FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W1551169308> ?p ?o ?g. }

• W1551169308 endingPage "2243" @default.
• W1551169308 startingPage "2242" @default.
• W1551169308 abstract "Have you seen?1 May 2012free access New romance between RNA degradation pathways: Mmi1 and RNAi meet on heterochromatic islands Lærke Rebekka Holm Lærke Rebekka Holm Department of Biology, University of Copenhagen, Copenhagen, Denmark Search for more papers by this author Geneviève Thon Corresponding Author Geneviève Thon Department of Biology, University of Copenhagen, Copenhagen, Denmark Search for more papers by this author Lærke Rebekka Holm Lærke Rebekka Holm Department of Biology, University of Copenhagen, Copenhagen, Denmark Search for more papers by this author Geneviève Thon Corresponding Author Geneviève Thon Department of Biology, University of Copenhagen, Copenhagen, Denmark Search for more papers by this author Author Information Lærke Rebekka Holm1 and Geneviève Thon 1 1Department of Biology, University of Copenhagen, Copenhagen, Denmark *Correspondence to: [email protected] The EMBO Journal (2012)31:2242-2243https://doi.org/10.1038/emboj.2012.138 There is an Article (May 2012) associated with this Have you seen?. PDFDownload PDF of article text and main figures. ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinked InMendeleyWechatReddit Figures & Info Meiosis is one of the most dramatic differentiation programmes a cell can undertake, since it leads to an irreversible reduction of the cell's genetic content. It therefore comes as no surprise that meiosis should be tightly regulated. In this issue Hiriart et al (2012) identify a new layer of regulation in which the RNA interference (RNAi) pathway dampens the expression of meiotic genes during vegetative growth in fission yeast. Their study converges with a recent publication by Zofall et al (2012) to reveal how components of the RNAi pathway, the Mmi1 RNA elimination system and chromatin modifications contribute to the maintenance of the vegetative state until a decision is made to enter meiosis. Cells express different parts of their genome depending on their function in an organism. Their expression programs can be altered according to intrinsic cues or in response to changes in the surroundings. When starved for nitrogen, fission yeast cells prepare for meiosis. Hundreds of genes are induced in successive waves (Mata et al, 2002), driving sexual differentiation and a cascade of events that culminate in the production of four haploid spores. The Ste11 and Mei4 transcription factors are master regulators in this programme. The wide changes in transcript abundance in ste11 and mei4 mutants underscore the importance of transcriptional regulation in meiosis. However, a remarkable discovery in the last few years has been that a number of meiotic genes, including mei4, are actually transcribed in vegetative yeast cells. Their transcripts though are unstable. How RNA-processing factors, the nuclear exosome and possibly other RNA degradation pathways control the expression of meiotic genes is currently the subject of intense study. One major source of meiotic transcript instability in vegetative yeast comes from the Mmi1 RNA elimination pathway (Harigaya et al, 2006; Figure 1). In this pathway the RNA-binding protein Mmi1 recognises DSR (determinant of selective removal) regions in a class of meiotic transcripts and orchestrates the recruitment of multiple factors including Red1, Pab2 and Rrp6 to target these transcripts for degradation (St-Andre et al, 2010; Yamanaka et al, 2010; Sugiyama and Sugioka-Sugiyama, 2011). At the onset of meiosis Mmi1 is sequestered into the Mei2 dot, a meiosis-specific subnuclear structure comprising the Mei2 protein and the non-coding meiRNA (Watanabe and Yamamoto, 1994). The resulting stabilization of DSR-containing transcripts is essential for meiotic progression. A large-scale expression array in the Hiriart et al (2012) work extends the number of known Mmi1 protein-coding targets in vegetative cells to 212, underscoring the importance of the system. Figure 1.Recruitment of RNAi and heterochromatin components to Mmi1 targets. During vegetative growth the Mmi1 protein targets DSR-containing transcripts for degradation. Mmi1 recruits the RNAi complex RITS and the Clr4-methyltransferase complex CLRC to participate in the repression of meiotic genes, as depicted in the