@article{Bartle2023,

title = {Methods that shaped telomerase research},

author = {Louise Bartle and Raymund J. Wellinger},

doi = {10.1007/s10522-023-10073-8},

issn = {1573-6768},

year  = {2024},

date = {2024-04-00},

journal = {Biogerontology},

volume = {25},

number = {2},

pages = {249--263},

publisher = {Springer Science and Business Media LLC},

abstract = {AbstractTelomerase, the ribonucleoprotein (RNP) responsible for telomere maintenance, has a complex life. Complex in that it is made of multiple proteins and an RNA, and complex because it undergoes many changes, and passes through different cell compartments. As such, many methods have been developed to discover telomerase components, delve deep into understanding its structure and function and to figure out how telomerase biology ultimately relates to human health and disease. While some old gold-standard methods are still key for determining telomere length and measuring telomerase activity, new technologies are providing promising new ways to gain detailed information that we have never had access to before. Therefore, we thought it timely to briefly review the methods that have revealed information about the telomerase RNP and outline some of the remaining questions that could be answered using new methodology.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Neumann2023,

title = {Ratcheted transport and sequential assembly of the yeast telomerase RNP},

author = {Hannah Neumann and Louise Bartle and Erin Bonnell and Raymund J. Wellinger},

doi = {10.1016/j.celrep.2023.113565},

issn = {2211-1247},

year  = {2023},

date = {2023-12-00},

journal = {Cell Reports},

volume = {42},

number = {12},

publisher = {Elsevier BV},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Khan2023,

title = {Distinct regulatory functions and biological roles of lncRNA splice variants},

author = {Muhammad Riaz Khan and Mariano Avino and Raymund J. Wellinger and Benoit Laurent},

doi = {10.1016/j.omtn.2023.03.004},

issn = {2162-2531},

year  = {2023},

date = {2023-06-00},

journal = {Molecular Therapy - Nucleic Acids},

volume = {32},

pages = {127--143},

publisher = {Elsevier BV},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Neumann2023b,

title = {The Histone Variant H2A.Z C-Terminal Domain Has Locus-Specific Differential Effects on H2A.Z Occupancy and Nucleosome Localization},

author = {Hannah Neumann and Celia Jeronimo and Jean-François Lucier and Emeline Pasquier and François Robert and Raymund J. Wellinger and Luc Gaudreau},

editor = {Adnane Sellam},

doi = {10.1128/spectrum.02550-22},

issn = {2165-0497},

year  = {2023},

date = {2023-04-13},

journal = {Microbiol Spectr},

volume = {11},

number = {2},

publisher = {American Society for Microbiology},

abstract = {

            We provide evidence that the

            Saccharomyces cerevisiae

            C-terminal region of histone variant H2A.Z can mediate its special function in performing gene regulation by interacting with effector proteins and chaperones. These functional interactions allow H2A.Z not only to incorporate to very specific gene regulatory regions, but also to facilitate the gene expression process.

          },

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Guintini2022,

title = {Transcription of ncRNAs promotes repair of UV induced DNA lesions in Saccharomyces cerevisiae subtelomeres},

author = {Laetitia Guintini and Audrey Paillé and Marco Graf and Brian Luke and Raymund J. Wellinger and Antonio Conconi},

editor = {Lorraine S. Symington},

doi = {10.1371/journal.pgen.1010167},

issn = {1553-7404},

year  = {2022},

date = {2022-04-29},

journal = {PLoS Genet},

volume = {18},

number = {4},

publisher = {Public Library of Science (PLoS)},

abstract = {Ultraviolet light causes DNA lesions that are removed by nucleotide excision repair (NER). The efficiency of NER is conditional to transcription and chromatin structure. UV induced photoproducts are repaired faster in the gene transcribed strands than in the non-transcribed strands or in transcriptionally inactive regions of the genome. This specificity of NER is known as transcription-coupled repair (TCR). The discovery of pervasive non-coding RNA transcription (ncRNA) advocates for ubiquitous contribution of TCR to the repair of UV photoproducts, beyond the repair of active gene-transcribed strands. Chromatin rules transcription, and telomeres form a complex structure of proteins that silences nearby engineered ectopic genes. The essential protective function of telomeres also includes preventing unwanted repair of double-strand breaks. Thus, telomeres were thought to be transcriptionally inert, but more recently, ncRNA transcription was found to initiate in subtelomeric regions. On the other hand, induced DNA lesions like the UV photoproducts must be recognized and repaired also at the ends of chromosomes. In this study, repair of UV induced DNA lesions was analyzed in the subtelomeric regions of budding yeast. The T4-endonuclease V nicking-activity at cyclobutene pyrimidine dimer (CPD) sites was exploited to monitor CPD formation and repair. The presence of two photoproducts, CPDs and pyrimidine (6,4)-pyrimidones (6-4PPs), was verified by the effective and precise blockage of Taq DNA polymerase at these sites. The results indicate that UV photoproducts in silenced heterochromatin are slowly repaired, but that ncRNA transcription enhances NER throughout one subtelomeric element, called Y’, and in distinct short segments of the second, more conserved element, called X. Therefore, ncRNA-transcription dependent TCR assists global genome repair to remove CPDs and 6-4PPs from subtelomeric DNA.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Bartle2021,

