SREBP Controls Oxygen-Dependent Mobilization of Retrotransposons in Fission Yeast

Abstract

Retrotransposons are mobile genetic elements that proliferate through an RNA intermediate. Transposons do not encode transcription factors and thus rely on host factors for mRNA expression and survival. Despite information regarding conditions under which elements are upregulated, much remains to be learned about the regulatory mechanisms or factors controlling retrotransposon expression. Here, we report that low oxygen activates the fission yeast Tf2 family of retrotransposons. Sre1, the yeast ortholog of the mammalian membrane-bound transcription factor sterol regulatory element binding protein (SREBP), directly induces the expression and mobilization of Tf2 retrotransposons under low oxygen. Sre1 binds to DNA sequences in the Tf2 long terminal repeat that functions as an oxygen-dependent promoter. We find that Tf2 solo long terminal repeats throughout the genome direct oxygendependent expression of adjacent coding and noncoding sequences, providing a potential mechanism for the generation of oxygen-dependent gene expression.

Host genome surveillance for retrotransposons by transposon-derived proteins

“…As Abp1 and Cbh1 can bind to distinct loci, and that these factors do not always colocalize with SHREC 23 , CENP-B binding in contexts other than heterochromatin and transposable elements might recruit activities important for other chromatin transactions, such as transcription and DNA replication. Accumulating evidence implicates transposable-element-derived sequences as regulators of gene expression in diverse species 1, [35][36][37] . A substantial fraction of human promoters contains transposable element sequences 38 , and instances of their contribution to gene regulation have been documented 1, 39 .…”

Mapping genomic hotspots of DNA damage by a single-strand-DNA-compatible and strand-specific ChIP-seq method

“…5F). Tf2 mobilization is often mediated by integrase-independent recombination between its cDNA and pre-existing genomic copies of Tf2 (Hoff et al 1998;Sehgal et al 2007). We speculate that the binding of Rad52 to an immature form of Tf2 cDNA may contribute to this main mode of Tf2 transposition.…”

“…To verify the SPI-seq results, we performed ChIP-PCR analysis using strains in which one Tf2 is tagged with a neo marker (Sehgal et al 2007). Indeed, in D1D3, we detected Rad52 enrichment on the neo marker gene (Fig.…”

Casein Kinase 1 Regulates Sterol Regulatory Element-binding Protein (SREBP) to Control Sterol Homeostasis

“…1B). The reporter gene consisted of four tandem Sre1N DNA-binding sites driving expression of ura4 ϩ that codes for orotidine 5-monophosphate decarboxylase and is required for growth in the absence of uracil (18,36). Orotidine 5-monophosphate decarboxylase also enables the cells to metabolize the compound 5-FOA to the toxin 5-fluorouracil; thus, cells that highly express ura4 ϩ fail to grow in the presence of 5-FOA (29).…”