title: RNA decay systems enhance reciprocal switching of sense and antisense transcripts in response to glucose starvation.
abstract: Antisense RNA has emerged as a crucial regulator of opposite-strand protein-coding genes in the long noncoding RNA (lncRNA) category, but little is known about their dynamics and decay process in the context of a stress response. Antisense transcripts from the fission yeast fbp1 locus (fbp1-as) are expressed in glucose-rich conditions and anticorrelated with transcription of metabolic stress-induced lncRNA (mlonRNA) and mRNA on the sense strand during glucose starvation. Here, we investigate the localization and decay of antisense RNAs at fbp1 and other loci, and propose a model to explain the rapid switch between antisense and sense mlonRNA/mRNA transcription triggered by glucose starvation. We show that fbp1-as shares many features with mRNAs, such as a 5'-cap and poly(A)-tail, and that its decay partially depends upon Rrp6, a cofactor of the nuclear exosome complex involved in 3'-5' degradation of RNA. Fluorescence in situ hybridization and polysome fractionation show that the majority of remaining fbp1-as localizes to the cytoplasm and binds to polyribosomes in glucose-rich conditions. Furthermore, fbp1-as and antisense RNA at other stress-responsive loci are promptly degraded via the cotranslational nonsense-mediated decay (NMD) pathway. These results suggest NMD may potentiate the swift disappearance of antisense RNAs in response to cellular stress.
authors.affiliation: Department of Biological Sciences, Graduate School of Science, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-8654, Japan.
authors.forename: Atsuko
authors.identifier: http://orcid.org/0000-0003-3898-8125
authors.initials: A
authors.lastname: Miki
authors.affiliation: Institute for Advanced Biosciences, Keio University, Tsuruoka, Yamagata, 997-0035, Japan.
authors.forename: Josephine
authors.initials: J
authors.lastname: Galipon
authors.affiliation: Department of Life Sciences, Graduate School of Arts and Sciences, The University of Tokyo, 3-8-1 Komaba, Meguro-ku, Tokyo, 153-8902, Japan.
authors.forename: Satoshi
authors.initials: S
authors.lastname: Sawai
authors.affiliation: Graduate School of Pharmaceutical Sciences, Tohoku University, Sendai, Miyagi, 980-8578, Japan.
authors.forename: Toshifumi
authors.initials: T
authors.lastname: Inada
authors.affiliation: Department of Biological Sciences, Graduate School of Science, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-8654, Japan.|Department of Life Sciences, Graduate School of Arts and Sciences, The University of Tokyo, 3-8-1 Komaba, Meguro-ku, Tokyo, 153-8902, Japan.
authors.forename: Kunihiro
authors.initials: K
authors.lastname: Ohta
mesh_terms: D003593:Cytoplasm / Q000378:metabolism; D015966:Gene Expression Regulation, Fungal; D005800:Genes, Fungal; D005947:Glucose / Q000378:metabolism*; D020871:RNA Stability; D016372:RNA, Antisense / Q000378:metabolism*; D012331:RNA, Fungal / Q000378:metabolism*; D062085:RNA, Long Noncoding / Q000378:metabolism*; D012270:Ribosomes / Q000378:metabolism; D012568:Schizosaccharomyces / Q000235:genetics* / Q000378:metabolism; D013312:Stress, Physiological
chemical_list: D016372:RNA, Antisense; D012331:RNA, Fungal; D062085:RNA, Long Noncoding; D005947:Glucose