetics, and induction coupled plasma mass spectrometry (ICP-MS), to develop a tissue sensitivity profile. In Specific Aim 2, we propose to explore the synergistic potential of combining GaM with radiation therapy, the backbone of many treatment protocols. Preliminary data suggest a potentiating cytotoxic effect, which requires confirmation in vivo. Collectively, these investigations will provide insights regarding how to maximize antineoplastic therapy with GaM to improve both the quality of life and extend survival in children with primary brain tumors.

Garfield Weston Foundation

One of the UK's largest family-funded charitable foundations distributing 90M+ GBP annually across arts, education, community, environment, health.

Garinagu Houngua Planning Committee

Garinagu Houngua Planning Committee will organize a series of workshops for community members to learn about various aspects of Garifuna culture. The series will take place at Casa Latina located at 317 17th Ave S. Workshops will be held from 3 pm - 5 pm each Saturday and Sunday beginning September 28, 2019 and ending April 11, 2020.

NIGMS - National Institute of General Medical Sciences

ABSTRACT Members of the voltage-gated superfamily of tetrameric cation channels have central roles in human physiology. My group's long-term objective is to understand the molecular mechanisms of gating, lipid modulation and cellular function of two families of channels within this group: the large conductance and calcium activated potassium (BK) channels and the cyclic nucleotide-modulated (CNM) channels, which have been the topics of 2 distinct RO1s from NIGMS (GM088352 – K channels, and GM124451 – CNM channels). BK channels have the ability to couple intracellular Ca2+ to membrane potential variations, play major physiological roles in vascular smooth muscle tone maintenance, regulation of circadian rhythms, hearing, neurotransmitter release. CNM channels are activated by cyclic nucleotides (CNG), and hyperpolarization (HCN), and are expressed in the heart and brain where they play key roles in pacemaking, vision, olfaction. They are excellent drug targets and understanding how they gate can be therapeutically useful. BK channels can associate with tissue-specific accessory subunits, endowing the channels with different functional properties. 2 and 3 subunits induce N-type (or ball-and-chain) inactivation of the otherwise non-inactivating BK channels. The structural correlates of this process were not known. We previously determined the structural correlates of ball-and-chain inactivation in MthK, a prokaryotic homolog of BK channels from Methanotropicum thermoautotrophicum, and found it has a strong lipid dependence. We propose to determine the structural correlates of ball-and-chain inactivation in BK channels and understand how lipids modulate inactivation in both BK and MthK channels. We previously used SthK, prokaryotic homolog of CNM channels from Spirochaeta thermophila, as model to investigate CNM channel gating. We determined the mechanisms of ligand selectivity and increase in activity with anionic lipids in SthK, and our preliminary data shows that lipids modulate the temperature dependence of SthK. We propose to elucidate the molecular mechanism of this process and determine whether it is conserved in eukaryotic thermo-sensitive channels. In addition, we propose to elucidate the structure of the olfactory CNG channel, proposed to be a heteromer of CNGA2, CNGA4, and CNGB subunits and determine the mechanism of lipid modulation and ligand selectivity. Since membrane lipid composition cannot be controlled in cells, we will use a bottom-up approach of purified channels in reconstituted systems, to rigorously control lipid content. We combine state-of-the-art techniques: single-particle cryo-EM, atomic force microscopy, computational approaches, and functional assays to reach our goals. The accomplishment of these projects will provide a comprehensive picture of ball- and-chain inactivation in calcium-gated potassium channels and its lipid dependence, as well as of ligand selectivity, lipid modulation and temperature dependence in select CNM channels.

