Autophagy-mediated control of ribosome homeostasis in oncogene-induced senescence

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Standard

Autophagy-mediated control of ribosome homeostasis in oncogene-induced senescence. / López, Aida Rodríguez; Jørgensen, Maria H.; Havelund, Jesper F.; Arendrup, Frederic S.; Kolapalli, Srinivasa Prasad; Nielsen, Thorbjørn M.; Pais, Eva; Beese, Carsten Jörn; Abdul-Al, Ahmad; Vind, Anna Constance; Bartek, Jiri; Bekker-Jensen, Simon; Montes, Marta; Galanos, Panagiotis; Faergeman, Nils; Happonen, Lotta; Frankel, Lisa B.

I: Cell Reports, Bind 42, Nr. 11, 113381, 2023.

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt

Harvard

López, AR, Jørgensen, MH, Havelund, JF, Arendrup, FS, Kolapalli, SP, Nielsen, TM, Pais, E, Beese, CJ, Abdul-Al, A, Vind, AC, Bartek, J, Bekker-Jensen, S, Montes, M, Galanos, P, Faergeman, N, Happonen, L & Frankel, LB 2023, 'Autophagy-mediated control of ribosome homeostasis in oncogene-induced senescence', Cell Reports, bind 42, nr. 11, 113381. https://doi.org/10.1016/j.celrep.2023.113381

APA

López, A. R., Jørgensen, M. H., Havelund, J. F., Arendrup, F. S., Kolapalli, S. P., Nielsen, T. M., Pais, E., Beese, C. J., Abdul-Al, A., Vind, A. C., Bartek, J., Bekker-Jensen, S., Montes, M., Galanos, P., Faergeman, N., Happonen, L., & Frankel, L. B. (2023). Autophagy-mediated control of ribosome homeostasis in oncogene-induced senescence. Cell Reports, 42(11), [113381]. https://doi.org/10.1016/j.celrep.2023.113381

Vancouver

López AR, Jørgensen MH, Havelund JF, Arendrup FS, Kolapalli SP, Nielsen TM o.a. Autophagy-mediated control of ribosome homeostasis in oncogene-induced senescence. Cell Reports. 2023;42(11). 113381. https://doi.org/10.1016/j.celrep.2023.113381

Author

López, Aida Rodríguez ; Jørgensen, Maria H. ; Havelund, Jesper F. ; Arendrup, Frederic S. ; Kolapalli, Srinivasa Prasad ; Nielsen, Thorbjørn M. ; Pais, Eva ; Beese, Carsten Jörn ; Abdul-Al, Ahmad ; Vind, Anna Constance ; Bartek, Jiri ; Bekker-Jensen, Simon ; Montes, Marta ; Galanos, Panagiotis ; Faergeman, Nils ; Happonen, Lotta ; Frankel, Lisa B. / Autophagy-mediated control of ribosome homeostasis in oncogene-induced senescence. I: Cell Reports. 2023 ; Bind 42, Nr. 11.

Bibtex

@article{414b15d9d0304f828196dcf51d3de62a,

title = "Autophagy-mediated control of ribosome homeostasis in oncogene-induced senescence",

abstract = "Oncogene-induced senescence (OIS) is a persistent anti-proliferative response that acts as a barrier against malignant transformation. During OIS, cells undergo dynamic remodeling, which involves alterations in protein and organelle homeostasis through autophagy. Here, we show that ribosomes are selectively targeted for degradation by autophagy during OIS. By characterizing senescence-dependent alterations in the ribosomal interactome, we find that the deubiquitinase USP10 dissociates from the ribosome during the transition to OIS. This release of USP10 leads to an enhanced ribosome ubiquitination, particularly of small subunit proteins, including lysine 275 on RPS2. Both reinforcement of the USP10-ribosome interaction and mutation of RPS2 K275 abrogate ribosomal delivery to lysosomes without affecting bulk autophagy. We show that the selective recruitment of ubiquitinated ribosomes to autophagosomes is mediated by the p62 receptor. While ribophagy is not required for the establishment of senescence per se, it contributes to senescence-related metabolome alterations and facilitates the senescence-associated secretory phenotype.",

keywords = "autophagy, CP: Cell biology, CP: Molecular biology, oncogene-induced senescence, ribosomes, selective autophagy, ubiquitin, USP10",

