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Antagonistic Regulation of PAF1C and p-TEFb Is Required for Oligodendrocyte Differentiation

Authors
Kim, SuhyunKim, Jun-DaeChung, Ah-YoungKim, Hyung-SeokKim, Young-SeopKim, Myoung-JinKoun, SoonilLee, You MieRhee, MyungchullPark, Hae-ChulHuh, Tae-Lin
Issue Date
13-Jun-2012
Publisher
SOC NEUROSCIENCE
Keywords
POLYMERASE-II TRANSCRIPTION; RNA-POLYMERASE; FACTOR SOX10; ZEBRAFISH; INHIBITOR; SPECIFICATION; MYELINATION; GENES
Citation
JOURNAL OF NEUROSCIENCE, v.32, no.24, pp 8201 - 8207
Pages
7
Indexed
SCI
SCIE
SCOPUS
Journal Title
JOURNAL OF NEUROSCIENCE
Volume
32
Number
24
Start Page
8201
End Page
8207
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/133851
DOI
10.1523/JNEUROSCI.5344-11.2012
ISSN
0270-6474
1529-2401
Abstract
Oligodendrocytes are myelinating glial cells in the CNS and are essential for proper neuronal function. During development, oligodendrocyte progenitor cells (OPCs) are specified from the motor neuron precursor domain of the ventral spinal cord and differentiate into myelinating oligodendrocytes after migration to the white matter of the neural tube. Cell cycle control of OPCs influences the balance between immature OPCs and myelinating oligodendrocytes, but the precise mechanism regulating the differentiation of OPCs into myelinating oligodendrocytes is unclear. To understand the mechanisms underlying oligodendrocyte differentiation, an N-ethyl-N-nitrosourea-based mutagenesis screen was performed and a zebrafish leo1 mutant, dalmuri (dal(knu6)) was identified in the current study. Leo1 is a component of the evolutionarily conserved RNA polymerase II-associated factor 1 complex (PAF1C), which is a positive regulator of transcription elongation. The dal(knu6) mutant embryos specified motor neurons and OPCs normally, and at the appropriate time, but OPCs subsequently failed to differentiate into myelinating oligodendrocytes and were eliminated by apoptosis. A loss-of-function study of cdc73, another member of PAF1C, showed the same phenotype in the CNS, indicating that PAF1C function is required for oligodendrocyte differentiation. Interestingly, inhibition of positive transcription elongation factor b (p-TEFb), rescued downregulated gene expression and impaired oligodendrocyte differentiation in the dal(knu6) mutant and Cdc73-deficient embryos. Together, these results indicate that antagonistic regulation of gene expression by PAF1C and p-TEFb plays a crucial role in oligodendrocyte development in the CNS.
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