Data from: Stabilization of primary cilia reduces abortive cell cyle re-entry to protect injured adult CNS neurons from apoptosis

Abortive cell cycle (ACC) re-entry of apoptotic neurons is a recently
characterized phenomenon that occurs after central nervous system (CNS)
injury or over the course of CNS disease. Consequently, inhibiting cell
cycle progression is neuroprotective in numerous CNS pathology models.
Primary cilia are ubiquitous, centriole-based cellular organelles that
prevent cell cycling, but their ability to modulate abortive cell cycle
has not been described. Here, we show that neuronal cilia are ablated
in-vitro and in-vivo following injury by hypoxia or optic nerve
transection (ONT), respectively. Furthermore, forced cilia resorption
sensitized neurons to these injuries and enhanced cell death. In contrast,
pharmacological inhibition or shRNA knockdown of the proteins that
disassemble the cilia increased neuron survival and decreased the
phosphorylation of retinoblastoma (Rb), a master switch for cell cycle
re-entry. Our findings show that the stabilization of neuronal primary
cilia inhibits apoptotic cell cycling, which has implications for future
therapeutic strategies that halt or slow the progression of
neurodegenerative diseases and acute CNS injuries.