title = {Maturation and shuttling of the yeast telomerase RNP: assembling something new using recycled parts},

author = {Louise Bartle and Yulia Vasianovich and Raymund J. Wellinger},

doi = {10.1007/s00294-021-01210-2},

issn = {1432-0983},

year  = {2022},

date = {2022-02-00},

journal = {Curr Genet},

volume = {68},

number = {1},

pages = {3--14},

publisher = {Springer Science and Business Media LLC},

abstract = {AbstractAs the limiting component of the budding yeast telomerase, the Tlc1 RNA must undergo multiple consecutive modifications and rigorous quality checks throughout its lifecycle. These steps will ensure that only correctly processed and matured molecules are assembled into telomerase complexes that subsequently act at telomeres. The complex pathway of Tlc1 RNA maturation, involving 5'- and 3'-end processing, stabilisation and assembly with the protein subunits, requires at least one nucleo-cytoplasmic passage. Furthermore, it appears that the pathway is tightly coordinated with the association of various and changing proteins, including the export factor Xpo1, the Mex67/Mtr2 complex, the Kap122 importin, the Sm7 ring and possibly the CBC and TREX-1 complexes. Although many of these maturation processes also affect other RNA species, the Tlc1 RNA exploits them in a new combination and, therefore, ultimately follows its own and unique pathway. In this review, we highlight recent new insights in maturation and subcellular shuttling of the budding yeast telomerase RNA and discuss how these events may be fine-tuned by the biochemical characteristics of the varying processing and transport factors as well as the final telomerase components. Finally, we indicate outstanding questions that we feel are important to be addressed for a complete understanding of the telomerase RNA lifecycle and that could have implications for the human telomerase as well.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Bonnell2021,

title = {Telomere Replication: Solving Multiple End Replication Problems},

author = {Erin Bonnell and Emeline Pasquier and Raymund J. Wellinger},

doi = {10.3389/fcell.2021.668171},

issn = {2296-634X},

year  = {2021},

date = {2021-04-01},

journal = {Front. Cell Dev. Biol.},

volume = {9},

publisher = {Frontiers Media SA},

abstract = {Eukaryotic genomes are highly complex and divided into linear chromosomes that require end protection from unwarranted fusions, recombination, and degradation in order to maintain genomic stability. This is accomplished through the conserved specialized nucleoprotein structure of telomeres. Due to the repetitive nature of telomeric DNA, and the unusual terminal structure, namely a protruding single stranded 3′ DNA end, completing telomeric DNA replication in a timely and efficient manner is a challenge. For example, the end replication problem causes a progressive shortening of telomeric DNA at each round of DNA replication, thus telomeres eventually lose their protective capacity. This phenomenon is counteracted by the recruitment and the activation at telomeres of the specialized reverse transcriptase telomerase. Despite the importance of telomerase in providing a mechanism for complete replication of telomeric ends, the majority of telomere replication is in fact carried out by the conventional DNA replication machinery. There is significant evidence demonstrating that progression of replication forks is hampered at chromosomal ends due to telomeric sequences prone to form secondary structures, tightly DNA-bound proteins, and the heterochromatic nature of telomeres. The telomeric loop (t-loop) formed by invasion of the 3′-end into telomeric duplex sequences may also impede the passage of replication fork. Replication fork stalling can lead to fork collapse and DNA breaks, a major cause of genomic instability triggered notably by unwanted repair events. Moreover, at chromosomal ends, unreplicated DNA distal to a stalled fork cannot be rescued by a fork coming from the opposite direction. This highlights the importance of the multiple mechanisms involved in overcoming fork progression obstacles at telomeres. Consequently, numerous factors participate in efficient telomeric DNA duplication by preventing replication fork stalling or promoting the restart of a stalled replication fork at telomeres. In this review, we will discuss difficulties associated with the passage of the replication fork through telomeres in both fission and budding yeasts as well as mammals, highlighting conserved mechanisms implicated in maintaining telomere integrity during replication, thus preserving a stable genome.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Pasquier2020,

title = {In vivo chromatin organization on native yeast telomeric regions is independent of a cis-telomere loopback conformation},