OD - NIH Office of the Director

ABSTRACT Drug metabolism and pharmacokinetics (DMPK) is critical for the successful development of new drugs ensuring they are both effective and safe for clinical use. Cytochrome P450 enzymes (P450s) are crucial in drug metabolism, responsible for the metabolism of approximately 75% of all marketed drugs. Determining the specific contribution of individual P450 enzyme to the metabolism of drugs facilitates understanding the role of a specific P450 isoform in pharmacokinetics, drug-drug interactions, and drug toxicity. Currently, P450- knockout animal models and specific chemical inhibitors are commonly used for these purposes. However, highly specific and effective chemical inhibitors in vivo are frequently unavailable. Although P450-KO mice are invaluable, the deletion of a specific or a cluster of P450 gene(s) can lead to compensatory changes of other P450s and cause developmental, or physiological abnormalities. Thus, creating new models to specifically manipulate P450s activities without the compensatory effects are extremely needed for DMPK studies. The state-of-the-art dTAG (degradable tag) system is a targeted protein degradation technology that enables the selective, rapid, and reversible degradation of a protein of interest within living cells or organisms. The unique features of dTAG system (e.g., minimizing the compensatory effects) render it ideal to generate animal model for assessing the impact of specific enzymes, transporters, or receptors on DMPK of drugs, especially for globally knocking out lethal genes (e.g., P450 reductase). In this proposal, we will employ dTAG system to create Cyp1a2dTAG and Cyp3a11dTAG models. Three Aims will be pursued: Aim 1: To generate and characterize Cyp1a2dTAG and Cyp3a11dTAG mice. Aim 2: To optimize dTAG molecule properties. Aim 3: To develop protocols to probe the roles of P450s in DMPK using homozygous P450dTAG mice. The proposed work is innovative as using dTAG system to modulate the drug metabolizing enzyme represents a transformative approach in this field. After completing the proposed work, we expect that two novel Cyp1a2dTAG and Cyp3a11dTAG mouse models that overcome the drawbacks of traditional models will be created and dTAG molecules that exhibit favorable physiological and pharmacokinetic properties will be developed. Our long-term goal is to extend the application of dTAG technology to regulate other significant drug metabolizing enzymes such as Cyp2d22, Cyp2e1, UGTs, and transporters, which will create a series of novel animal models for DMPK, toxicity, and functional studies. This work will have a great potential to significantly advance the fields of preclinical DMPK studies in drug development, and toxicity.

NIA - National Institute on Aging

PROJECT SUMMARY Microglia are the macrophages of the brain and become activated in response to amyloid. Recently, single cell sequencing has defined multiple activated states of microglia including two states that are robustly induced in animals of Alzheimer’s disease (AD): disease associated microglia (DAM), and interferon responding microglia (IRM). It is now established that in response to amyloid microglia initiate the classical pathway of the complement cascade, and that the complement cascade is a critical mediator of neuronal synapse loss during disease progression. Synapse loss is among the strongest neurobiological correlates of cognitive decline in AD. Global ablation of the C1 complex (via C1qa gene knockout) preserves synapses in AD mouse models, highlighting the importance of determining the mechanisms determining the role of microglia in complement-mediated synapse loss. Yet despite much work, key knowledge gaps remain. First, the relationships among the different transcriptionally defined microglia states have not been determined. Second, all microglia express C1Q and it remains unknown whether microglia belonging to distinct states trigger synapse loss on neurons. Third, the complement cascade requires downstream components such as complement factors C2 through C9 that are not expressed by microglia, but virtually nothing is known about the spatial and temporal coordination of the specific cell types expressing these components in the brain. Filling these knowledge gaps may lead to new therapeutic avenues that prevent or intervene in synapse loss in AD. By leveraging floxed alleles of Csf1r, Trem2, Sting1, C1qa, C3, C5 and C7, microglia state specific Cre driver lines such as Cx3cr1-cre, Tmem119-cre, Itgax-cre, and Mx1-cre, and reporter lines to lineage trace distinct states, we will take a multi-modal approach based on genetic strategies to address these questions with cellular specificity. We will use distinct mouse genetic contexts we have shown are susceptible (C57BL/6J) or resilient (PWK/PhJ) to synapse loss, and we will employ state-of-the- art methodologies including single cell myeloid cell sequencing, spatial transcriptomics and protein visualization, and circuit-specific labeling of synapses. In three aims we will test the model that IRM are an intermediate microglia state necessary to recruit DAM to plaques, and that DAM are the critical state driving complement- mediated synapse loss. In Aim 1, to test whether IRM are the intermediate state between homeostatic microglia and DAM, we will lineage trace IRM, ablate DAM or IRM, and conditionally delete Sting1 (a key mediator of interferon signaling) from DAM. In Aim 2, to determine whether DAM are the primary initiators of complement mediated synapse loss, we will conditionally delete Trem2 from homeostatic microglia, ablate DAM, and conditionally delete C1qa from DAM. In Aim 3, to uncover the cell types producing the downstream components of the complement cascade, we will perform spatial transcriptomics and protein visualization. We will then conditionally delete a downstream component from its parent cell type. Successful completion of these aims will result in the identification of critical cellular and genetic contributors to complement-mediate synapse loss in AD.

