Regulating retrotransposon activity through the use of alternative transcription start sites

Research output: Contribution to journal › Journal article › Research › peer-review

Standard

Regulating retrotransposon activity through the use of alternative transcription start sites. / Persson, Jenna; Steglich, Babett; Smialowska, Agata; Boyd, Mette; Lange, Jette Bornholdt; Andersson, Robin; Schurra, Catherine; Arcangioli, Benoit; Sandelin, Albin Gustav; Nielsen, Olaf; Ekwall, Karl.

In: E M B O Reports, Vol. 17, No. 5, 2016, p. 753-768.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Persson, J, Steglich, B, Smialowska, A, Boyd, M, Lange, JB, Andersson, R, Schurra, C, Arcangioli, B, Sandelin, AG, Nielsen, O & Ekwall, K 2016, 'Regulating retrotransposon activity through the use of alternative transcription start sites', E M B O Reports, vol. 17, no. 5, pp. 753-768. https://doi.org/10.15252/embr.201541866

APA

Persson, J., Steglich, B., Smialowska, A., Boyd, M., Lange, J. B., Andersson, R., Schurra, C., Arcangioli, B., Sandelin, A. G., Nielsen, O., & Ekwall, K. (2016). Regulating retrotransposon activity through the use of alternative transcription start sites. E M B O Reports, 17(5), 753-768. https://doi.org/10.15252/embr.201541866

Vancouver

Persson J, Steglich B, Smialowska A, Boyd M, Lange JB, Andersson R et al. Regulating retrotransposon activity through the use of alternative transcription start sites. E M B O Reports. 2016;17(5):753-768. https://doi.org/10.15252/embr.201541866

Author

Persson, Jenna ; Steglich, Babett ; Smialowska, Agata ; Boyd, Mette ; Lange, Jette Bornholdt ; Andersson, Robin ; Schurra, Catherine ; Arcangioli, Benoit ; Sandelin, Albin Gustav ; Nielsen, Olaf ; Ekwall, Karl. / Regulating retrotransposon activity through the use of alternative transcription start sites. In: E M B O Reports. 2016 ; Vol. 17, No. 5. pp. 753-768.

Bibtex

@article{cb5f64f8f1ce439dbf124e1072bd78f2,
title = "Regulating retrotransposon activity through the use of alternative transcription start sites",
abstract = "Retrotransposons, the ancestors of retroviruses, have the potential for gene disruption and genomic takeover if not kept in check. Paradoxically, although host cells repress these elements by multiple mechanisms, they are transcribed and are even activated under stress conditions. Here, we describe a new mechanism of retrotransposon regulation through transcription start site (TSS) selection by altered nucleosome occupancy. We show that Fun30 chromatin remodelers cooperate to maintain a high level of nucleosome occupancy at retrotransposon-flanking long terminal repeat (LTR) elements. This enforces the use of a downstream TSS and the production of a truncated RNA incapable of reverse transcription and retrotransposition. However, in stressed cells, nucleosome occupancy at LTR elements is reduced, and the TSS shifts to allow for productive transcription. We propose that controlled retrotransposon transcription from a nonproductive TSS allows for rapid stress-induced activation, while preventing uncontrolled transposon activity in the genome.",
author = "Jenna Persson and Babett Steglich and Agata Smialowska and Mette Boyd and Lange, {Jette Bornholdt} and Robin Andersson and Catherine Schurra and Benoit Arcangioli and Sandelin, {Albin Gustav} and Olaf Nielsen and Karl Ekwall",
note = "{\textcopyright} 2016 The Authors. Published under the terms of the CC BY NC ND 4.0 license.",
year = "2016",
doi = "10.15252/embr.201541866",
language = "English",
volume = "17",
pages = "753--768",
journal = "E M B O Reports",
issn = "1469-221X",
publisher = "Wiley-Blackwell",
number = "5",

}

RIS

TY - JOUR

T1 - Regulating retrotransposon activity through the use of alternative transcription start sites

AU - Persson, Jenna

AU - Steglich, Babett

AU - Smialowska, Agata

AU - Boyd, Mette

AU - Lange, Jette Bornholdt

AU - Andersson, Robin

AU - Schurra, Catherine

AU - Arcangioli, Benoit

AU - Sandelin, Albin Gustav

AU - Nielsen, Olaf

AU - Ekwall, Karl

N1 - © 2016 The Authors. Published under the terms of the CC BY NC ND 4.0 license.

PY - 2016

Y1 - 2016

N2 - Retrotransposons, the ancestors of retroviruses, have the potential for gene disruption and genomic takeover if not kept in check. Paradoxically, although host cells repress these elements by multiple mechanisms, they are transcribed and are even activated under stress conditions. Here, we describe a new mechanism of retrotransposon regulation through transcription start site (TSS) selection by altered nucleosome occupancy. We show that Fun30 chromatin remodelers cooperate to maintain a high level of nucleosome occupancy at retrotransposon-flanking long terminal repeat (LTR) elements. This enforces the use of a downstream TSS and the production of a truncated RNA incapable of reverse transcription and retrotransposition. However, in stressed cells, nucleosome occupancy at LTR elements is reduced, and the TSS shifts to allow for productive transcription. We propose that controlled retrotransposon transcription from a nonproductive TSS allows for rapid stress-induced activation, while preventing uncontrolled transposon activity in the genome.

AB - Retrotransposons, the ancestors of retroviruses, have the potential for gene disruption and genomic takeover if not kept in check. Paradoxically, although host cells repress these elements by multiple mechanisms, they are transcribed and are even activated under stress conditions. Here, we describe a new mechanism of retrotransposon regulation through transcription start site (TSS) selection by altered nucleosome occupancy. We show that Fun30 chromatin remodelers cooperate to maintain a high level of nucleosome occupancy at retrotransposon-flanking long terminal repeat (LTR) elements. This enforces the use of a downstream TSS and the production of a truncated RNA incapable of reverse transcription and retrotransposition. However, in stressed cells, nucleosome occupancy at LTR elements is reduced, and the TSS shifts to allow for productive transcription. We propose that controlled retrotransposon transcription from a nonproductive TSS allows for rapid stress-induced activation, while preventing uncontrolled transposon activity in the genome.

U2 - 10.15252/embr.201541866

DO - 10.15252/embr.201541866

M3 - Journal article

C2 - 26902262

VL - 17

SP - 753

EP - 768

JO - E M B O Reports

JF - E M B O Reports

SN - 1469-221X

IS - 5

ER -

ID: 159429244