Rad52 SUMOylation functions as a molecular switch that determines a balance between the Rad5- and Rad59-dependent survivors

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Rad52 SUMOylation functions as a molecular switch that determines a balance between the Rad5- and Rad59-dependent survivors. / Charifi, Ferose; Churikov, Dmitri; Eckert-Boulet, Nadine; Minguet, Christopher; Jourquin, Frédéric; Hardy, Julien; Lisby, Michael; Simon, Marie Noëlle; Géli, Vincent.

In: iScience, Vol. 24, No. 3, 102231, 2021.

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

Harvard

Charifi, F, Churikov, D, Eckert-Boulet, N, Minguet, C, Jourquin, F, Hardy, J, Lisby, M, Simon, MN & Géli, V 2021, 'Rad52 SUMOylation functions as a molecular switch that determines a balance between the Rad5- and Rad59-dependent survivors', iScience, vol. 24, no. 3, 102231. https://doi.org/10.1016/j.isci.2021.102231

APA

Charifi, F., Churikov, D., Eckert-Boulet, N., Minguet, C., Jourquin, F., Hardy, J., Lisby, M., Simon, M. N., & Géli, V. (2021). Rad52 SUMOylation functions as a molecular switch that determines a balance between the Rad5- and Rad59-dependent survivors. iScience, 24(3), [102231]. https://doi.org/10.1016/j.isci.2021.102231

Vancouver

Charifi F, Churikov D, Eckert-Boulet N, Minguet C, Jourquin F, Hardy J et al. Rad52 SUMOylation functions as a molecular switch that determines a balance between the Rad5- and Rad59-dependent survivors. iScience. 2021;24(3). 102231. https://doi.org/10.1016/j.isci.2021.102231

Author

Charifi, Ferose ; Churikov, Dmitri ; Eckert-Boulet, Nadine ; Minguet, Christopher ; Jourquin, Frédéric ; Hardy, Julien ; Lisby, Michael ; Simon, Marie Noëlle ; Géli, Vincent. / Rad52 SUMOylation functions as a molecular switch that determines a balance between the Rad5- and Rad59-dependent survivors. In: iScience. 2021 ; Vol. 24, No. 3.

Bibtex

@article{a837513d4c38454580c19c50615aac2c,
title = "Rad52 SUMOylation functions as a molecular switch that determines a balance between the Rad5- and Rad59-dependent survivors",
abstract = "Functional telomeres in yeast lacking telomerase can be restored by rare Rad51- or Rad59-dependent recombination events that lead to type I and type II survivors, respectively. We previously proposed that polySUMOylation of proteins and the SUMO-targeted ubiquitin ligase Slx5-Slx8 are key factors in type II recombination. Here, we show that SUMOylation of Rad52 favors the formation of type I survivors. Conversely, preventing Rad52 SUMOylation partially bypasses the requirement of Slx5-Slx8 for type II recombination. We further report that SUMO-dependent proteasomal degradation favors type II recombination. Finally, inactivation of Rad59, but not Rad51, impairs the relocation of eroded telomeres to the Nuclear Pore complexes (NPCs). We propose that Rad59 cooperates with non-SUMOylated Rad52 to promote type II recombination at NPCs, resulting in the emergence of more robust survivors akin to ALT cancer cells. Finally, neither Rad59 nor Rad51 is required by itself for the survival of established type II survivors. Biological Sciences; Molecular Biology; Cell Biology",
keywords = "Biological Sciences, Cell Biology, Molecular Biology",
author = "Ferose Charifi and Dmitri Churikov and Nadine Eckert-Boulet and Christopher Minguet and Fr{\'e}d{\'e}ric Jourquin and Julien Hardy and Michael Lisby and Simon, {Marie No{\"e}lle} and Vincent G{\'e}li",
year = "2021",
doi = "10.1016/j.isci.2021.102231",
language = "English",
volume = "24",
journal = "iScience",
issn = "2589-0042",
publisher = "Elsevier",
number = "3",

}

RIS

TY - JOUR

T1 - Rad52 SUMOylation functions as a molecular switch that determines a balance between the Rad5- and Rad59-dependent survivors

AU - Charifi, Ferose

AU - Churikov, Dmitri

AU - Eckert-Boulet, Nadine

AU - Minguet, Christopher

AU - Jourquin, Frédéric

AU - Hardy, Julien

AU - Lisby, Michael

AU - Simon, Marie Noëlle

AU - Géli, Vincent

PY - 2021

Y1 - 2021

N2 - Functional telomeres in yeast lacking telomerase can be restored by rare Rad51- or Rad59-dependent recombination events that lead to type I and type II survivors, respectively. We previously proposed that polySUMOylation of proteins and the SUMO-targeted ubiquitin ligase Slx5-Slx8 are key factors in type II recombination. Here, we show that SUMOylation of Rad52 favors the formation of type I survivors. Conversely, preventing Rad52 SUMOylation partially bypasses the requirement of Slx5-Slx8 for type II recombination. We further report that SUMO-dependent proteasomal degradation favors type II recombination. Finally, inactivation of Rad59, but not Rad51, impairs the relocation of eroded telomeres to the Nuclear Pore complexes (NPCs). We propose that Rad59 cooperates with non-SUMOylated Rad52 to promote type II recombination at NPCs, resulting in the emergence of more robust survivors akin to ALT cancer cells. Finally, neither Rad59 nor Rad51 is required by itself for the survival of established type II survivors. Biological Sciences; Molecular Biology; Cell Biology

AB - Functional telomeres in yeast lacking telomerase can be restored by rare Rad51- or Rad59-dependent recombination events that lead to type I and type II survivors, respectively. We previously proposed that polySUMOylation of proteins and the SUMO-targeted ubiquitin ligase Slx5-Slx8 are key factors in type II recombination. Here, we show that SUMOylation of Rad52 favors the formation of type I survivors. Conversely, preventing Rad52 SUMOylation partially bypasses the requirement of Slx5-Slx8 for type II recombination. We further report that SUMO-dependent proteasomal degradation favors type II recombination. Finally, inactivation of Rad59, but not Rad51, impairs the relocation of eroded telomeres to the Nuclear Pore complexes (NPCs). We propose that Rad59 cooperates with non-SUMOylated Rad52 to promote type II recombination at NPCs, resulting in the emergence of more robust survivors akin to ALT cancer cells. Finally, neither Rad59 nor Rad51 is required by itself for the survival of established type II survivors. Biological Sciences; Molecular Biology; Cell Biology

KW - Biological Sciences

KW - Cell Biology

KW - Molecular Biology

U2 - 10.1016/j.isci.2021.102231

DO - 10.1016/j.isci.2021.102231

M3 - Journal article

C2 - 33748714

AN - SCOPUS:85102301957

VL - 24

JO - iScience

JF - iScience

SN - 2589-0042

IS - 3

M1 - 102231

ER -

ID: 259990712