NIDA - National Institute on Drug Abuse

PROJECT SUMMARY Early initiation of cannabis use (<16 years of age) increases risk for cannabis use disorder (CUD), mental illness, cognitive impairment, later unemployment, and poor social relationships. Prevention of early initiation is critical for improving social and health outcomes. Precision prevention programs have reduced youth substance use, but no approaches have specifically targeted cannabis use. Furthermore, no studies have comprehensively considered risk factors for early cannabis initiation (genetic, social, behavioral, environmental, and cognitive) to enhance the prediction of early use and inform precision prevention approaches. Comprehensive multivariable prediction models for early cannabis initiation that include genetics and social/environmental factors are needed. Cannabis use is polygenic, influenced by multiple genetic variants with weak-to-moderate effects, and polygenicity makes it difficult to translate genetics for clinical application. One method for clinically applying genetics is through the development of polygenic risk scores (PRS) that are composite scores representative of overall genetic risk. Prior PRS have typically lacked portability to non-European populations; however, a state- of-the-art method has been developed to build PRS with significantly improved risk prediction (34% improvement) across ancestries. There is a need to apply this method to develop cross-ancestry PRS for cannabis use for inclusion of overall genetic risk in comprehensive prediction models. Furthermore, given the complex interplay between genetics and social/environmental factors, research is needed to understand gene by environment (GxE) interactions in which social/environmental factors synergistically impact the risk conferred by genetics. Research into GxE interactions is statistically and computationally challenging, and traditional single-variant and more recent polygenic approaches focus on lower order 2-way interactions. Our logic forest (LF) algorithm efficiently searches all possible interactions up to 8 variables without a priori specification. This study will apply these state-of-the-art computational methods to the Adolescent Brain Cognitive Development (ABCD) Study, which examines childhood risk factors and initiation of substance use from ages 9-10 years to early adulthood in a population demographically reflective of the U.S. Nearly all youth had not used cannabis at recruitment, enabling the prospective measurement of initiation and the development of prediction models integrating genetics with pre-substance use measurements of cognitive, social, and environmental factors. This research will 1) develop cross-ancestry PRS for inclusion in prediction models that comprehensively consider genetic, sociodemographic, behavioral, cognitive, and environmental factors, and 2) apply LF to gene-sets within known biological pathways across the whole genome to identify pathway-specific GxE interactions. Comprehensive models coupled with a more complete understanding of GxE factors influencing early cannabis initiation can identify 1) high risk youth populations for targeted prevention, 2) targetable factors present among high-risk clusters for tailored interventions, and 3) biological pathways for therapeutic development.

NIAID - National Institute of Allergy and Infectious Diseases

ABSTRACT The goal of the studies in this proposal is to establish how disease-associated genetic variation regulates antibody responses at the level of B cell help by follicular helper T cells (TFH). In Aim 1, we will use a powerful combination of state-of-the-art, variant-to-gene mapping approaches in follicular T cells ‘caught in the act’ of helping B cell antibody responses in human lymphoid tissue: 1) chromosome conformation data to reveal physical associations between regulatory variants and gene promoters in the context of the 3D structure of the genome, 2) quantitative expression-trait mapping to reveal statistical associations between disease-associated variants and gene expression in TFH cells, 3) massively-parallel reporter assays to identify expression- modulating variants, and 4) CRISPR interference screens to identify genes regulated by antibody disease variants in TFH cells. In Aim 2, ‘novel’ effector genes prioritized by the approaches in Aim 1 will be assessed for roles in TFH function in an in vitro lymphoid organoid model human humoral immunity and in in vivo mouse models of lupus and influenza vaccination. The proposed studies are supported by the extensive experience and preliminary data of the research team, and will use a confluence of evidence from orthogonal approaches to power discovery of novel mechanisms that regulate T cell-dependent humoral immunity, refine our understanding of how common genetic variation contributes to autoimmune disease susceptibility, and point to novel therapeutic interventions to modulate humoral immunity in the context of vaccines, infectious disease, and autoimmune disorders.

