Publication details

Possible mechanisms responsible for absence of a retrotransposon family on a plant Y chromosome

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Authors

KUBÁT Zdeněk ŽLUVOVÁ Jitka VOGEL Ivan KOVÁČOVÁ Viera ČERMÁK Tomáš CEGAN Radim HOBZA Roman VYSKOT Boris KEJNOVSKÝ Eduard

Year of publication 2014
Type Article in Periodical
Magazine / Source New Phytologist
MU Faculty or unit

Central European Institute of Technology

Citation
Web http://onlinelibrary.wiley.com/doi/10.1111/nph.12669/epdf
Doi http://dx.doi.org/10.1111/nph.12669
Field Genetics and molecular biology
Keywords epigenetics; genome size; long terminal repeat (LTR) retrotransposon; plant sex chromosomes; silencing; Silene latifolia (white campion); small RNA
Description Some transposable elements (TEs) show extraordinary variance in abundance along sex chromosomes but the mechanisms responsible for this variance are unknown. Here, we studied Ogre long terminal repeat (LTR) retrotransposons in Silene latifolia, a dioecious plant with evolutionarily young heteromorphic sex chromosomes. Ogre elements are ubiquitous in the S.latifolia genome but surprisingly absent on the Y chromosome. Bacterial artificial chromosome (BAC) library analysis and fluorescence in situ hybridization (FISH) were used to determine Ogre structure and chromosomal localization. Next generation sequencing (NGS) data were analysed to assess the transcription level and abundance of small RNAs. Methylation of Ogres was determined by bisulphite sequencing. Phylogenetic analysis was used to determine mobilization time and selection forces acting on Ogre elements. We characterized three Ogre families ubiquitous in the S.latifolia genome. One family is nearly absent on the Y chromosome despite all the families having similar structures and spreading mechanisms. We showed that Ogre retrotransposons evolved before sex chromosomes appeared but were mobilized after formation of the Y chromosome. Our data suggest that the absence of one Ogre family on the Y chromosome may be caused by 24-nucleotide (24-nt) small RNA-mediated silencing leading to female-specific spreading. Our findings highlight epigenetic silencing mechanisms as potentially crucial factors in sex-specific spreading of some TEs, but other possible mechanisms are also discussed.
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