Abstract
An analysis of the nuclear β-fibrinogen intron 7 locus from 30 taxa representing 12 placental orders of mammals reveals the enriched occurrences of short interspersed element (SINE) insertion events. Mammalian-wide interspersed repeats (MIRs) are present at orthologous sites of all examined species except those in the order Rodentia. The higher substitution rate in mouse and a rare MIR deletion from rat account for the absence of MIR in the rodents. A minimum of five lineage-specific SINE sequences are also found to have independently inserted into this intron in Carnivora, Artiodactyla and Lagomorpha. In the case of Carnivora, the unique amplification pattern of order-specific CAN SINE provides important evidence for the “pan-carnivore” hypothesis of this repeat element and reveals that the CAN SINE family may still be active today. Particularly interesting is the finding that all identified lineage-specific SINE elements show a strong tendency to insert within or in very close proximity to the preexisting MIRs for their efficient integrations, suggesting that the MIR element is a hot spot for successive insertions of other SINEs. The unexpected MIR excision as a result of a random deletion in the rat intron locus and the non-random site targeting detected by this study indicate that SINEs actually have a greater insertional flexibility and regional specificity than had previously been recognized. Implications for SINE sequence evolution upon and following integration, as well as the fascinating interactions between retroposons and the host genomes are discussed.
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Acknowledgments
This work was supported by the grants from National Natural Science Foundation of China (NSFC) and Chinese Academy of Science. Additionally, we thank Dr. Alfred Roca, Dr. Warren Johnson and Ms. Luo Shujin, National Cancer Institute, Laboratory of Genomic Diversity for improving the English of the manuscript.
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Yu, L., Zhang, Yp. Evolutionary implications of multiple SINE insertions in an intronic region from diverse mammals. Mamm Genome 16, 651–660 (2005). https://doi.org/10.1007/s00335-004-2456-3
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DOI: https://doi.org/10.1007/s00335-004-2456-3