author = {Emeline Pasquier and Raymund J. Wellinger},

doi = {10.1186/s13072-020-00344-w},

issn = {1756-8935},

year  = {2020},

date = {2020-12-00},

journal = {Epigenetics & Chromatin},

volume = {13},

number = {1},

publisher = {Springer Science and Business Media LLC},

abstract = {AbstractBackgroundDNA packaging into chromatin regulates all DNA-related processes and at chromosomal ends could affect both essential functions of telomeres: protection against DNA damage response and telomere replication. Despite this primordial role of chromatin, little is known about chromatin organization, and in particular about nucleosome positioning on unmodified subtelomere–telomere junctions inSaccharomyces cerevisiae.ResultsBy ChEC experiments and indirect end-labeling, we characterized nucleosome positioning as well as specialized protein–DNA associations on most subtelomere–telomere junctions present in budding yeast. The results show that there is a relatively large nucleosome-free region at chromosome ends. Despite the absence of sequence homologies between the two major classes of subtelomere–telomere junctions (i.e.: Y’-telomeres and X-telomeres), all analyzed subtelomere–telomere junctions show a terminal nucleosome-free region just distally from the known Rap1-covered telomeric repeats. Moreover, previous evidence suggested a telomeric chromatin fold-back structure onto subtelomeric areas that supposedly was implicated in chromosome end protection. The in vivo ChEC method used herein in conjunction with several proteins in a natural context revealed no evidence for such structures in bulk chromatin.ConclusionsOur study allows a structural definition of the chromatin found at chromosome ends in budding yeast. This definition, derived with direct in vivo approaches, includes a terminal area that is free of nucleosomes, certain positioned nucleosomes and conserved DNA-bound protein complexes. This organization of subtelomeric and telomeric areas however does not include a telomeric cis-loopback conformation. We propose that the observations on such fold-back structures may report rare and/or transient associations and not stable or constitutive structures.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Vasianovich2020,

title = {Telomerase biogenesis requires a novel Mex67 function and a cytoplasmic association with the Sm7 complex},

author = {Yulia Vasianovich and Emmanuel Bajon and Raymund J Wellinger},

doi = {10.7554/elife.60000},

issn = {2050-084X},

year  = {2020},

date = {2020-10-23},

volume = {9},

publisher = {eLife Sciences Publications, Ltd},

abstract = {The templating RNA is the core of the telomerase reverse transcriptase. In Saccharomyces cerevisiae, the complex life cycle and maturation of telomerase includes a cytoplasmic stage. However, timing and reason for this cytoplasmic passage are poorly understood. Here, we use inducible RNA tagging experiments to show that immediately after transcription, newly synthesized telomerase RNAs undergo one round of nucleo-cytoplasmic shuttling. Their export depends entirely on Crm1/Xpo1, whereas re-import is mediated by Kap122 plus redundant, kinetically less efficient import pathways. Strikingly, Mex67 is essential to stabilize newly transcribed RNA before Xpo1-mediated nuclear export. The results further show that the Sm7 complex associates with and stabilizes the telomerase RNA in the cytoplasm and promotes its nuclear re-import. Remarkably, after this cytoplasmic passage, the nuclear stability of telomerase RNA no longer depends on Mex67. These results underscore the utility of inducible RNA tagging and challenge current models of telomerase maturation.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Langston2020,

title = {Loss of Cdc13 causes genome instability by a deficiency in replication-dependent telomere capping},

author = {Rachel E. Langston and Dominic Palazzola and Erin Bonnell and Raymund J. Wellinger and Ted Weinert},

editor = {Lorraine S. Symington},

doi = {10.1371/journal.pgen.1008733},

issn = {1553-7404},

year  = {2020},

date = {2020-04-14},

journal = {PLoS Genet},

volume = {16},

number = {4},

publisher = {Public Library of Science (PLoS)},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Červenák2019,

title = {Identification of telomerase RNAs in species of the Yarrowia clade provides insights into the co-evolution of telomerase, telomeric repeats and telomere-binding proteins},

author = {Filip Červenák and Katarína Juríková and Hugo Devillers and Binyamin Kaffe and Areej Khatib and Erin Bonnell and Martina Sopkovičová and Raymund J. Wellinger and Jozef Nosek and Yehuda Tzfati and Cécile Neuvéglise and Ľubomír Tomáška},

doi = {10.1038/s41598-019-49628-6},

issn = {2045-2322},

year  = {2019},

date = {2019-12-00},

journal = {Sci Rep},

volume = {9},

number = {1},

publisher = {Springer Science and Business Media LLC},

abstract = {AbstractTelomeric repeats in fungi of the subphylum Saccharomycotina exhibit great inter- and intra-species variability in length and sequence. Such variations challenged telomeric DNA-binding proteins that co-evolved to maintain their functions at telomeres. Here, we compare the extent of co-variations in telomeric repeats, encoded in the telomerase RNAs (TERs), and the repeat-binding proteins from 13 species belonging to the Yarrowia clade. We identified putative TER loci, analyzed their sequence and secondary structure conservation, and predicted functional elements. Moreover, in vivo complementation assays with mutant TERs showed the functional importance of four novel TER substructures. The TER-derived telomeric repeat unit of all species, except for one, is 10 bp long and can be represented as 5′-TTNNNNAGGG-3′, with repeat sequence variations occuring primarily outside the vertebrate telomeric motif 5′-TTAGGG-3′. All species possess a homologue of the Yarrowia lipolytica Tay1 protein, YlTay1p. In vitro, YlTay1p displays comparable DNA-binding affinity to all repeat variants, suggesting a conserved role among these species. Taken together, these results add significant insights into the co-evolution of TERs, telomeric repeats and telomere-binding proteins in yeasts.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Gauchier2019,

title = {SETDB1-dependent heterochromatin stimulates alternative lengthening of telomeres},

