TARE1, a Mutated Copia-Like LTR Retrotransposon Followed by Recent Massive Amplification in Tomato
文献类型: 外文期刊
作者: Yin, Hao 1 ; Liu, Jing 1 ; Xu, Yingxiu 1 ; Liu, Xing 1 ; Zhang, Shaoling 2 ; Ma, Jianxin 3 ; Du, Jianchang 1 ;
作者机构: 1.Jiangsu Acad Agr Sci, Bioinformat Grp, Inst Ind Crops, Nanjing, Jiangsu, Peoples R China
2.Nanjing Agr Univ, State Key Lab Crop Genet & Germplasm Enhancement, Ctr Pear Engn Technol Res, Nanjing, Jiangsu, Peoples R China
3.Purdue Univ, Dept Agron, W Lafayette, IN 47907 USA
期刊名称:PLOS ONE ( 影响因子:3.24; 五年影响因子:3.788 )
ISSN: 1932-6203
年卷期: 2013 年 8 卷 7 期
页码:
收录情况: SCI
摘要: Long terminal repeat retrotransposons (LTR-RTs) are the major DNA components in flowering plants. Most LTR-RTs contain dinucleotides 'TG' and 'CA' at the ends of the two LTRs. Here we report the structure, evolution, and propensity of a tomato atypical retrotransposon element (TARE1) with both LTRs starting as 'TA'. This family is also characterized by high copy numbers (354 copies), short LTR size (194 bp), extremely low ratio of solo LTRs to intact elements (0.05: 1), recent insertion (most within 0.75 similar to 1.75 million years, Mys), and enrichment in pericentromeric region. The majority (83%) of the TARE1 elements are shared between S. lycopersicum and its wild relative S. pimpinellifolium, but none of them are found in potato. In the present study, we used shared LTR-RTs as molecular markers and estimated the divergence time between S. lycopersicum and S. pimpinellifolium to be <0.5 Mys. Phylogenetic analysis showed that the TARE1 elements, together with two closely related families, TARE2 and TGRE1, have formed a sub-lineage belonging to a Copia-like Ale lineage. Although TARE1 and TARE2 shared similar structural characteristics, the timing, scale, and activity of their amplification were found to be substantially different. We further propose a model wherein a single mutation from 'G' to 'A' in 39 LTR followed by amplification is responsible for the origin of TARE1, thus providing evidence that the proliferation of a spontaneous mutation can be mediated by the amplification of LTR-RTs at the level of RNA.
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