CELL IN DISTRESS: In cultured neurons, damage to the axon results in a wave of calcium ions surging toward the cell body (1). Subsequently, the enzyme PKCμ is phosphorylated (2), resulting in the release of histone deacetylase 5 (HDAC5) from the nucleus (3). Following HDAC5’s departure, acetylation of histone H3 increases (4), upregulating the expression of genes involved in regeneration. HDAC5 then ends up congregating at the site of injury (5). © SCOTT LEIGHTON
The paper
Y. Cho et al., “Injury-induced HDAC5 nuclear export is essential for axon regeneration,” Cell, 155:894–908, 2013.
To regenerate after injury, a nerve cell must turn on gene programs that have been silenced since development. Epigenetic modifications, important players in the activation and silencing of genes, may underlie the ability for a cell to rebuild. “At some level, some epigenetic change must occur globally to allow the neuron to reprogram itself,” says Valeria Cavalli of the Washington University School of Medicine in St. Louis, Missouri.
In 2012, Cavalli’s group showed that when axons are injured in peripheral sensory neurons, a wave of calcium ions courses from the site of the injury down the axon to the cell body. Subsequently, histone deacetylase 5 (HDAC5)—an epigenetic ...
