title: Overproduction of non-translatable mRNA silences. The transcription of Ty1 retrotransposons in S. cerevisiae via functional inactivation of the nuclear cap-binding complex and subsequent hyperstimulation of the TORC1 pathway.
abstract: Co-suppression is high gene copy number-triggered homology-dependent gene silencing, and co-suppression may have evolved in eukaryotes to counter invasive molecular parasites, such as viruses and transposons. We previously reported 'Ty1 transcriptional co-suppression'-high Ty1 copy number-triggered transient transcriptional silencing of Ty1 retrotransposons in S. cerevisiae. We report here that this phenomenon is unlikely to be homology-dependent, despite the copy number dependence. The Ty1 mRNA is an extremely poor template for translation, and overproduction of non-translatable mRNA without Ty1 homology is sufficient to initiate the transient Ty1 transcriptional silencing. We present genetic evidence that overproduction of non-translatable mRNA may functionally inactivate the nuclear cap-binding complex (CBC), and inactivation of CBC may then hyperstimulate the TORC1 pathway to mediate Ty1 transcriptional silencing. Our results point to a potent regulatory function of non-translatable mRNA in vivo (via CBC and TORC1) to potentially modulate a variety of intracellular activities, such as Ty1 transcription. Although overproduction of non-translatable mRNA causes transient Ty1 transcriptional silencing, it does not play a detectable role in controlling Ty1 retrotransposition.
authors.affiliation: Department of Cell Biology and Genetics, University of North Texas Health Science Center, Fort Worth, TX 76107, USA.
authors.forename: Xiaofeng
authors.initials: X
authors.lastname: Wu
authors.forename: Yi Wei
authors.initials: YW
authors.lastname: Jiang
mesh_terms: D000900:Anti-Bacterial Agents / Q000494:pharmacology; D018628:Gene Dosage; D015966:Gene Expression Regulation, Fungal; D020868:Gene Silencing; D005947:Glucose / Q000378:metabolism; D008958:Models, Molecular; D039502:Nuclear Cap-Binding Protein Complex / Q000235:genetics* / Q000378:metabolism; D028861:Nuclear Pore Complex Proteins / Q000235:genetics / Q000378:metabolism; D014176:Protein Biosynthesis; D017346:Protein Serine-Threonine Kinases; D012333:RNA, Messenger / Q000235:genetics* / Q000378:metabolism; D018626:Retroelements / Q000235:genetics*; D012441:Saccharomyces cerevisiae / Q000187:drug effects / Q000235:genetics* / Q000378:metabolism; D029701:Saccharomyces cerevisiae Proteins / Q000235:genetics / Q000378:metabolism*; D015398:Signal Transduction; D020123:Sirolimus / Q000494:pharmacology; D014158:Transcription, Genetic
chemical_list: D000900:Anti-Bacterial Agents; D039502:Nuclear Cap-Binding Protein Complex; D028861:Nuclear Pore Complex Proteins; D012333:RNA, Messenger; D018626:Retroelements; D029701:Saccharomyces cerevisiae Proteins; D017346:Protein Serine-Threonine Kinases; C500749:target of rapamycin protein, S cerevisiae; D005947:Glucose; D020123:Sirolimus