|ZFIN ID: ZDB-PUB-050603-4|
Oligodendrocyte development and myelination in GFP-transgenic zebrafish
Yoshida, M., and Macklin, W.B.
|Source:||Journal of neuroscience research 81(1): 1-8 (Journal)|
|Registered Authors:||Macklin, Wendy B.|
|Keywords:||transgenic zebrafish; oligodendrocytes; EGFP; myelination|
|PubMed:||15920740 Full text @ J. Neurosci. Res.|
Yoshida, M., and Macklin, W.B. (2005) Oligodendrocyte development and myelination in GFP-transgenic zebrafish. Journal of neuroscience research. 81(1):1-8.
ABSTRACTGreen fluorescent protein (GFP) transgenic zebrafish technology has been employed to directly visualize and analyze dynamic developmental processes, such as cell migration and morphogenesis. Stable transgenic zebrafish that express GFP in oligodendrocytes can be a valuable tool to visualize complex myelination processes in vivo, as well as to conduct rapid mutagenesis screens for defective myelination mutants. We investigated whether two myelin gene promoters, the zebrafish P0 promoter and the mouse proteolipid protein (PLP) promoter, drive GFP expression in zebrafish oligodendrocytes. Transiently, both promoters drive enhanced GFP (EGFP) expression in morphologically identifiable oligodendrocytes, premyelinating oligodendrocytes, and possible oligodendrocyte precursors. We have established a stable transgenic zebrafish line, tg(plp:EGFP) zebrafish, at the F1 generation, which expresses enhanced GFP (EGFP) driven by the mouse PLP promoter. In this transgenic line, EGFP-expressing cells are visually detectable around 24-hr postfertilization (hpf), and later at 54 hpf, these cells start exhibiting the clear morphologic characteristics of oligodendrocytes. Shortly afterward, EGFP-expressing oligodendrocytes establish a ventral dominant distribution pattern throughout the central nervous system. This transgenic zebrafish line is likely to serve as a useful tool, in which normal myelination as well as abnormal myelination can be recorded under time-lapse confocal microscopy. Furthermore, it has the potential to greatly facilitate mutagenesis screening for novel dysmyelinating mutants. (c) 2005 Wiley-Liss, Inc.