期刊
ELIFE
卷 2, 期 -, 页码 -出版社
ELIFE SCIENCES PUBLICATIONS LTD
DOI: 10.7554/eLife.00668
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资金
- Wellcome Trust [093160/Z/10/Z]
- Royal Society
- National Institute of General Medical Sciences [91687]
- National Institutes of Health [R01GM086615-01]
- Microsoft Research Faculty Fellowship
- Apple Research & Technology Support
- EU-IndiaGrid2
- Wellcome Trust [093160/Z/10/Z] Funding Source: Wellcome Trust
How do DNA transposons live in harmony with their hosts? Bacteria provide the only documented mechanisms for autoregulation, but these are incompatible with eukaryotic cell biology. Here we show that autoregulation of Hsmar1 operates during assembly of the transpososome and arises from the multimeric state of the transposase, mediated by a competition for binding sites. We explore the dynamics of a genomic invasion using a computer model, supported by in vitro and in vivo experiments, and show that amplification accelerates at first but then achieves a constant rate. The rate is proportional to the genome size and inversely proportional to transposase expression and its affinity for the transposon ends. Mariner transposons may therefore resist post-transcriptional silencing. Because regulation is an emergent property of the reaction it is resistant to selfish exploitation. The behavior of distantly related eukaryotic transposons is consistent with the same mechanism, which may therefore be widely applicable.
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