case of mei4. During meiotic induction Mmi1 is sequestered in the Mei2 dot, causing dissociation of the complexes and expression of DSR-containing meiotic genes. The anti-silencing protein Epe1 helps remove H3K9me. Download figure Download PowerPoint An essential contribution of Hiriart et al (2012) is to establish a functional connection between Mmi1-mediated RNA elimination and another repressive pathway, RNAi. RNAi in S. pombe has been dissected in great detail in connection with its role in the formation of constitutive heterochromatin at centromeres and telomeres, and in the mating-type region. Central to the pathway at these locations are the ribonuclease Dicer and the RITS complex consisting of Ago1, Tas3, and Chp1 (reviewed by Creamer and Partridge, 2011). Dicer processes double-stranded RNA molecules transcribed from heterochromatic regions into 21–23-nucleotide siRNAs. siRNAs loaded onto Ago1 are believed to guide RITS to heterochromatic transcripts through base-pairing. One of the RITS-interacting complexes, CLRC, contains the Clr4 methyltransferase. By methylating histone H3 at lysine 9 (H3K9me), Clr4 creates a binding site for the chromodomain protein Chp1, thereby providing an alternate path of association for RITS to chromatin. The combined action of RNAi and histone modifications silences gene expression in constitutive heterochromatin both transcriptionally and post-transcriptionally. Here, Hiriart et al (2012) find that in addition to being present in constitutive heterochromatin, RITS is also associated with Mmi1 targets in vegetative cells. The association of RITS with meiotic genes is documented for the three subunits of RITS at mei4 and for Chp1 at numerous other targets. The physical association of RITS with meiotic genes suggests that RITS participates in the repression of these genes. Consistently, the mei4 and ssm4 steady-state transcript levels double in mutants lacking a RITS subunit and in dcr1Δ mutants. Furthermore, the association of RITS with Mmi1 targets is lost when cells are induced to undergo sexual differentiation by nitrogen starvation, coinciding with the sequestration of Mmi1 in the Mei2 dot. These findings extend the work recently published by Zofall et al (2012) on facultative heterochromatic islands. H3K9me was clearly detected at approximately 30 chromosomal locations in the study by Zofall et al (2012) and possibly in a latent state at a far greater number of locations. According to their diverse dependency on trans-acting factors, H3K9me islands do not represent one homogenous group corresponding to a single biological function. One subset corresponds to the Mmi1-regulated loci characterized here by Hiriart et al (2012). Nitrogen starvation reduces H3K9me at these islands, which include mei4 and ssm4, as it reduces their association with RITS. A picture emerges where the combined action of RNAi and heterochromatin regulates Mmi1 targets. The mechanism of association of RITS with Mmi1 targets differs quite strikingly from its association with constitutive heterochromatin, permitting and perhaps facilitating the dynamic changes that occur during differentiation. At centromeres the association of RITS depends very strongly on Dcr1 and Clr4, but at meiotic genes it rather relies on the Mmi1 protein and its co-factors, Rrp6, Red1 and Pab2 (Figure 1). Red1 facilitates the association of RITS with chromatin—perhaps through direct binding of Red1 and Clr4 and resulting H3K9me as suggested by Zofall et al (2012)—while Pab2 appears to facilitate association through RNA. A pending question is the extent to which siRNAs from meiotic transcripts contribute to the association of RITS with meiotic genes and the biogenesis of these siRNAs. How does RITS help silence its meiotic targets? H3K9me, the histone deacetylase Clr3 and Mit1 are detected at these targets (Hiriart et al, 2012; Zofall et al, 2012), suggesting that RITS might bring the same mechanisms of silencing to meiotic genes as to constitutive heterochromatin. Consistent with this scenario, a previous study found increased expression of meiotic genes in histone deacetylase and clr4 mutants (Hansen et al, 2005). The amplitude of the repression by RITS and heterochromatin is notably small compared to the changes occurring in a meiotic time course (Mata et al, 2002; Hansen et al, 2005) and unlike Hiriart et al (2012), Zofall et al (2012) did not detect increased