author = {Mathilde Gauchier and Sophie Kan and Amandine Barral and Sandrine Sauzet and Eneritz Agirre and Erin Bonnell and Nehmé Saksouk and Teresa K. Barth and Satoru Ide and Serge Urbach and Raymund J. Wellinger and Reini F. Luco and Axel Imhof and Jérôme Déjardin},

doi = {10.1126/sciadv.aav3673},

issn = {2375-2548},

year  = {2019},

date = {2019-05-03},

journal = {Sci. Adv.},

volume = {5},

number = {5},

publisher = {American Association for the Advancement of Science (AAAS)},

abstract = {Atypical heterochromatin forms on telomeres and correlates with ALT activities.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Mersaoui2018,

title = {Fine tuning the level of the Cdc13 telomere-capping protein for maximal chromosome stability performance},

author = {Sofiane Y. Mersaoui and Raymund J. Wellinger},

doi = {10.1007/s00294-018-0871-3},

issn = {1432-0983},

year  = {2019},

date = {2019-02-00},

journal = {Curr Genet},

volume = {65},

number = {1},

pages = {109--118},

publisher = {Springer Science and Business Media LLC},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Laterreur2018,

title = {The yeast telomerase module for telomere recruitment requires a specific RNA architecture},

author = {Nancy Laterreur and Bruno Lemieux and Hannah Neumann and Jean-Christophe Berger-Dancause and Daniel Lafontaine and Raymund J. Wellinger},

doi = {10.1261/rna.066696.118},

issn = {1469-9001},

year  = {2018},

date = {2018-08-00},

journal = {RNA},

volume = {24},

number = {8},

pages = {1067--1079},

publisher = {Cold Spring Harbor Laboratory},

abstract = {Telomerases are ribonucleoprotein (RNP) reverse transcriptases. While telomerases maintain genome stability, their composition varies significantly between species. Yeast telomerase RNPs contain an RNA that is comparatively large, and its overall folding shows long helical segments with distal functional parts. Here we investigated the essential stem IVc module of the budding yeast telomerase RNA, called Tlc1. The distal part of stem IVc includes a conserved sequence element CS2a and structurally conserved features for binding Pop1/Pop6/Pop7 proteins, which together function analogously to the P3 domains of the RNase P/MRP RNPs. A more proximal bulged stem with the CS2 element is thought to associate with Est1, a telomerase protein required for telomerase recruitment to telomeres. Previous work found that changes in CS2a cause a loss of all stem IVc proteins, not just the Pop proteins. Here we show that the association of Est1 with stem IVc indeed requires both the proximal bulged stem and the P3 domain with the associated Pop proteins. Separating the P3 domain from the Est1 binding site by inserting only 2 base pairs into the helical stem between the two sites causes a complete loss of Est1 from the RNP and hence a telomerase-negative phenotype in vivo. Still, the distal P3 domain with the associated Pop proteins remains intact. Moreover, the P3 domain ensures Est2 stability on the RNP independently of Est1 association. Therefore, the Tlc1 stem IVc recruitment module of the RNA requires a very tight architectural organization for telomerase function in vivo.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Mersaoui2018b,

title = {Nuclear import of Cdc13 limits chromosomal capping},

author = {Sofiane Y Mersaoui and Erin Bonnell and Raymund J Wellinger},

doi = {10.1093/nar/gky085},

issn = {1362-4962},

year  = {2018},

date = {2018-04-06},

volume = {46},

number = {6},

pages = {2975--2989},

publisher = {Oxford University Press (OUP)},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Laterreur2017,

title = {La télomérase de la levure subit une cure de rajeunissement},

author = {Nancy Laterreur and Raymund J. Wellinger},

doi = {10.1051/medsci/20173312011},

issn = {1958-5381},

year  = {2017},

date = {2017-12-00},

journal = {Med Sci (Paris)},

volume = {33},

number = {12},

pages = {1051--1054},

publisher = {EDP Sciences},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Vasianovich2017,

title = {Life and Death of Yeast Telomerase RNA},

author = {Yulia Vasianovich and Raymund J. Wellinger},

doi = {10.1016/j.jmb.2017.01.013},

issn = {0022-2836},

year  = {2017},

date = {2017-10-00},

journal = {Journal of Molecular Biology},

volume = {429},

number = {21},

pages = {3242--3254},

publisher = {Elsevier BV},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Guintini2017,

title = {Repair of UV-induced DNA lesions in natural Saccharomyces cerevisiae telomeres is moderated by Sir2 and Sir3, and inhibited by yKu–Sir4 interaction},

author = {Laetitia Guintini and Maxime Tremblay and Martin Toussaint and Annie D’Amours and Ralf E. Wellinger and Raymund J. Wellinger and Antonio Conconi},

doi = {10.1093/nar/gkx123},

issn = {1362-4962},

year  = {2017},

date = {2017-05-05},

volume = {45},

number = {8},

pages = {4577--4589},

publisher = {Oxford University Press (OUP)},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Larcher2016,

title = {Ku Binding on Telomeres Occurs at Sites Distal from the Physical Chromosome Ends},

