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PIKE is essential for oligodendroglia development and CNS myelination

Significance Accumulation of a lipid-rich substance (myelin sheath) around the axon of neurons enables the nerve cells to transmit information faster. However, the molecular mechanism that controls this important process is not well understood. Here, we report that the GTPase phosphoinositide 3-kinase enhancer is a regulator of myelin sheath formation during development and myelin repair. Oligodendrocyte (OL) differentiation and myelin development are complex events regulated by numerous signal transduction factors. Here, we report that phosphoinositide-3 kinase enhancer L (PIKE-L) is required for OL development and myelination. PIKE-L expression is up-regulated when oligodendrocyte progenitor cells commit to differentiation. Conversely, depleting phosphoinositide-3 kinase enhancer (PIKE) expression by shRNA prevents oligodendrocyte progenitor cell differentiation. In both conventional PIKE knockout (PIKE−/−) and OL-specific PIKE knockout mice, the number of OLs is reduced in the corpus callosum. PIKE−/− OLs also display defects when forming myelin sheath on neuronal axons during neonatal development, which is partially rescued when PTEN is ablated. In addition, Akt/mTOR signaling is impaired in OL-enriched tissues of the PIKE−/− mutant, leading to reduced expression of critical proteins for myelin development and hypomyelination. Moreover, myelin repair of lysolecithin-induced lesions is delayed in PIKE−/− brain. Thus, PIKE plays pivotal roles to advance OL development and myelinogenesis through Akt/mTOR activation.