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DNA transposons mediate duplications via transposition-independent and -dependent mechanisms in metazoans

Despite long being considered as “junk”, transposable elements (TEs) are now accepted as catalysts of evolution. One example is Mutator -like elements (MULEs, one type of terminal inverted repeat DNA TEs, or TIR TEs) capturing sequences as Pack-MULEs in plants. However, their origination mechanism r...

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Published in:Nature communications 2021-07, Vol.12 (1), p.4280-14, Article 4280
Main Authors: Tan, Shengjun, Ma, Huijing, Wang, Jinbo, Wang, Man, Wang, Mengxia, Yin, Haodong, Zhang, Yaqiong, Zhang, Xinying, Shen, Jieyu, Wang, Danyang, Banes, Graham L., Zhang, Zhihua, Wu, Jianmin, Huang, Xun, Chen, Hua, Ge, Siqin, Chen, Chun-Long, Zhang, Yong E.
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Language:English
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Summary:Despite long being considered as “junk”, transposable elements (TEs) are now accepted as catalysts of evolution. One example is Mutator -like elements (MULEs, one type of terminal inverted repeat DNA TEs, or TIR TEs) capturing sequences as Pack-MULEs in plants. However, their origination mechanism remains perplexing, and whether TIR TEs mediate duplication in animals is almost unexplored. Here we identify 370 Pack-TIRs in 100 animal reference genomes and one Pack-TIR ( Ssk-FB4 ) family in fly populations. We find that single-copy Pack-TIRs are mostly generated via transposition-independent gap filling, and multicopy Pack-TIRs are likely generated by transposition after replication fork switching. We show that a proportion of Pack-TIRs are transcribed and often form chimeras with hosts. We also find that Ssk-FB4s represent a young protein family, as supported by proteomics and signatures of positive selection. Thus, TIR TEs catalyze new gene structures and new genes in animals via both transposition-independent and -dependent mechanisms. Transposons are accepted as evolutionary catalysts but how they do so remains less clear. Analyzing 100 animal genomes finds that terminal inverted repeat-type transposable elements catalyze new gene structures and new genes in animals via both transposition-independent and -dependent mechanisms.
ISSN:2041-1723
2041-1723
DOI:10.1038/s41467-021-24585-9