mei4 or ssm4 transcript in ago1Δ cells. However, Hiriart et al (2012) provide genetic evidence that the contribution of RNAi to the repression of meiosis is physiologically important, by showing that deletion of chp1 or dcr1 partially suppresses the meiotic block in sme2Δ cells defective in producing meiRNA. Hiriart et al (2012) also identify meiRNA as one of the most sensitive Mmi1 targets, which reveals that the transition between vegetative state and meiosis is regulated through a double-negative loop where Mmi1 and meiRNA inhibit each other. RNAi and heterochromatin stabilize the Mmi1-dependent state in this bistable system, their repressive effects adding up with several other mechanisms (i.e. Cremona et al, 2011) for a tight and robust repression of meiotic genes in vegetative cells. Conflict of Interest The authors declare that they have no conflict of interest. References Creamer KM, Partridge JF (2011) RITS-connecting transcription, RNA interference, and heterochromatin assembly in fission yeast. Wiley Interdiscip Rev RNA 2: 632–646Wiley Online LibraryCASPubMedWeb of Science®Google Scholar Cremona N, Potter K, Wise JA (2011) A meiotic gene regulatory cascade driven by alternative fates for newly synthesized transcripts. Mol Biol Cell 22: 66–77CrossrefCASPubMedWeb of Science®Google Scholar Hansen KR, Burns G, Mata J, Volpe TA, Martienssen RA, Bähler J, Thon G (2005) Global effects on gene expression in fission yeast by silencing and RNA interference machineries. Mol Cell Biol 25: 590–601CrossrefCASPubMedWeb of Science®Google Scholar Harigaya Y, Tanaka H, Yamanaka S, Tanaka K, Watanabe Y, Tsutsumi C, Chikashige Y, Hiraoka Y, Yamashita A, Yamamoto M (2006) Selective elimination of messenger RNA prevents an incidence of untimely meiosis. Nature 442: 45–50CrossrefCASPubMedWeb of Science®Google Scholar Hiriart E, Vavasseur A, Touat-Todescini L, Yamashita A, Gilquin B, Lambert E, Perot J, Shichino Y, Nazaret N, Boyault C, Lachuer J, Perazza D, Yamamoto M, Verdel A (2012) Mmi1 RNA surveillance machinery directs RNAi complex RITS to specific meiotic genes in fission yeast. EMBO J 31: 2296–2308Wiley Online LibraryCASPubMedWeb of Science®Google Scholar Mata J, Lyne R, Burns G, Bahler J (2002) The transcriptional program of meiosis and sporulation in fission yeast. Nat Genet 32: 143–147CrossrefCASPubMedWeb of Science®Google Scholar St-Andre O, Lemieux C, Perreault A, Lackner DH, Bahler J, Bachand F (2010) Negative regulation of meiotic gene expression by the nuclear poly(a)-binding protein in fission yeast. J Biol Chem 285: 27859–27868CrossrefCASPubMedWeb of Science®Google Scholar Sugiyama T, Sugioka-Sugiyama R (2011) Red1 promotes the elimination of meiosis-specific mRNAs in vegetatively growing fission yeast. EMBO J 30: 1027–1039Wiley Online LibraryCASPubMedWeb of Science®Google Scholar Watanabe Y, Yamamoto M (1994) S. pombe mei2+ encodes an RNA-binding protein essential for premeiotic DNA synthesis and meiosis I, which cooperates with a novel RNA species meiRNA. Cell 78: 487–498CrossrefCASPubMedWeb of Science®Google Scholar Yamanaka S, Yamashita A, Harigaya Y, Iwata R, Yamamoto M (2010) Importance of polyadenylation in the selective elimination of meiotic mRNAs in growing S. pombe cells. EMBO J 29: 2173–2181Wiley Online LibraryCASPubMedWeb of Science®Google Scholar Zofall M, Yamanaka S, Reyes-Turcu FE, Zhang K, Rubin C, Grewal SI (2012) RNA elimination machinery targeting meiotic mRNAs promotes facultative heterochromatin formation. Science 335: 96–100CrossrefCASPubMedWeb of Science®Google Scholar Previous ArticleNext Article Read MoreAbout the coverClose modalView large imageVolume 31,Issue 10,May 16, 2012This month's cover image, Blue Mitosis, is a watercolour painting of cells in various stages of mitosis by Michele Banks, a painter based in Washington, DC. Most of Banks' artwork is inspired by science, particularly biology. Her work has been featured in The Scientist Online and Scientific American and has been exhibited at the National Institutes of Health. You can see more of her paintings and collages at http://artologica.etsy.com. Volume 31Issue 1016 May 2012In this issue FiguresReferencesRelatedDetailsLoading ..." @default.
• W1551169308 created "2016-06-24" @default.
• W1551169308 creator A5022569927 @default.
• W1551169308 creator A5027055248 @default.
• W1551169308 date "2012-05-01" @default.
• W1551169308 modified "2023-10-17" @default.
