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Huskins, S. N.

Publications and source records attributed to Huskins, S. N..

2 recordsLinked to original sources

Radiotherapy Reshapes the 3D Genome in Medulloblastoma Cells

Radiotherapy is central to medulloblastoma treatment, yet the molecular and three-dimensional (3D) genome responses to irradiation remain poorly understood. Here, we integrated RNA sequencing, proteomics, and Micro-C to characterise the response of ONS-76 medulloblastoma cells to clinically relevant radiation exposures. A single 2 Gy dose induced widespread transcriptional and proteomic changes, including altered cell adhesion, migration, DNA replication, and ribosome biogenesis pathways. Integrated analysis identified LAMB3 and AKR1B10 as candidate mediators of radioresponse that remained elevated following fractionated irradiation. Micro-C profiling following single and repeated 2 Gy exposures revealed radiation-induced 3D genome remodelling. While global genome organisation remained largely stable, irradiation promoted shifts towards active A compartments, new TAD boundary formation, and transient boundary strengthening. Together, these findings provide the first genome-wide characterisation of radiation-induced 3D chromatin reorganisation in a medulloblastoma model and identify molecular and structural features associated with radioresponse.

cancer biology↗

H3K4me3 enrichment defines neuronal age, while a youthful H3K27ac signature is recapitulated in aged neurons

Neurons live for the lifespan of the individual and underlie our ability for lifelong learning and memory. However, aging alters neuron morphology and function resulting in age-related cognitive decline. It is well established that epigenetic alterations are essential for learning and memory, yet few neuron-specific genome-wide epigenetic maps exist into old age. Comprehensive mapping of H3K4me3 and H3K27ac in mouse neurons across lifespan revealed plastic H3K4me3 marking that differentiates neuronal age linked to known characteristics of cellular and neuronal aging. We determined that neurons in old age recapitulate the H3K27ac enrichment at promoters, enhancers and super enhancers from young adult neurons, likely representing a re-activation of pathways to maintain neuronal output. Finally, this study identified new characteristics of neuronal aging, including altered rDNA regulation and epigenetic regulatory mechanisms. Collectively, these findings indicate a key role for epigenetic regulation in neurons, that is inextricably linked with aging.

molecular biology↗