author = {Mélanie V. Larcher and Emeline Pasquier and R. Stephen MacDonald and Raymund J. Wellinger},

editor = {Jin-Qiu Zhou},

doi = {10.1371/journal.pgen.1006479},

issn = {1553-7404},

year  = {2016},

date = {2016-12-08},

journal = {PLoS Genet},

volume = {12},

number = {12},

publisher = {Public Library of Science (PLoS)},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Lemieux2016,

title = {Active Yeast Telomerase Shares Subunits with Ribonucleoproteins RNase P and RNase MRP},

author = {Bruno Lemieux and Nancy Laterreur and Anna Perederina and Jean-François Noël and Marie-Line Dubois and Andrey S. Krasilnikov and Raymund J. Wellinger},

doi = {10.1016/j.cell.2016.04.018},

issn = {0092-8674},

year  = {2016},

date = {2016-05-00},

journal = {Cell},

volume = {165},

number = {5},

pages = {1171--1181},

publisher = {Elsevier BV},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Mersaoui2015,

title = {DNA damage checkpoint adaptation genes are required for division of cells harbouring eroded telomeres},

author = {Sofiane Mersaoui and Serge Gravel and Victor Karpov and Raymund Wellinger},

doi = {10.15698/mic2015.10.229},

issn = {2311-2638},

year  = {2015},

date = {2015-10-05},

journal = {MIC},

volume = {2},

number = {10},

pages = {394--405},

publisher = {Shared Science Publishers OG},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Bajon2015,

title = {A Single Templating RNA in Yeast Telomerase},

author = {Emmanuel Bajon and Nancy Laterreur and Raymund J. Wellinger},

doi = {10.1016/j.celrep.2015.06.045},

issn = {2211-1247},

year  = {2015},

date = {2015-07-00},

journal = {Cell Reports},

volume = {12},

number = {3},

pages = {441--448},

publisher = {Elsevier BV},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Lemieux2015,

title = {A Function for the hnRNP A1/A2 Proteins in Transcription Elongation},

author = {Bruno Lemieux and Marco Blanchette and Anne Monette and Andrew J. Mouland and Raymund J. Wellinger and Benoit Chabot},

editor = {Massimo Caputi},

doi = {10.1371/journal.pone.0126654},

issn = {1932-6203},

year  = {2015},

date = {2015-05-26},

journal = {PLoS ONE},

volume = {10},

number = {5},

publisher = {Public Library of Science (PLoS)},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Wellinger2015,

title = {Turning Telomerase into a Jekyll and Hyde Case?},

author = {Raymund J. Wellinger},

doi = {10.1158/2159-8290.cd-14-1346},

issn = {2159-8290},

year  = {2015},

date = {2015-01-01},

volume = {5},

number = {1},

pages = {19--21},

publisher = {American Association for Cancer Research (AACR)},

abstract = {Abstract

               Summary: It may be possible to coerce telomerase to incorporate modified guanine nucleotides into telomeric repeat DNA, thereby seriously compromising the functionality of the telomeres. Thus, a guanine analogue such as 6-thio-dG could turn active telomerase into a chromosome de-protecting enzyme, the opposite of what it is normally, namely a chromosome-protecting enzyme. Cancer Discov; 5(1); 19–21. ©2015 AACR.

               See related article by Mender et al., p. 82},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Wellinger2014,

title = {In the End, What’s the Problem?},

author = {Raymund J. Wellinger},

doi = {10.1016/j.molcel.2014.03.008},

issn = {1097-2765},

year  = {2014},

date = {2014-03-00},

journal = {Molecular Cell},

volume = {53},

number = {6},

pages = {855--856},

publisher = {Elsevier BV},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Laterreur2013,

title = {A new telomerase RNA element that is critical for telomere elongation},

author = {Nancy Laterreur and Sébastien H. Eschbach and Daniel A. Lafontaine and Raymund J. Wellinger},

doi = {10.1093/nar/gkt514},

issn = {1362-4962},

year  = {2013},

date = {2013-09-00},

volume = {41},

number = {16},

pages = {7713--7724},

publisher = {Oxford University Press (OUP)},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Dionne2013,

title = {Cell cycle–dependent transcription factors control the expression of yeast telomerase RNA},

author = {Isabelle Dionne and Stéphanie Larose and Alain T. Dandjinou and Sherif Abou Elela and Raymund J. Wellinger},

