scholarly journals DNMT and HDAC inhibitors induce cryptic transcription start sites encoded in long terminal repeats

2017 ◽  
Vol 49 (7) ◽  
pp. 1052-1060 ◽  
Author(s):  
David Brocks ◽  
Christopher R Schmidt ◽  
Michael Daskalakis ◽  
Hyo Sik Jang ◽  
Nakul M Shah ◽  
...  
Keyword(s):  
Hdac Inhibitors ◽  
Long Terminal Repeats ◽  
Transcription Start ◽  
Transcription Start Sites ◽  
Cryptic Transcription ◽  
Terminal Repeats

scholarly journals Erratum: DNMT and HDAC inhibitors induce cryptic transcription start sites encoded in long terminal repeats

2017 ◽  
Vol 49 (11) ◽  
pp. 1661-1661 ◽  
Author(s):  
David Brocks ◽  
Christopher R Schmidt ◽  
Michael Daskalakis ◽  
Hyo Sik Jang ◽  
Nakul M Shah ◽  
...  
Keyword(s):  
Hdac Inhibitors ◽  
Long Terminal Repeats ◽  
Transcription Start ◽  
Transcription Start Sites ◽  
Cryptic Transcription ◽  
Terminal Repeats

scholarly journals Chromatin-sensitive cryptic promoters encode alternative protein isoforms in yeast

2018 ◽  
Author(s):  
Wu Wei ◽  
Bianca P. Hennig ◽  
Jingwen Wang ◽  
Yujie Zhang ◽  
Ilaria Piazza ◽  
...  
Keyword(s):  
Rna Degradation ◽  
Chromatin Accessibility ◽  
Protein Isoforms ◽  
Transcription Start ◽  
Mrna Isoforms ◽  
Rna Molecules ◽  
Transcription Start Sites ◽  
Cryptic Transcription ◽  
Functional Consequences ◽  
Cryptic Promoters

AbstractCryptic transcription is widespread and generates a heterogeneous group of RNA molecules of unknown function. To improve our understanding of cryptic transcription, we investigated their transcription start site usage, chromatin organization and post-transcriptional consequences in Saccharomyces cerevisiae. We show that transcription start sites (TSSs) of chromatin-sensitive internal cryptic transcripts retain comparable features of canonical TSSs in terms of DNA sequence, directionality and chromatin accessibility. We degine the 5’ and 3’ boundaries of cryptic transcripts and show that, contrary to RNA degradation-sensitive ones, they often overlap with the end of the gene thereby using the canonical polyadenylation site and associate to polyribosomes. We show that chromatin-sensitive cryptic transcripts can be recognized by ribosomes and may produce truncated polypeptides from downstream, in-frame start codons. Finally, we congirm the presence of the predicted polypeptides by reanalyzing N-terminal proteomic datasets. Our work suggests that a fraction of chromatin-sensitive internal cryptic promoters are in fact alternative truncated mRNA isoforms. The expression of these chromatin-sensitive isoforms is conserved from yeast to human expanding the functional consequences of cryptic transcription and proteome complexity.

scholarly journals Functional Activity of HERV-K-T47D-Related Long Terminal Repeats

Virology ◽  
2001 ◽  
Vol 283 (2) ◽  
pp. 262-272 ◽  
Author(s):  
Corinna Baust ◽  
Wolfgang Seifarth ◽  
Ulrike Schön ◽  
Rüdiger Hehlmann ◽  
Christine Leib-Mösch
Keyword(s):  
Functional Activity ◽  
Long Terminal Repeats ◽  
Terminal Repeats

scholarly journals Transactivation of Naturally Occurring HIV-1 Long Terminal Repeats by the JNK Signaling Pathway

2000 ◽  
Vol 275 (27) ◽  
pp. 20382-20390 ◽  
Author(s):  
Peifeng Chen ◽  
Egbert Flory ◽  
Andris Avots ◽  
Bruce W. M. Jordan ◽  
Frank Kirchhoff ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Long Terminal Repeats ◽  
Jnk Signaling ◽  
Naturally Occurring ◽  
Jnk Signaling Pathway ◽  
Terminal Repeats ◽  
Hiv 1

scholarly journals Genome-Wide Identification of Transcription Start Sites, Promoters and Transcription Factor Binding Sites in E. coli

