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With dramatic advancements in biological data generation, genetic rescue and reproductive technologies, and inter-institutional coordination of care across entire animal populations, zoos, aquariums, and their collaborators are uniquely positioned to lead population-wide research benefiting animal wellbeing and species survival. However, procedural and inter-institutional barriers make it exceedingly difficult to access existing zoological biospecimens and data at scale. To address this, the Zoonomics Working Group, representing diverse roles across three zoological associations (AZA, EAZA, WAZA), proposes a biodiversity biobank alliance that develops and delivers shared resources to support the collection, storage, and sharing of biological samples and associated data across the zoological and conservation community. By biobank alliance, we mean a community-guided effort that develops shared resources, standards, ethos, and practices for collecting, storing, and sharing biological samples and associated data voluntarily through transparent processes, consistent with professional accreditation standards and international best practices. While initially focused on addressing the needs and regulatory landscape of U.S. institutions, the alliance is designed to create frameworks that are adaptable and adoptable for international expansion. Such a framework would help the zoological community navigate the ethical, legal, and practical challenges of managing biospecimen collections, making access more efficient, reliable, and robust. Achieving this vision requires collective agreement on ethical principles such as reciprocity, transparency, and data stewardship, ensuring that research is both feasible and proactively supported. Such coordination will drive advances in fundamental biology and accelerate progress in animal health, welfare, management, and biodiversity conservation. 

Individuals with disabilities, including individuals with an autism spectrum disorder (ASD), are underrepresented in science, technology, engineering, and mathematics (STEM) fields. With the importance of STEM skills in future employment and other disciplines, effective instructional strategies must be identified to enhance early and sustained access to STEM for students with ASD. However, the literature identifying effective STEM-specific supports and practices for this population of students is sparse and regarding engineering, there are no empirical studies that focus on teaching engineering skills to students with ASD. Therefore, the article aims to provide an overview of the available literature on the perspectives of engineering educators and suggested strategies aimed at supporting students with ASD in K-12 instruction and higher education. Additionally, recommendations regarding employment preparation and shifting the workplace environment to support individuals with ASD are presented. The available literature reveals limitations and implications for future research including the presentation of the voices of individuals with ASD across the spectrum. Furthermore, there continues to be work that must be done to prepare educators, employers, peers, and colleagues to better understand the disability and support individuals with ASD in all contexts. 

Rationale: NAA15 (N-alpha-acetyltransferase 15) is a component of the NatA (N-terminal acetyltransferase complex). The mechanism by which NAA15 haploinsufficiency causes congenital heart disease remains unknown. To better understand molecular processes by which NAA15 haploinsufficiency perturbs cardiac development, we introduced NAA15 variants into human induced pluripotent stem cells (iPSCs) and assessed the consequences of these mutations on RNA and protein expression. Objective: We aim to understand the role of NAA15 haploinsufficiency in cardiac development by investigating proteomic effects on NatA complex activity and identifying proteins dependent upon a full amount of NAA15. Methods and Results: We introduced heterozygous loss of function, compound heterozygous, and missense residues (R276W) in iPSCs using CRISPR/Cas9. Haploinsufficient NAA15 iPSCs differentiate into cardiomyocytes, unlike NAA15 -null iPSCs, presumably due to altered composition of NatA. Mass spectrometry analyses reveal ≈80% of identified iPSC NatA targeted proteins displayed partial or complete N-terminal acetylation. Between null and haploinsufficient NAA15 cells, N-terminal acetylation levels of 32 and 9 NatA-specific targeted proteins were reduced, respectively. Similar acetylation loss in few proteins occurred in NAA15 R276W induced pluripotent stem cells. In addition, steady-state protein levels of 562 proteins were altered in both null and haploinsufficient NAA15 cells; 18 were ribosomal-associated proteins. At least 4 proteins were encoded by genes known to cause autosomal dominant congenital heart disease. Conclusions: These studies define a set of human proteins that requires a full NAA15 complement for normal synthesis and development. A 50% reduction in the amount of NAA15 alters levels of at least 562 proteins and N-terminal acetylation of only 9 proteins. One or more modulated proteins are likely responsible for NAA15-haploinsufficiency mediated congenital heart disease. Additionally, genetically engineered induced pluripotent stem cells provide a platform for evaluating the consequences of amino acid sequence variants of unknown significance on NAA15 function. 

Damaging GATA6 variants cause cardiac outflow tract defects, sometimes with pancreatic and diaphragmic malformations. To define molecular mechanisms for these diverse developmental defects, we studied transcriptional and epigenetic responses to GATA6 loss of function (LoF) and missense variants during cardiomyocyte differentiation of isogenic human induced pluripotent stem cells. We show that GATA6 is a pioneer factor in cardiac development, regulating SMYD1 that activates HAND2, and KDR that with HAND2 orchestrates outflow tract formation. LoF variants perturbed cardiac genes and also endoderm lineage genes that direct PDX1 expression and pancreatic development. Remarkably, an exon 4 GATA6 missense variant, highly associated with extra-cardiac malformations, caused ectopic pioneer activities, profoundly diminishing GATA4 , FOXA1/2, and PDX1 expression and increasing normal retinoic acid signaling that promotes diaphragm development. These aberrant epigenetic and transcriptional signatures illuminate the molecular mechanisms for cardiovascular malformations, pancreas and diaphragm dysgenesis that arise in patients with distinct GATA6 variants.