bioRxiv Science⌕ Search

Biology subjects

Ertaylan, G.

Publications and source records attributed to Ertaylan, G..

3 recordsLinked to original sources

PRISM-G: an interpretable privacy scoring method for assessing risk in synthetic human genome data

Synthetic genomic data promises broader access, but unresolved privacy risks persist. In Europe, these risks increasingly hinder cross-border use of national genomic resources due to limitations in trust and legal interoperability rather than scientific demand. At the same time, privacy risk is not uniformly distributed: leakage driven by relatedness structure and rare-variant uniqueness can disproportionately affect underrepresented or vulnerable populations when shared data are misused or linked with external resources, making transparent, domain-aware measurement of privacy exposure central to responsible governance. We introduce PRISM-G, a model-agnostic framework that quantifies privacy exposure in synthetic genome data cross three complementary components: proximity to real genomes in genetic-coordinate space, replay of familial or population-structure patterns, and trait-linked exposure via rare variants and membership-inference signals. These components are normalized and combined through a risk-averse aggregation into a single 0-100 PRISM-G score. We evaluated PRISM-G on synthetic cohorts generated by a generative adversarial network (GAN), a restricted Boltzmann machine (RBM), and a logic-based SAT-solver (Genomator). Our results show that privacy vulnerabilities concentrate along different axes across models and marker densities, demonstrating that a single similarity-based metric is sufficient to characterize genomic privacy risk.

bioinformatics↗

The guardians of mitochondrial dynamics: a novel role for intermediate filament proteins

Mitochondria are dynamic organelles and the main source of cellular energy. Their dynamic nature is crucial to meet cellular requirements. However, the processes and proteins involved in mitochondrial dynamics are not fully understood. Using a computational protein-protein interaction approach, we identified ITPRIPL2, which caused mitochondrial elongation upon knockdown. ITPRIPL2 co-localizes with the intermediate filament protein vimentin and interacts with vimentin according to protein simulations. ITPRIPL2 knockdown alters vimentin processing, disrupts intermediate filaments and transcriptomics analysis revealed changes in vimentin-related pathways. Our data illustrates that ITPRIPL2 is essential for vimentin related intermediate filament structure. Interestingly, like ITPRIPL2 knockdown, vimentin knockdown results in mitochondrial elongation. Our data highlights ITPRIPL2 as a vimentin-associated protein and reveals a role for intermediate filaments in mitochondrial dynamics, improving our understanding of mitochondrial dynamics regulators. Moreover, our study demonstrates that protein- protein interaction analysis is a powerful approach for identifying novel mitochondrial dynamics proteins.

systems biology↗

Adipose tissue in health and disease through the lens of its building blocks

BackgroundHighly specialized cells work in synergy forming tissues to perform functions required for the survival of organisms. Understanding this tissue-specific cellular heterogeneity and homeostasis is essential to comprehend the development of diseases within the tissue and also for developing regenerative therapies. Cellular subpopulations in the adipose tissue have been related to disease development, but efforts towards characterizing the adipose tissue cell type composition are limited due to lack of robust cell surface markers, limited access to tissue samples, and the labor-intensive process required to identify them.\n\nResultsWe propose a framework, identifying cellular heterogeneity while providing state-of-the-art cellular markers for each cell type present in tissues using transcriptomics level analysis. We validate our approach with an independent dataset and present the most comprehensive study of adipose tissue cell type composition to date, determining the relative amounts of 21 different cell types in 779 adipose tissue samples detailing differences across four adipose tissue depots, between genders, across ranges of BMI and in different stages of type-2 diabetes. We also highlight the heterogeneity in reported marker-based studies of adipose tissue cell type composition and provide novel cellular markers to distinguish different cell types within the adipose tissue.\n\nConclusionsOur study provides a systematic framework for studying cell type composition in a given tissue and valuable insights into adipose tissue cell type heterogeneity in health and disease.

systems biology↗