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DNA damage induces p53-independent apoptosis through ribosome stalling
In response to excessive DNA damage, human cells can activate p53 to induce apoptosis. Cells lacking p53 can still undergo apoptosis upon DNA damage, yet the responsible pathways are unknown. We observed that p53-independent apoptosis in response to DNA damage coincided with translation inhibition,...
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| Published in: | Science (American Association for the Advancement of Science) 2024-05, Vol.384 (6697), p.785-792 |
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| Main Authors: | , , , , , , , , , , , , , , , , , |
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| container_title | Science (American Association for the Advancement of Science) |
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| creator | Boon, Nicolaas J Oliveira, Rafaela A Körner, Pierré-René Kochavi, Adva Mertens, Sander Malka, Yuval Voogd, Rhianne van der Horst, Suzanne E M Huismans, Maarten A Smabers, Lidwien P Draper, Jonne M Wessels, Lodewyk F A Haahr, Peter Roodhart, Jeanine M L Schumacher, Ton N M Snippert, Hugo J Agami, Reuven Brummelkamp, Thijn R |
| description | In response to excessive DNA damage, human cells can activate p53 to induce apoptosis. Cells lacking p53 can still undergo apoptosis upon DNA damage, yet the responsible pathways are unknown. We observed that p53-independent apoptosis in response to DNA damage coincided with translation inhibition, which was characterized by ribosome stalling on rare leucine-encoding UUA codons and globally curtailed translation initiation. A genetic screen identified the transfer RNAse SLFN11 and the kinase GCN2 as factors required for UUA stalling and global translation inhibition, respectively. Stalled ribosomes activated a ribotoxic stress signal conveyed by the ribosome sensor ZAKα to the apoptosis machinery. These results provide an explanation for the frequent inactivation of SLFN11 in chemotherapy-unresponsive tumors and highlight ribosome stalling as a signaling event affecting cell fate in response to DNA damage. |
| doi_str_mv | 10.1126/science.adh7950 |
| format | article |
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Cells lacking p53 can still undergo apoptosis upon DNA damage, yet the responsible pathways are unknown. We observed that p53-independent apoptosis in response to DNA damage coincided with translation inhibition, which was characterized by ribosome stalling on rare leucine-encoding UUA codons and globally curtailed translation initiation. A genetic screen identified the transfer RNAse SLFN11 and the kinase GCN2 as factors required for UUA stalling and global translation inhibition, respectively. Stalled ribosomes activated a ribotoxic stress signal conveyed by the ribosome sensor ZAKα to the apoptosis machinery. 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No claim to original U.S. Government Works</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c325t-808ac2a09024d9ce36fd0ae162acbd5f03cd703ab3a6b556b50aa94c962ffd4e3</citedby><cites>FETCH-LOGICAL-c325t-808ac2a09024d9ce36fd0ae162acbd5f03cd703ab3a6b556b50aa94c962ffd4e3</cites><orcidid>0000-0003-1556-0820 ; 0000-0002-3066-7071 ; 0000-0001-6495-3482 ; 0009-0004-7664-212X ; 0000-0002-2848-2473 ; 0000-0002-1656-8480 ; 0009-0009-5328-2543 ; 0009-0007-9631-1012 ; 0000-0002-9964-234X ; 0000-0001-9680-2304 ; 0000-0002-1656-6995 ; 0000-0002-6274-1942 ; 0000-0003-1398-8970 ; 0000-0003-0517-8804</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,2884,2885,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38753784$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Boon, Nicolaas J</creatorcontrib><creatorcontrib>Oliveira, Rafaela A</creatorcontrib><creatorcontrib>Körner, Pierré-René</creatorcontrib><creatorcontrib>Kochavi, Adva</creatorcontrib><creatorcontrib>Mertens, Sander</creatorcontrib><creatorcontrib>Malka, Yuval</creatorcontrib><creatorcontrib>Voogd, Rhianne</creatorcontrib><creatorcontrib>van der Horst, Suzanne E M</creatorcontrib><creatorcontrib>Huismans, Maarten