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Evolution of sequence-specific anti-silencing systems in Arabidopsis

Aoi Hosaka (), Raku Saito, Kazuya Takashima, Taku Sasaki, Yu Fu, Akira Kawabe, Tasuku Ito, Atsushi Toyoda, Asao Fujiyama, Yoshiaki Tarutani and Tetsuji Kakutani ()
Additional contact information
Aoi Hosaka: National Institute of Genetics
Raku Saito: National Institute of Genetics
Kazuya Takashima: National Institute of Genetics
Taku Sasaki: National Institute of Genetics
Yu Fu: National Institute of Genetics
Akira Kawabe: Faculty of Life Sciences, Kyoto Sangyo University, Motoyama Kamigamo
Tasuku Ito: National Institute of Genetics
Atsushi Toyoda: Center for Information Biology, National Institute of Genetics
Asao Fujiyama: Center for Information Biology, National Institute of Genetics
Yoshiaki Tarutani: National Institute of Genetics
Tetsuji Kakutani: National Institute of Genetics

Nature Communications, 2017, vol. 8, issue 1, 1-10

Abstract: Abstract The arms race between parasitic sequences and their hosts is a major driving force for evolution of gene control systems. Since transposable elements (TEs) are potentially deleterious, eukaryotes silence them by epigenetic mechanisms such as DNA methylation. Little is known about how TEs counteract silencing to propagate during evolution. Here, we report behavior of sequence-specific anti-silencing proteins used by Arabidopsis TEs and evolution of those proteins and their target sequences. We show that VANC, a TE-encoded anti-silencing protein, induces extensive DNA methylation loss throughout TEs. Related VANC proteins have evolved to hypomethylate TEs of completely different spectra. Targets for VANC proteins often form tandem repeats, which vary considerably between related TEs. We propose that evolution of VANC proteins and their targets allow propagation of TEs while causing minimal host damage. Our findings provide insight into the evolutionary dynamics of these apparently “selfish” sequences. They also provide potential tools to edit epigenomes in a sequence-specific manner.

Date: 2017
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DOI: 10.1038/s41467-017-02150-7

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