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Reprogramming of Retrotransposon Activity during Speciation of the Genus Citrus.

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URI
http://hdl.handle.net/20.500.11939/6316
DOI
10.1093/gbe/evz246
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openAccess
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Author
Borredá, Carles; Pérez-Román, Estela; Ibanez, Victoria; Terol, Javier; Talón, Manuel
Date
2019
Cita bibliográfica
Borreda, C., Perez-Roman, E., Ibanez, V., Terol, J., & Talon, M. (2019). Reprogramming of Retrotransposon Activity during Speciation of the Genus Citrus. Genome biology and evolution, 11(12), 3478-3495.
Abstract
Speciation of the genus Citrus from a common ancestor has recently been established to begin 8Ma during the late Miocene, a period of major climatic alterations. Here, we report the changes in activity of Citrus LTR retrotransposons during the process of diversification that gave rise to the current Citrus species. To reach this goal, we analyzed four pure species that diverged early during Citrus speciation, three recent admixtures derived from those species and an outgroup of the Citrus clade. More than 30,000 retrotransposons were grouped in ten linages. Estimations of LTR insertion times revealed that retrotransposon activity followed a species-specific pattern of change that could be ascribed to one of three different models. In some genomes, the expected pattern of gradual transposon accumulation was suddenly arrested during the radiation of the ancestor that gave birth to the current Citrus species. The individualized analyses of retrotransposon lineages showed that in each and every species studied, not all lineages follow the general pattern of the species itself. For instance, in most of the genomes, the retrotransposon activity of elements from the SIRE lineage reached its highest level just before Citrus speciation, while for Retrofit elements, it has been steadily growing. Based on these observations, we propose that Citrus retrotransposons may respond to stressful conditions driving speciation as a part of the genetic response involved in adaptation. This proposal implies that the evolving conditions of each species interact with the internal regulatory mechanisms of the genome controlling the proliferation of mobile elements.
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