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• W2035281648 endingPage "20142874" @default.
• W2035281648 startingPage "20142874" @default.
• W2035281648 abstract "Interspecific hybridization leads to new interactions among divergent genomes, revealing the nature of genetic incompatibilities having accumulated during and after the origin of species. Conflicts associated with misregulation of transposable elements (TEs) in hybrids expectedly result in their activation and genome-wide changes that may be key to species boundaries. Repetitive genomes of wild wheats have diverged under differential dynamics of specific long terminal repeat retrotransposons (LTR-RTs), offering unparalleled opportunities to address the underpinnings of plant genome reorganization by selfish sequences. Using reciprocal F 1 hybrids between three Aegilops species, restructuring and epigenetic repatterning was assessed at random and LTR-RT sequences with amplified fragment length polymorphism and sequence-specific amplified polymorphisms as well as their methylation-sensitive counterparts, respectively. Asymmetrical reorganization of LTR-RT families predicted to cause conflicting interactions matched differential survival of F 1 hybrids. Consistent with the genome shock model, increasing divergence of merged LTR-RTs yielded higher levels of changes in corresponding genome fractions and lead to repeated reorganization of LTR-RT sequences in F 1 hybrids. Such non-random reorganization of hybrid genomes is coherent with the necessary repression of incompatible TE loci in support of hybrid viability and indicates that TE-driven genomic conflicts may represent an overlooked factor supporting reproductive isolation." @default.
• W2035281648 created "2016-06-24" @default.
• W2035281648 creator A5023968309 @default.
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• W2035281648 date "2015-04-07" @default.
• W2035281648 modified "2023-09-27" @default.
• W2035281648 title "Genome reorganization in F ₁ hybrids uncovers the role of retrotransposons in reproductive isolation" @default.
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• W2035281648 doi "https://doi.org/10.1098/rspb.2014.2874" @default.
• W2035281648 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4375867" @default.
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