NHLBI - National Heart Lung and Blood Institute

PROJECT SUMMARY Gene editing offers the prospect of directly modifying any nucleotide(s) in the genome, including correction of pathogenic variants underlying disease. These technologies could form the basis of cures for currently untreatable genetic conditions. The work proposed in this application aims to identify genome editing strategies to prevent aortic pathology in Marfan syndrome (MFS). MFS is the most prevalent hereditary connective tissue disorder and is associated with significantly increased morbidity and mortality due to life-limiting thoracic aortic aneurysm and dissection. MFS is caused by heterozygous pathogenic variants in FBN1, the gene encoding the main structural component of extracellular microfibrils, fibrillin-1. Microfibrils are essential for providing structural elasticity and resilience, in addition to having a signaling role, and defects in both features are thought to contribute to elastic lamina fragmentation and aortic wall weakness. We hypothesize that gene editing correction of FBN1 pathogenic variants or genome editing-based upregulation of the structurally related protein FBN2 within aortic vascular smooth muscle will reduce risk of aortic root dilation and dissection, thereby limiting the major cause of morbidity and mortality in this disease. In the first aim, the candidate will identify a prime editing strategy to correct the Fbn1 C1041G pathogenic variant in aortic vascular smooth muscle of a murine model of MFS and will test this therapeutic strategy by monitoring aortic aneurysm. In the second aim, a machine learning model will be used to identify promoter variants, putative enhancers, and transcription factor binding site motifs within the FBN2 promoter region that are predicted to augment FBN2 expression. These elements will be functionally evaluated in a massively parallel reporter assay (MPRA). Finally, in vivo genome editing will be used to introduce an optimized FBN2 upregulatory strategy established through these analyses in the Fbn1C1041G/+ mouse model of MFS for correction of aortic pathology. In addition to establishing potential gene editing treatment strategies for aortic aneurysm in Marfan syndrome, these studies will enable the candidate to obtain expertise in the design and application of state-of-the-art gene editing tools that can be used to generate disease models and investigate therapies for many different genetic disorders, which he plans to pursue throughout his career as a physician-scientist.

NHGRI - National Human Genome Research Institute

Project Summary This proposed MAGen development site aims to develop genomics and multi-modal artificial intelligence (AI) models to transform personalized cancer risk assessment, monitoring, and prevention. A substantial gap exists between the theoretical potential of genomics-based AI predictions and their practical application in clinical and population healthcare settings. The clinical classification of genetic variants is hindered by insufficient data to classify ultra-rare variants, particularly those found in non-European populations. Moreover, despite significant advances in AI across fields, we lack AI models that can combine diverse streams of health data to accurately predict disease risk across a person’s life course. Finally, the real-world effectiveness of these AI models remains untested and their ethical, legal, and social implications (ELSI) are unclear. To address these challenges, our primary goal is to develop state-of-the-art (SOTA) AI models that can accurately identify pathogenic variants affecting DNA repair genes and predict cancer risks over the life course of high-risk carriers, thereby optimizing screening and prevention strategies in an ELSI-informed manner. Our multidisciplinary team comprises experts in computational genomics, AI/ML, health informatics, statistical genetics, medical genetics, population health, oncology, and ELSI research from Icahn School of Medicine at Mount Sinai (ISMMS), Boston Children’s Hospital/Harvard, and Columbia University, and has complementary and extensive experience in consortium and team science projects. In our proposed project for MAGen, Aim 1 will develop robust genomic AI models for identifying protein-disrupting missense variants that confer high cancer risks. Aim 2 will combine other genetic factors, including common and rare variant polygenic risk scores (PRS), and non-genetic factors, including EHR, longitudinal lab markers, SDoH, and digital pathology, to predict cancer risk over the life course and optimize screening recommendations for carriers. Aim 3 will cross-validate AI models in real-world population biobanks and determine their clinical impact. Aim 4 will construct an ELSI framework and conduct ELSI projects to evaluate the multi-faceted impacts of AI-driven genetic diagnostics. Aim 5 will disseminate AI model/predictions, cross-validation data, and ELSI recommendations. The completion of these Aims will bring genomics-based and multi-modal AI closer to the advancement of personalized medicine in real-world settings by more accurately classifying pathogenic variants, optimizing the timing of screening, and identifying key lifestyle and medical prevention strategies that could ultimately save lives from cancer.