doi = {10.1261/rna.037663.112},

issn = {1469-9001},

year  = {2013},

date = {2013-07-00},

journal = {RNA},

volume = {19},

number = {7},

pages = {992--1002},

publisher = {Cold Spring Harbor Laboratory},

abstract = {Telomerase is a specialized ribonucleoprotein that adds repeated DNA sequences to the ends of eukaryotic chromosomes to preserve genome integrity. Some secondary structure features of the telomerase RNA are very well conserved, and it serves as a central scaffold for the binding of associated proteins. The Saccharomyces cerevisiae telomerase RNA, TLC1, is found in very low copy number in the cell and is the limiting component of the known telomerase holoenzyme constituents. The reasons for this low abundance are unclear, but given that the RNA is very stable, transcriptional control mechanisms must be extremely important. Here we define the sequences forming the TLC1 promoter and identify the elements required for its low expression level, including enhancer and repressor elements. Within an enhancer element, we found consensus sites for Mbp1/Swi4 association, and chromatin immunoprecipitation (ChIP) assays confirmed the binding of Mbp1 and Swi4 to these sites of the TLC1 promoter. Furthermore, the enhancer element conferred cell cycle–dependent regulation to a reporter gene, and mutations in the Mbp1/Swi4 binding sites affected the levels of telomerase RNA and telomere length. Finally, ChIP experiments using a TLC1 RNA-binding protein as target showed cell cycle–dependent transcription of the TLC1 gene. These results indicate that the budding yeast TLC1 RNA is transcribed in a cell cycle–dependent fashion late in G1 and may be part of the S phase–regulated group of genes involved in DNA replication.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Balestrini2013,

title = {The Ku Heterodimer and the Metabolism of Single-Ended DNA Double-Strand Breaks},

author = {Alessia Balestrini and Dejan Ristic and Isabelle Dionne and Xiao Z. Liu and Claire Wyman and Raymund J. Wellinger and John H.J. Petrini},

doi = {10.1016/j.celrep.2013.05.026},

issn = {2211-1247},

year  = {2013},

date = {2013-06-00},

journal = {Cell Reports},

volume = {3},

number = {6},

pages = {2033--2045},

publisher = {Elsevier BV},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Londoño-Vallejo2012,

title = {Telomeres and telomerase dance to the rhythm of the cell cycle},

author = {J. Arturo Londoño-Vallejo and Raymund J. Wellinger},

doi = {10.1016/j.tibs.2012.05.004},

issn = {0968-0004},

year  = {2012},

date = {2012-09-00},

journal = {Trends in Biochemical Sciences},

volume = {37},

number = {9},

pages = {391--399},

publisher = {Elsevier BV},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Gallardo2012,

title = {Telomerase caught in the act},

author = {Franck Gallardo and Nancy Laterreur and Raymund J. Wellinger and Pascal Chartrand},

doi = {10.4161/rna.21498},

issn = {1555-8584},

year  = {2012},

date = {2012-09-00},

journal = {RNA Biology},

volume = {9},

number = {9},

pages = {1139--1143},

publisher = {Informa UK Limited},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Wellinger2012,

title = {Everything You Ever Wanted to Know About \textit{Saccharomyces cerevisiae} Telomeres: Beginning to End},

author = {Raymund J Wellinger and Virginia A Zakian},

doi = {10.1534/genetics.111.137851},

issn = {1943-2631},

year  = {2012},

date = {2012-08-01},

volume = {191},

number = {4},

pages = {1073--1105},

publisher = {Oxford University Press (OUP)},

abstract = {Abstract

               The mechanisms that maintain the stability of chromosome ends have broad impact on genome integrity in all eukaryotes. Budding yeast is a premier organism for telomere studies. Many fundamental concepts of telomere and telomerase function were first established in yeast and then extended to other organisms. We present a comprehensive review of yeast telomere biology that covers capping, replication, recombination, and transcription. We think of it as yeast telomeres—soup to nuts.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Noël2012,

title = {Exposing Secrets of Telomere-Telomerase Encounters},

author = {Jean-François Noël and Raymund J. Wellinger},

doi = {10.1016/j.cell.2012.07.015},

issn = {0092-8674},

year  = {2012},

date = {2012-08-00},

journal = {Cell},

volume = {150},

number = {3},

pages = {453--454},

publisher = {Elsevier BV},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Noël2012b,

title = {Budding yeast telomerase RNA transcription termination is dictated by the Nrd1/Nab3 non-coding RNA termination pathway},

author = {Jean-François Noël and Stéphanie Larose and Sherif Abou Elela and Raymund J. Wellinger},

doi = {10.1093/nar/gks200},

issn = {1362-4962},

year  = {2012},

date = {2012-07-00},

volume = {40},

number = {12},

pages = {5625--5636},

publisher = {Oxford University Press (OUP)},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Gallardo2011,

title = {Live Cell Imaging of Telomerase RNA Dynamics Reveals Cell Cycle-Dependent Clustering of Telomerase at Elongating Telomeres},

author = {Franck Gallardo and Nancy Laterreur and Emilio Cusanelli and Faissal Ouenzar and Emmanuelle Querido and Raymund J. Wellinger and Pascal Chartrand},

doi = {10.1016/j.molcel.2011.09.020},

issn = {1097-2765},

year  = {2011},

date = {2011-12-00},

journal = {Molecular Cell},

volume = {44},

number = {5},

pages = {819--827},

publisher = {Elsevier BV},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Parenteau2011,

title = {Introns within Ribosomal Protein Genes Regulate the Production and Function of Yeast Ribosomes},

author = {Julie Parenteau and Mathieu Durand and Geneviève Morin and Jules Gagnon and Jean-François Lucier and Raymund J. Wellinger and Benoit Chabot and Sherif Abou Elela},

