Journal
HEREDITY
Volume 110, Issue 2, Pages 194-204Publisher
SPRINGERNATURE
DOI: 10.1038/hdy.2012.99
Keywords
DNA amplification; genome size variation; polyploidy; repetitive DNA; sample sequence analysis; transposable elements
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Funding
- NSF [0607123]
- NIH [T32 GM07103-31]
- Georgia Research Alliance
- Direct For Biological Sciences [1118550] Funding Source: National Science Foundation
- Division Of Integrative Organismal Systems [1118550] Funding Source: National Science Foundation
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Sample sequence analysis was employed to investigate the repetitive DNAs that were most responsible for the evolved variation in genome content across seven panicoid grasses with >5-fold variation in genome size and different histories of polyploidy. In all cases, the most abundant repeats were LTR retrotransposons, but the particular families that had become dominant were found to be different in the Pennisetum, Saccharum, Sorghum and Zea lineages. One element family, Huck, has been very active in all of the studied species over the last few million years. This suggests the transmittal of an active or quiescent autonomous set of Huck elements to this lineage at the founding of the panicoids. Similarly, independent recent activity of Ji and Opie elements in Zea and of Leviathan elements in Sorghum and Saccharum species suggests that members of these families with exceptional activation potential were present in the genome(s) of the founders of these lineages. In a detailed analysis of the Zea lineage, the combined action of several families of LTR retrotransposons were observed to have approximately doubled the genome size of Zea luxurians relative to Zea mays and Zea diploperennis in just the last few million years. One of the LTR retrotransposon amplification bursts in Zea may have been initiated by polyploidy, but the great majority of transposable element activations are not. Instead, the results suggest random activation of a few or many LTR retrotransposons families in particular lineages over evolutionary time, with some families especially prone to future activation and hyper-amplification. Heredity (2013) 110, 194-204; doi:10.1038/hdy.2012.99
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