A study led by Dr. Hyun Kyoung Lee, associate professor at Baylor College of Medicine and investigator at the Jan and Dan Duncan Neurological Research Institute at Texas Children's Hospital, has discovered a new biological mechanism to regenerate and repair myelin, a protective sheath that insulates neuronal fibers and plays a vital role in ensuring rapid and accurate neurotransmission.
The Duncan NRI team found novel roles for the Disheveled associated activator of morphogenesis 2 protein and CK2α kinase in regulating myelin repair and regeneration. The study was published in theMyelin is produced by a type of glial precursor cells called oligodendrocytes which are among the most numerous cells in the nervous system. Damage or loss of myelin sheath is the hallmark of various neurological diseases in adults and infants and is common after brain injuries.
A few years back, Dr. Lee and others found that a glial protein, Daam2 inhibits the differentiation of oligodendrocytes during development as well as myelin regeneration and repair. However, until now precise mechanisms underlying this process have remained a mystery. To explore if Daam2 phosphorylation affected the progression of OL lineage, they analyzed differentially expressed genes in wild-type and mutant animals whose Daam2 is constitutively phosphorylated. DEGs downregulated in the mutant OLs were enriched in genes involved in lipid/cholesterol metabolism whereas DEGs upregulated in the mutant OLs were involved in multiple signaling processes, including the Wnt pathway.
"Intriguingly, we found Daam2 phosphorylation differentially impacts distinct stages of oligodendrocyte development—in early stages, it accelerates the conversion of precursor OLs to glial cells but in later stages, it slows down their maturation and their ability to produce myelin," Dr. Lee said.
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