• W1551169308 title "New romance between RNA degradation pathways: Mmi1 and RNAi meet on heterochromatic islands" @default.
• W1551169308 cites W1969636175 @default.
• W1551169308 cites W1988952096 @default.
• W1551169308 cites W2008344131 @default.
• W1551169308 cites W2013094037 @default.
• W1551169308 cites W2027950141 @default.
• W1551169308 cites W2054229788 @default.
• W1551169308 cites W2054663548 @default.
• W1551169308 cites W2097363081 @default.
• W1551169308 cites W2099358398 @default.
• W1551169308 cites W2156991031 @default.
• W1551169308 cites W2157289789 @default.
• W1551169308 doi "https://doi.org/10.1038/emboj.2012.138" @default.
• W1551169308 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3364736" @default.
• W1551169308 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/22549465" @default.
• W1551169308 hasPublicationYear "2012" @default.
• W1551169308 type Work @default.
• W1551169308 sameAs 1551169308 @default.
• W1551169308 citedByCount "4" @default.
• W1551169308 countsByYear W15511693082014 @default.
• W1551169308 countsByYear W15511693082016 @default.
• W1551169308 countsByYear W15511693082021 @default.
• W1551169308 countsByYear W15511693082022 @default.
• W1551169308 crossrefType "journal-article" @default.
• W1551169308 hasAuthorship W1551169308A5022569927 @default.
• W1551169308 hasAuthorship W1551169308A5027055248 @default.
• W1551169308 hasBestOaLocation W15511693082 @default.
• W1551169308 hasConcept C103435993 @default.
• W1551169308 hasConcept C104317684 @default.
• W1551169308 hasConcept C166703698 @default.
• W1551169308 hasConcept C2779679103 @default.
• W1551169308 hasConcept C41008148 @default.
• W1551169308 hasConcept C54355233 @default.
• W1551169308 hasConcept C67705224 @default.
• W1551169308 hasConcept C70721500 @default.
• W1551169308 hasConcept C76155785 @default.
• W1551169308 hasConcept C78458016 @default.
• W1551169308 hasConcept C83640560 @default.
• W1551169308 hasConcept C86803240 @default.
• W1551169308 hasConcept C95444343 @default.
• W1551169308 hasConceptScore W1551169308C103435993 @default.
• W1551169308 hasConceptScore W1551169308C104317684 @default.
• W1551169308 hasConceptScore W1551169308C166703698 @default.
• W1551169308 hasConceptScore W1551169308C2779679103 @default.
• W1551169308 hasConceptScore W1551169308C41008148 @default.
• W1551169308 hasConceptScore W1551169308C54355233 @default.
• W1551169308 hasConceptScore W1551169308C67705224 @default.
• W1551169308 hasConceptScore W1551169308C70721500 @default.
• W1551169308 hasConceptScore W1551169308C76155785 @default.
• W1551169308 hasConceptScore W1551169308C78458016 @default.
• W1551169308 hasConceptScore W1551169308C83640560 @default.
• W1551169308 hasConceptScore W1551169308C86803240 @default.
• W1551169308 hasConceptScore W1551169308C95444343 @default.
• W1551169308 hasIssue "10" @default.
• W1551169308 hasLocation W15511693081 @default.
• W1551169308 hasLocation W15511693082 @default.
• W1551169308 hasLocation W15511693083 @default.
• W1551169308 hasLocation W15511693084 @default.
• W1551169308 hasOpenAccess W1551169308 @default.
• W1551169308 hasPrimaryLocation W15511693081 @default.
• W1551169308 hasRelatedWork W107772589 @default.
• W1551169308 hasRelatedWork W1991523530 @default.
• W1551169308 hasRelatedWork W2002128513 @default.
• W1551169308 hasRelatedWork W2102789602 @default.
• W1551169308 hasRelatedWork W2128468599 @default.
• W1551169308 hasRelatedWork W2141919058 @default.
• W1551169308 hasRelatedWork W2894391419 @default.
• W1551169308 hasRelatedWork W3014735164 @default.
• W1551169308 hasRelatedWork W4233657100 @default.
• W1551169308 hasRelatedWork W2092874662 @default.
• W1551169308 hasVolume "31" @default.
• W1551169308 isParatext "false" @default.
• W1551169308 isRetracted "false" @default.
• W1551169308 magId "1551169308" @default.
• W1551169308 workType "article" @default.