doi = {10.1016/j.cell.2011.08.044},

issn = {0092-8674},

year  = {2011},

date = {2011-10-00},

journal = {Cell},

volume = {147},

number = {2},

pages = {320--331},

publisher = {Elsevier BV},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Bah2011,

title = {Telomerase Is Required to Protect Chromosomes with Vertebrate-type T2AG3 3′ Ends in Saccharomyces cerevisiae},

author = {Amadou Bah and Eric Gilson and Raymund J. Wellinger},

doi = {10.1074/jbc.m111.220186},

issn = {0021-9258},

year  = {2011},

date = {2011-08-00},

journal = {Journal of Biological Chemistry},

volume = {286},

number = {31},

pages = {27132--27138},

publisher = {Elsevier BV},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Prinos2011,

title = {Alternative splicing of SYK regulates mitosis and cell survival},

author = {Panagiotis Prinos and Daniel Garneau and Jean-François Lucier and Daniel Gendron and Sonia Couture and Marianne Boivin and Jean-Philippe Brosseau and Elvy Lapointe and Philippe Thibault and Mathieu Durand and Karine Tremblay and Julien Gervais-Bird and Hanad Nwilati and Roscoe Klinck and Benoit Chabot and Jean-Pierre Perreault and Raymund J Wellinger and Sherif Abou Elela},

doi = {10.1038/nsmb.2040},

issn = {1545-9985},

year  = {2011},

date = {2011-06-00},

journal = {Nat Struct Mol Biol},

volume = {18},

number = {6},

pages = {673--679},

publisher = {Springer Science and Business Media LLC},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Noël2011,

title = {Abrupt telomere losses and reduced end-resection can explain accelerated senescence of Smc5/6 mutants lacking telomerase},

author = {Jean-François Noël and Raymund J. Wellinger},

doi = {10.1016/j.dnarep.2010.11.010},

issn = {1568-7864},

year  = {2011},

date = {2011-03-07},

journal = {DNA Repair},

volume = {10},

number = {3},

pages = {271--282},

publisher = {Elsevier BV},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Leduc2011,

title = {Genome-Wide Mapping of DNA Strand Breaks},

author = {Frédéric Leduc and David Faucher and Geneviève Bikond Nkoma and Marie-Chantal Grégoire and Mélina Arguin and Raymund J. Wellinger and Guylain Boissonneault},

editor = {Martin Marinus},

doi = {10.1371/journal.pone.0017353},

issn = {1932-6203},

year  = {2011},

date = {2011-02-25},

journal = {PLoS ONE},

volume = {6},

number = {2},

publisher = {Public Library of Science (PLoS)},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Wellinger2010,

title = {When the caps fall off: Responses to telomere uncapping in yeast},

author = {Raymund J. Wellinger},

doi = {10.1016/j.febslet.2010.06.031},

issn = {1873-3468},

year  = {2010},

date = {2010-09-10},

journal = {FEBS Letters},

volume = {584},

number = {17},

pages = {3734--3740},

publisher = {Wiley},

abstract = {Telomeres protect the ends of linear chromosomes from activities that cause sequence losses or challenge chromosome integrity. Furthermore, these ends must be hidden from detection by the DNA damage recognition and response pathways. In particular, they must not fuse with each other. These fundamental and very first functions attributed to telomeres are also summarized with the term ‘chromosome capping’. However, telomeres can become uncapped and the foremost cellular responses to such events aim to restore genome stability in the most conservative fashion possible. I will provide an outline of cellular responses to uncapping in budding yeast and briefly discuss the reverse, namely avoidance mechanisms that prevent telomere formation at inappropriate places.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Vodenicharov2010,

title = {Telomere capping in non-dividing yeast cells requires Yku and Rap1},

author = {Momchil D Vodenicharov and Nancy Laterreur and Raymund J Wellinger},

doi = {10.1038/emboj.2010.155},

issn = {1460-2075},

year  = {2010},

date = {2010-09-01},

journal = {EMBO J},

volume = {29},

number = {17},

pages = {3007--3019},

publisher = {Springer Science and Business Media LLC},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Faucher2010,

title = {Methylated H3K4, a Transcription-Associated Histone Modification, Is Involved in the DNA Damage Response Pathway},

author = {David Faucher and Raymund J. Wellinger},

editor = {Gregory P. Copenhaver},

doi = {10.1371/journal.pgen.1001082},

issn = {1553-7404},

year  = {2010},

date = {2010-08-26},

journal = {PLoS Genet},

volume = {6},

number = {8},

publisher = {Public Library of Science (PLoS)},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Toussaint2010,

title = {Differential participation of homologous recombination and nucleotide excision repair in yeast survival to ultraviolet light radiation},

author = {Martin Toussaint and Raymund J. Wellinger and Antonio Conconi},

doi = {10.1016/j.mrgentox.2010.03.013},

issn = {1383-5718},

year  = {2010},

date = {2010-04-00},

journal = {Mutation Research/Genetic Toxicology and Environmental Mutagenesis},

volume = {698},

number = {1-2},

pages = {52--59},

publisher = {Elsevier BV},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Wellinger2009,

title = {The CST Complex and Telomere Maintenance: The Exception Becomes the Rule},