Georgetown Merchants Association

The Georgetown Carnival is a free, one-day, arts & music-focused street fair centered in Georgetown’s historic business district. The 2025 Carnival will take place on June 14, 12-10 pm, on Airport Way S between 12th Ave S & Corson Ave. The Carnival is a celebration of the neighborhood and its unique place as an artistic and small business haven surrounded by large-scale industry. It brings visibility to the neighborhood artists and businesses, and gives our small residential community a day of fun focused on our special neighborhood. With a residential population of only 1700, Georgetown’s small businesses rely on customers from other parts of Seattle to remain viable. Events like Carnival are vital in increasing the visibility of our local artists and businesses, and create a lasting economic impact by introducing new people to the neighborhood and encouraging them to return. In 2023, we welcomed over 5,000 people to the Carnival, many of whom were first time visitors to Georgetown.

Georgetown Merchants Association

Our project is the revival of the annual Georgetown Carnival. Carnival has been a tradition going on 14 years, with 2023 being it's official return post-COVID. Carnival is a one day music and arts festival, taking place from 12pm - 10 pm along Airport Way S, and 12th Ave S in the Georgetown Neighborhood. Featuring live performances on three stages, booths for local vendors and artists, industrial art displays, and children's activities. The purpose of Carnival is to increase visibility of businesses in Georgetown. The businesses in Georgetown cannot be sustained by our small residential population alone.

Georgetown Association of Arts and Culture

The Georgetown Halloween Parade is a free community event on October 31, 2024. The family-friendly parade will be open to the public for participation and for viewing. Georgetown Association of Arts and Culture will host a number of free workshops leading up to the parade teaching people to do special effects make-up and prop-building, among other skills that can help them prepare for the parade. Many businesses and venues along Airport Way are coordinating with GTAAC to provide post-parade programming that night. This project will be completed by December 31, 2024.

Urban ArtWorks

The Georgetown Mural Program is an arts-based employment opportunity for up to 10 teens experiencing economic barriers and systemic inequality in the Georgetown neighborhood. This program is a partnership between Urban ArtWorks (UA)s and Mini Mart City Park (MMCP), a new community arts center in Georgetown. Mentored by a UA professional teaching artist, teens will be paid a stipend to design and install a mural at MMCP. The project will culminate in a publicly accessible mural unveiling and solo art exhibit at the new MMCP gallery. The anticipate project completion date is September 30, 2021.

Coltura

On November 5th, 2017, community group, Coltura, will create a Georgetown No-Gas Mural. The mural will be installed at 969 S. Nebraska St. The public will be invited to Georgetown Art Attack Day to dedicate and celebrate the unveiling of the mural on November 11th. The goal of the Georgetown No-Gas Mural is to invite viewers to think about the use of gasoline in all the ways it touches them - the effect on their community and society, and to transform their thoughts to action. This mural is an effort to address community concerns regarding environmental justice through art.

Georgetown Steam Plant CDA

The Georgetown Steam Plant Science Fair is a two-day, community-driven celebration of SHTEAM – science, history, technology, engineering, art, and math. Curated to spark curiosity, connection, and critical thinking for all ages, this event empowers participants by moving them from the role of “observer” into “active contributor” to community development. Hosted at the historic Georgetown Steamplant, the fair blends hands-on experiments, scientific demos, community dialogue, data visualizations, interactive exhibits, art installations, and more to inspire makers, thinkers, and problem solvers. With the theme “Break the System,” this year’s fair challenges participants to reimagine outdated systems and structures – industrial, social, or ecological – and explore bold and regenerative solutions for the future. Along with exhibits, there will be food trucks, performances, and more! The event is free, family-friendly, and rooted in the values of community and collaboration.

Georgia Council for the Arts

Georgia Council for the Arts provides grants to support arts and cultural programming, artist fellowships, arts education, and community-based arts projects across GA.

Georgia Council for the Arts

Georgia Council for the Arts Arts Education grants support in-school and community arts education programs, artist residencies, and initiatives that bring arts experiences to Georgia students and youth.

Georgia Council for the Arts

The Georgia Council for the Arts provides operational support grants to Georgia nonprofit arts organizations, enabling them to sustain programming, build organizational capacity, and deliver arts and cultural experiences statewide.