GEO series
Repeat expansions in C9orf72 rewire the 3D chromatin landscape in ALS
GSE313074
Homo sapiens
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing; Other
39 samples
2026/02/09
GPL24676GPL30173GPL34281
Summary
Amyotrophic lateral sclerosis (ALS) is frequently driven by GGGGCC short tandem repeat (STR) expansions in C9orf72, yet the mechanisms by which these expansions lead to neurodegeneration remain incompletely understood. Here, we propose a novel mechanism involving higher-order chromatin architecture where C9orf72-STR expansions induce widespread, neuron-specific gains in chromatin loops that are closely linked to transcriptomic dysregulation in ALS. These ectopic loops colocalize with the genomic binding sites of C9orf72-STR RNAs and the architectural protein CTCF, supporting a model in which RNA-DNA interactions promote aberrant loop formation.
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