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Katsuhiko Ono,Hirohide Takebayashi,Kazuhiro Ikenaka 한국분자세포생물학회 2009 Molecules and cells Vol.27 No.4
Olig2 transcription factor is widely expressed throughout the central nervous system; therefore, it is considered to have multiple functions in the developing, mature and injured brain. In this mini-review, we focus on Olig2 in the forebrain (telencephalon and diencephalon) and discuss the functional significance of Olig2 and the differentiation properties of Olig2-expressing progenitors in the development and injured states. Short- and long-term lineage analysis in the developing forebrain elucidated that not all late Olig2+ cells are direct cohorts of early cells and that Olig2 lineage cells differentiate into neurons or glial cells in a region- and stage-dependent manner. Olig2-deficient mice revealed large elimination of oligodendrocyte precursor cells and a decreased number of astrocyte progenitors in the dorsal cortex, whereas no reduction in the number of GABAergic neurons. In addition to Olig2 function in the developing cortex, Olig2 is also reported to be important for glial scar formation after injury. Thus, Olig2 can be essential for glial differentiation during development and after injury.
Hashimoto, Hirokazu,Jiang, Wen,Yoshimura, Takeshi,Moon, Kyeong-Hye,Bok, Jinwoong,Ikenaka, Kazuhiro Elsevier 2018 Neurochemistry International Vol.119 No.-
<P><B>Abstract</B></P> <P>In the mouse neural tube, sonic hedgehog (Shh) secreted from the floor plate (FP) and the notochord (NC) regulates ventral patterning of the neural tube, and later is essential for the generation of oligodendrocyte precursor cells (OPCs). During early development, the NC is adjacent to the neural tube and induces ventral domains in it, including the FP. In the later stage of development, during gliogenesis in the spinal cord, the pMN domain receives strong Shh signaling input. While this is considered to be essential for the generation of OPCs, the actual role of this strong input in OPC generation remains unclear. Here we studied OPC generation in <I>bromi</I> mutant mice which show abnormal ciliary structure. Shh signaling occurs within cilia and has been reported to be weak in <I>bromi</I> mutants. At E11.5, accumulation of <I>Patched1</I> mRNA, a Shh signaling reporter, is observed in the pMN domain of wild type but not <I>bromi</I> mutants, whereas expression of <I>Gli1</I> mRNA, another Shh reporter, disappeared. Thus, Shh signaling input to the pMN domain at E12.5 was reduced in <I>bromi</I> mutant mice. In these mutants, induction of the FP structure was delayed and its size was reduced compared to wild type mice. Furthermore, while the p3 and pMN domains were induced, the length of the Nkx2.2-positive region and the number of Olig2-positive cells decreased. The number of OPCs was also significantly decreased in the E12.5 and E14.5 <I>bromi</I> mutant spinal cord. In contrast, motor neuron (MN) production, detected by HB9 expression, significantly increased. It is likely that the transition from MN production to OPC generation in the pMN domain is impaired in <I>bromi</I> mutant mice. These results suggest that strong Shh input to the pMN domain is not required for OPC generation but is essential for producing a sufficient number of OPCs.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Induction of the floor plate structure is attenuated in E12.5 <I>bromi</I> mutants. </LI> <LI> Shh signaling input to the pMN domain is insufficient in <I>bromi</I> mutants. </LI> <LI> Motor neuron generation increases at E12.5 by <I>bromi</I> mutation. </LI> <LI> Oligodendrocyte precursor cell number decreases in the embryonic <I>bromi</I> spinal cord. </LI> </UL> </P>