author = "L{\'o}pez, {Aida Rodr{\'i}guez} and J{\o}rgensen, {Maria H.} and Havelund, {Jesper F.} and Arendrup, {Frederic S.} and Kolapalli, {Srinivasa Prasad} and Nielsen, {Thorbj{\o}rn M.} and Eva Pais and Beese, {Carsten J{\"o}rn} and Ahmad Abdul-Al and Vind, {Anna Constance} and Jiri Bartek and Simon Bekker-Jensen and Marta Montes and Panagiotis Galanos and Nils Faergeman and Lotta Happonen and Frankel, {Lisa B.}",

note = "Publisher Copyright: {\textcopyright} 2023 The Authors",

year = "2023",

doi = "10.1016/j.celrep.2023.113381",

language = "English",

volume = "42",

journal = "Cell Reports",

issn = "2211-1247",

publisher = "Cell Press",

number = "11",

}

RIS

TY - JOUR

T1 - Autophagy-mediated control of ribosome homeostasis in oncogene-induced senescence

AU - López, Aida Rodríguez

AU - Jørgensen, Maria H.

AU - Havelund, Jesper F.

AU - Arendrup, Frederic S.

AU - Kolapalli, Srinivasa Prasad

AU - Nielsen, Thorbjørn M.

AU - Pais, Eva

AU - Beese, Carsten Jörn

AU - Abdul-Al, Ahmad

AU - Vind, Anna Constance

AU - Bartek, Jiri

AU - Bekker-Jensen, Simon

AU - Montes, Marta

AU - Galanos, Panagiotis

AU - Faergeman, Nils

AU - Happonen, Lotta

AU - Frankel, Lisa B.

PY - 2023

Y1 - 2023

N2 - Oncogene-induced senescence (OIS) is a persistent anti-proliferative response that acts as a barrier against malignant transformation. During OIS, cells undergo dynamic remodeling, which involves alterations in protein and organelle homeostasis through autophagy. Here, we show that ribosomes are selectively targeted for degradation by autophagy during OIS. By characterizing senescence-dependent alterations in the ribosomal interactome, we find that the deubiquitinase USP10 dissociates from the ribosome during the transition to OIS. This release of USP10 leads to an enhanced ribosome ubiquitination, particularly of small subunit proteins, including lysine 275 on RPS2. Both reinforcement of the USP10-ribosome interaction and mutation of RPS2 K275 abrogate ribosomal delivery to lysosomes without affecting bulk autophagy. We show that the selective recruitment of ubiquitinated ribosomes to autophagosomes is mediated by the p62 receptor. While ribophagy is not required for the establishment of senescence per se, it contributes to senescence-related metabolome alterations and facilitates the senescence-associated secretory phenotype.

AB - Oncogene-induced senescence (OIS) is a persistent anti-proliferative response that acts as a barrier against malignant transformation. During OIS, cells undergo dynamic remodeling, which involves alterations in protein and organelle homeostasis through autophagy. Here, we show that ribosomes are selectively targeted for degradation by autophagy during OIS. By characterizing senescence-dependent alterations in the ribosomal interactome, we find that the deubiquitinase USP10 dissociates from the ribosome during the transition to OIS. This release of USP10 leads to an enhanced ribosome ubiquitination, particularly of small subunit proteins, including lysine 275 on RPS2. Both reinforcement of the USP10-ribosome interaction and mutation of RPS2 K275 abrogate ribosomal delivery to lysosomes without affecting bulk autophagy. We show that the selective recruitment of ubiquitinated ribosomes to autophagosomes is mediated by the p62 receptor. While ribophagy is not required for the establishment of senescence per se, it contributes to senescence-related metabolome alterations and facilitates the senescence-associated secretory phenotype.

KW - autophagy

KW - CP: Cell biology

KW - CP: Molecular biology

KW - oncogene-induced senescence

KW - ribosomes

KW - selective autophagy

KW - ubiquitin

KW - USP10

U2 - 10.1016/j.celrep.2023.113381

DO - 10.1016/j.celrep.2023.113381

M3 - Journal article

C2 - 37930887

AN - SCOPUS:85175818246

VL - 42

JO - Cell Reports

JF - Cell Reports

SN - 2211-1247

IS - 11

M1 - 113381

ER -

ID: 373468767

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