author = {Raymund J. Wellinger},

doi = {10.1016/j.molcel.2009.10.001},

issn = {1097-2765},

year  = {2009},

date = {2009-10-00},

journal = {Molecular Cell},

volume = {36},

number = {2},

pages = {168--169},

publisher = {Elsevier BV},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Gunisova2009,

title = {Identification and comparative analysis of telomerase RNAs from \textit{Candida} species reveal conservation of functional elements},

author = {Stanislava Gunisova and Elhanan Elboher and Jozef Nosek and Valentin Gorkovoy and Yogev Brown and Jean-Francois Lucier and Nancy Laterreur and Raymund J. Wellinger and Yehuda Tzfati and Lubomir Tomaska},

doi = {10.1261/rna.1194009},

issn = {1469-9001},

year  = {2009},

date = {2009-04-00},

journal = {RNA},

volume = {15},

number = {4},

pages = {546--559},

publisher = {Cold Spring Harbor Laboratory},

abstract = {The RNA component of telomerase (telomerase RNA; TER) varies substantially both in sequence composition and size (from ∼150 nucleotides [nt] to >1500 nt) across species. This dramatic divergence has hampered the identification of TER genes and a large-scale comparative analysis of TER sequences and structures among distantly related species. To identify by phylogenetic analysis conserved sequences and structural features of TER that are of general importance, it is essential to obtain TER sequences from evolutionarily distant groups of species, providing enough conservation within each group and enough variation among the groups. To this end, we identified TER genes in several yeast species with relatively large (>20 base pairs) and nonvariant telomeric repeats, mostly from the genus Candida. Interestingly, several of the TERs reported here are longer than all other yeast TERs known to date. Within these TERs, we predicted a pseudoknot containing U-A·U base triples (conserved in vertebrates, budding yeasts, and ciliates) and a three-way junction element (conserved in vertebrates and budding yeasts). In addition, we identified a novel conserved sequence (CS2a) predicted to reside within an internal-loop structure, in all the budding yeast TERs examined. CS2a is located near the Est1p-binding bulge-stem previously identified in Saccharomyces cerevisiae. Mutational analyses in both budding yeasts S. cerevisiae and Kluyveromyces lactis demonstrate that CS2a is essential for in vivo telomerase function. The comparative and mutational analyses of conserved TER elements reported here provide novel insights into the structure and function of the telomerase ribonucleoprotein complex.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Knecht2008,

title = {The 3D nuclear organization of telomeres marks the transition from Hodgkin to Reed–Sternberg cells},

author = {H Knecht and B Sawan and D Lichtensztejn and B Lemieux and R J Wellinger and S Mai},

doi = {10.1038/leu.2008.314},

issn = {1476-5551},

year  = {2009},

date = {2009-03-00},

journal = {Leukemia},

volume = {23},

number = {3},

pages = {565--573},

publisher = {Springer Science and Business Media LLC},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Venables2008,

title = {Identification of Alternative Splicing Markers for Breast Cancer},

author = {Julian P. Venables and Roscoe Klinck and Anne Bramard and Lyna Inkel and Geneviève Dufresne-Martin and ChuShin Koh and Julien Gervais-Bird and Elvy Lapointe and Ulrike Froehlich and Mathieu Durand and Daniel Gendron and Jean-Philippe Brosseau and Philippe Thibault and Jean-Francois Lucier and Karine Tremblay and Panagiotis Prinos and Raymund J. Wellinger and Benoit Chabot and Claudine Rancourt and Sherif Abou Elela},

doi = {10.1158/0008-5472.can-08-1769},

issn = {1538-7445},

year  = {2008},

date = {2008-11-15},

volume = {68},

number = {22},

pages = {9525--9531},

publisher = {American Association for Cancer Research (AACR)},

abstract = {Abstract

               Breast cancer is the most common cause of cancer death among women under age 50 years, so it is imperative to identify molecular markers to improve diagnosis and prognosis of this disease. Here, we present a new approach for the identification of breast cancer markers that does not measure gene expression but instead uses the ratio of alternatively spliced mRNAs as its indicator. Using a high-throughput reverse transcription-PCR–based system for splicing annotation, we monitored the alternative splicing profiles of 600 cancer-associated genes in a panel of 21 normal and 26 cancerous breast tissues. We validated 41 alternative splicing events that significantly differed in breast tumors relative to normal breast tissues. Most cancer-specific changes in splicing that disrupt known protein domains support an increase in cell proliferation or survival consistent with a functional role for alternative splicing in cancer. In a blind screen, a classifier based on the 12 best cancer-associated splicing events correctly identified cancer tissues with 96% accuracy. Moreover, a subset of these alternative splicing events could order tissues according to histopathologic grade, and 5 markers were validated in a further blind set of 19 grade 1 and 19 grade 3 tumor samples. These results provide a simple alternative for the classification of normal and cancerous breast tumor tissues and underscore the putative role of alternative splicing in the biology of cancer. [Cancer Res 2008;68(22):9525–31]},

keywords = {},

pubstate = {published},

tppubtype = {article}

}