| Literature DB >> 26358720 |
Anthony Hickey1, Caroline Esnault1, Anasuya Majumdar1, Atreyi Ghatak Chatterjee1, James R Iben2, Philip G McQueen1, Andrew X Yang1, Takeshi Mizuguchi3, Shiv I S Grewal3, Henry L Levin4.
Abstract
Transposable elements (TEs) constitute a substantial fraction of the eukaryotic genome and, as a result, have a complex relationship with their host that is both adversarial and dependent. To minimize damage to cellular genes, TEs possess mechanisms that target integration to sequences of low importance. However, the retrotransposon Tf1 of Schizosaccharomyces pombe integrates with a surprising bias for promoter sequences of stress-response genes. The clustering of integration in specific promoters suggests that Tf1 possesses a targeting mechanism that is important for evolutionary adaptation to changes in environment. We report here that Sap1, an essential DNA-binding protein, plays an important role in Tf1 integration. A mutation in Sap1 resulted in a 10-fold drop in Tf1 transposition, and measures of transposon intermediates support the argument that the defect occurred in the process of integration. Published ChIP-Seq data on Sap1 binding combined with high-density maps of Tf1 integration that measure independent insertions at single-nucleotide positions show that 73.4% of all integration occurs at genomic sequences bound by Sap1. This represents high selectivity because Sap1 binds just 6.8% of the genome. A genome-wide analysis of promoter sequences revealed that Sap1 binding and amounts of integration correlate strongly. More important, an alignment of the DNA-binding motif of Sap1 revealed integration clustered on both sides of the motif and showed high levels specifically at positions +19 and -9. These data indicate that Sap1 contributes to the efficiency and position of Tf1 integration.Entities:
Keywords: Sap1; Schizosaccharomyces pombe; Tf1; integration; transposition
Mesh:
Substances:
Year: 2015 PMID: 26358720 PMCID: PMC4649660 DOI: 10.1534/genetics.115.181602
Source DB: PubMed Journal: Genetics ISSN: 0016-6731 Impact factor: 4.562