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Targeted reduction of the DNA methylation level with 5-azacytidine promotes excision of the medaka fish Tol2 transposable element

Published online by Cambridge University Press:  04 July 2006

ATSUO IIDA
Affiliation:
Division of Biological Science, Graduate School of Science, Nagoya University, Nagoya 464-8602, Japan
ATSUKO SHIMADA
Affiliation:
Department of Biological Sciences, Graduate School of Sciences, University of Tokyo, Tokyo 113-0033, Japan
AKIHIRO SHIMA
Affiliation:
Department of Integrated Biosciences, Graduate School of Frontier Sciences, University of Tokyo, Kashiwa 277-8562, Japan Present address: Institute for Environmental Sciences, Rokkasho, Aomori 039-3212, Japan.
NAOFUMI TAKAMATSU
Affiliation:
Division of Biological Science, Graduate School of Science, Nagoya University, Nagoya 464-8602, Japan
HIROSHI HORI
Affiliation:
Division of Biological Science, Graduate School of Science, Nagoya University, Nagoya 464-8602, Japan
KOSEI TAKEUCHI
Affiliation:
Division of Biological Science, Graduate School of Science, Nagoya University, Nagoya 464-8602, Japan Present address: Laboratory for Neuronal Circuit, KAN Research Institute, Kyoto 600-8815, Japan.
AKIHIKO KOGA
Affiliation:
Division of Biological Science, Graduate School of Science, Nagoya University, Nagoya 464-8602, Japan
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Abstract

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The Tol2 element of the medaka fish Oryzias latipes is a member of the hAT (hobo/Activator/Tam3) transposable element family. There is evidence for rapid expansion in the genome and throughout the species in the past but a high spontaneous transposition rate is not observed with current fish materials, suggesting that the Tol2 element and its host species have already acquired an interactive mechanism to control the transposition frequency. DNA methylation is a possible contributing factor, given its involvement with many other transposable elements. We therefore soaked embryos in 5-azacytidine, a reagent that causes reduction in the DNA methylation level, and examined amounts of PCR products reflecting the somatic excision frequency, obtaining direct evidence that exposure promotes Tol2 excision. Our results thus suggest that methylation of the genome DNA is a factor included in the putative mechanisms of control of transposition of the Tol2 element.

Type
Research Article
Copyright
© 2006 Cambridge University Press