The failure of adult central nervous system neurons to regenerate after injury has been
attributed to transcriptional and epigenetic barriers, but whether three-dimensional genome
organization constitutes an independent regulatory layer encoding regenerative potential
remains unknown. Here we present the first genome-wide map of chromatin compartments,
topologically associating domains, and loops across postnatal development, adult
homeostasis, and spinal cord injury in the mouse motor cortex. Postnatal maturation
progressively consolidates a growth-restrictive three-dimensional architecture, and spinal cord
injury alone partially reverses this consolidation, re-engaging neonatal gene programs through
reorganized but functionally recapitulative architecture despite minimal transcriptional
activation. This reversion is directed rather than stochastic, preferentially targeting
pro-growth gene networks, and reveals a latent three-dimensional memory of
developmental growth states in the adult cortical genome. Strikingly, NR2F6, a
transcription factor that promotes corticospinal axon regeneration, extends this reversion
beyond the neonatal state toward an earlier embryonic chromatin configuration, a depth of
developmental plasticity that injury alone cannot reach. These findings establish
three-dimensional genome topology as a regulatory layer encoding regenerative potential in
adult cortical neurons, demonstrating that successful CNS regeneration requires accessing
embryonic rather than merely neonatal chromatin states, and reframing regenerative
failure as a topological problem with new therapeutic targets.