PLoS ONE ◽  
2009 ◽  
Vol 4 (10) ◽  
pp. e7526 ◽  
Author(s):  
Alfredo Mendoza-Vargas ◽  
Leticia Olvera ◽  
Maricela Olvera ◽  
Ricardo Grande ◽  
Leticia Vega-Alvarado ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Binding Sites ◽  
Transcription Factor Binding Sites ◽  
Transcription Factor Binding ◽  
Transcription Start ◽  
Transcription Start Sites ◽  
E Coli ◽  
Factor Binding ◽  
Genome Wide

Transcription shapes 3D chromatin organization by interacting with loop-extruding cohesin complexes

2022 ◽  
Author(s):  
Edward J Banigan ◽  
Wen Tang ◽  
Aafke A van den Berg ◽  
Roman R Stocsits ◽  
Gordana Wutz ◽  
...  
Keyword(s):  
Functional Organization ◽  
Regulatory Elements ◽  
General Shape ◽  
Transcription Start ◽  
Double Knockout ◽  
Transcription Start Sites ◽  
Contact Patterns ◽  
New Type ◽  
Active Transcription ◽  
Distal Regulatory Elements

Cohesin organizes mammalian interphase chromosomes by reeling chromatin fibers into dynamic loops (Banigan and Mirny, 2020; Davidson et al., 2019; Kim et al., 2019; Yatskevich et al., 2019). "Loop extrusion" is obstructed when cohesin encounters a properly oriented CTCF protein (Busslinger et al., 2017; de Wit et al., 2015; Fudenberg et al., 2016; Nora et al., 2017; Sanborn et al., 2015; Wutz et al., 2017), and recent work indicates that other factors, such as the replicative helicase MCM (Dequeker et al., 2020), can also act as barriers to loop extrusion. It has been proposed that transcription relocalizes (Busslinger et al., 2017; Glynn et al., 2004; Lengronne et al., 2004) or interferes with cohesin (Heinz et al., 2018; Jeppsson et al., 2020; Valton et al., 2021; S. Zhang et al., 2021), and that active transcription start sites function as cohesin loading sites (Busslinger et al., 2017; Kagey et al., 2010; Zhu et al., 2021; Zuin et al., 2014), but how these effects, and transcription in general, shape chromatin is unknown. To determine whether transcription can modulate loop extrusion, we studied cells in which the primary extrusion barriers could be removed by CTCF depletion and cohesin's residence time and abundance on chromatin could be increased by Wapl knockout. We found evidence that transcription directly interacts with loop extrusion through a novel "moving barrier" mechanism, but not by loading cohesin at active promoters. Hi-C experiments showed intricate, cohesin-dependent genomic contact patterns near actively transcribed genes, and in CTCF-Wapl double knockout (DKO) cells (Busslinger et al., 2017), genomic contacts were enriched between sites of transcription-driven cohesin localization ("cohesin islands"). Similar patterns also emerged in polymer simulations in which transcribing RNA polymerases (RNAPs) acted as "moving barriers" by impeding, slowing, or pushing loop-extruding cohesins. The model predicts that cohesin does not load preferentially at promoters and instead accumulates at TSSs due to the barrier function of RNAPs. We tested this prediction by new ChIP-seq experiments, which revealed that the "cohesin loader" Nipbl (Ciosk et al., 2000) co-localizes with cohesin, but, unlike in previous reports (Busslinger et al., 2017; Kagey et al., 2010; Zhu et al., 2021; Zuin et al., 2014), Nipbl did not accumulate at active promoters. We propose that RNAP acts as a new type of barrier to loop extrusion that, unlike CTCF, is not stationary in its precise genomic position, but is itself dynamically translocating and relocalizes cohesin along DNA. In this way, loop extrusion could enable translocating RNAPs to maintain contacts with distal regulatory elements, allowing transcriptional activity to shape genomic functional organization.

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