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Sas-Nowosielska, H.

Publications and source records attributed to Sas-Nowosielska, H..

2 recordsLinked to original sources

SWING domains prime chromatin for nuclear body mediated gene regulation

Nuclear speckles have long been recognized as RNA-rich nuclear bodies, yet their role in genome organization and gene regulation remains incompletely understood. Using a rapid dTAG-mediated degradation system to simultaneously deplete SON and SRRM2--the core structural components of nuclear speckles--we identify a novel class of genomic regions, which we term SWING regions. Upon speckle disruption, SWING regions relocate to the nuclear periphery and acquire repressive histone marks such as H3K9me3, accompanied by gene downregulation, particularly of genes involved in developmental pathways. Consistent with this, depletion of Lamin A reduces lamina association of SWING regions and enhances their association with nuclear speckles, supporting a bidirectional balance between these two nuclear compartments. Notably, human mutations in SON and SRRM2 are associated with neurodevelopmental disorders characterized by intellectual disability and global developmental delay. Patient-derived cells bearing such mutations similarly exhibit SWING-region relocalization and gene repression, underlining a role for speckles in developmental gene regulation. We also report that drug-induced speckle rejuvenation partially rescues aberrant SWING-region localization to the nuclear lamina in patient-derived cells and iPSCs with acute depletion of SON. These findings identify SWING regions as an intermediate chromatin state positioned between nuclear speckles and the lamina, maintained by opposing functions from both structures. Our work reveals a mechanism underlying the contribution of nuclear bodies to 3D genome organization, highlights the importance of nuclear speckles and SWING regions in developmental regulation, and provides a potential therapeutic intervention in speckle dysfunction. Impact StatementIdentification of nuclear speckles as determinants of specific 3D genome organization. Demonstration of functional interactions between opposing nuclear structures (speckle versus lamina) through SWING regions. Establishment of developmental and human disease relevance of speckle-mediated genome organization. Providing potential avenues for therapeutic intervention in speckleopathies.

genetics↗

Histone acetylation in an Alzheimer's disease cell model promotes homeostatic amyloid-reducing pathways

Alzheimers Disease (AD) is a disorder characterized by cognitive decline, neurodegeneration, and accumulation of amyloid plaques and tau neurofibrillary tangles in the brain. Dysregulation of epigenetic histone modifications may lead to expression of transcriptional programs that play a role either in protecting against disease genesis or in worsening of disease pathology. One such histone modification, acetylation of histone H3 lysine residue 27 (H3K27ac), is primarily localized to genomic enhancer regions and promotes active gene transcription. We previously discovered H3K27ac to be more abundant in AD patient brain tissue compared to the brains of age-matched non-demented controls. In this study, we use iPSC-neurons derived from familial AD patients with an amyloid precursor protein (APP) duplication (APPDup neurons) as a model to study the functional effect of lowering CBP/P300 enzymes that catalyze H3K27ac primarily at gene enhancers. We found that homeostatic amyloid-reducing genes were upregulated in the APPDup neurons compared to non- demented controls. We lowered CBP/P300 to reduce H3K27ac, which led to decreased expression of numerous of these homeostatic amyloid-reducing genes, along with increased extracellular secretion of a toxic amyloid-{beta} species, A{beta}(1-42). Our findings suggest that epigenomic histone acetylation, including H3K27ac, drives expression of compensatory genetic programs in response to AD-associated insults, specifically those resulting from APP duplication, and thus may play a role in mitigating AD pathology in neurons.

neuroscience↗