A</creatorcontrib><creatorcontrib>Smabers, Lidwien P</creatorcontrib><creatorcontrib>Draper, Jonne M</creatorcontrib><creatorcontrib>Wessels, Lodewyk F A</creatorcontrib><creatorcontrib>Haahr, Peter</creatorcontrib><creatorcontrib>Roodhart, Jeanine M L</creatorcontrib><creatorcontrib>Schumacher, Ton N M</creatorcontrib><creatorcontrib>Snippert, Hugo J</creatorcontrib><creatorcontrib>Agami, Reuven</creatorcontrib><creatorcontrib>Brummelkamp, Thijn R</creatorcontrib><title>DNA damage induces p53-independent apoptosis through ribosome stalling</title><title>Science (American Association for the Advancement of Science)</title><addtitle>Science</addtitle><description>In response to excessive DNA damage, human cells can activate p53 to induce apoptosis. Cells lacking p53 can still undergo apoptosis upon DNA damage, yet the responsible pathways are unknown. We observed that p53-independent apoptosis in response to DNA damage coincided with translation inhibition, which was characterized by ribosome stalling on rare leucine-encoding UUA codons and globally curtailed translation initiation. A genetic screen identified the transfer RNAse SLFN11 and the kinase GCN2 as factors required for UUA stalling and global translation inhibition, respectively. Stalled ribosomes activated a ribotoxic stress signal conveyed by the ribosome sensor ZAKα to the apoptosis machinery. These results provide an explanation for the frequent inactivation of SLFN11 in chemotherapy-unresponsive tumors and highlight ribosome stalling as a signaling event affecting cell fate in response to DNA damage.</description><subject>Apoptosis</subject><subject>Cell death</subject><subject>Cell Line, Tumor</subject><subject>Chemotherapy</subject><subject>Codon - genetics</subject><subject>Damage</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA Damage</subject><subject>Endonuclease</subject><subject>Genetic screening</subject><subject>Humans</subject><subject>Leucine - genetics</subject><subject>MAP Kinase Kinase Kinases - genetics</subject><subject>MAP Kinase Kinase Kinases - metabolism</subject><subject>Nuclear Proteins - genetics</subject><subject>Nuclear Proteins - metabolism</subject><subject>p53 Protein</subject><subject>Protein Biosynthesis</subject><subject>Protein Serine-Threonine Kinases - genetics</subject><subject>Protein Serine-Threonine Kinases - metabolism</subject><subject>Ribosomes - metabolism</subject><subject>Signal Transduction</subject><subject>Stalling</subject><subject>Tumor Suppressor Protein p53 - genetics</subject><subject>Tumor Suppressor Protein p53 - metabolism</subject><issn>0036-8075</issn><issn>1095-9203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><recordid>eNpdkL1PwzAQxS0EoqUws6FILCxpL3bPiceqUECqYIE5cmynTZXEwU4G_ntcNTAw3Id0v3t6eoTcJjBPEsoXXlWmVWYu9T4VCGdkmoDAWFBg52QKwHicQYoTcuX9ASDcBLskE5alyNJsOSWbx7dVpGUjdyaqWj0o46MOWRx205nQ2j6Sne166ysf9Xtnh90-clVhvW1M5HtZ11W7uyYXpay9uRnnjHxunj7WL_H2_fl1vdrGilHsg5dMKipBAF1qoQzjpQZpEk6lKjSWwJROgcmCSV4ghgIpxVIJTstSLw2bkYeTbufs12B8nzeVV6auZWvs4HMGyDlHZCKg9__Qgx1cG9wdKURAilmgFidKOeu9M2XeuaqR7jtPID9GnI8R52PE4eNu1B2Kxug__jdT9gMNMHl-</recordid><startdate>20240517</startdate><enddate>20240517</enddate><creator>Boon, Nicolaas J</creator><creator>Oliveira, Rafaela A</creator><creator>Körner, Pierré-René</creator><creator>Kochavi, Adva</creator><creator>Mertens, Sander</creator><creator>Malka, Yuval</creator><creator>Voogd, Rhianne</creator><creator>van der Horst, Suzanne E M</creator><creator>Huismans, Maarten A</creator><creator>Smabers, Lidwien P</creator><creator>Draper, Jonne M</creator><creator>Wessels, Lodewyk F A</creator><creator>Haahr, Peter</creator><creator>Roodhart, Jeanine M L</creator><creator>Schumacher, Ton N M</creator><creator>Snippert, Hugo J</creator><creator>Agami, Reuven</creator><creator>Brummelkamp, Thijn R</creator><general>The American Association for the Advancement of Science</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QF</scope><scope>7QG</scope><scope>7QL</scope><scope>7QP</scope><scope>7QQ</scope><scope>7QR</scope><scope>7SC</scope><scope>7SE</scope><scope>7SN</scope><scope>7SP</scope><scope>7SR</scope><scope>7SS</scope><scope>7T7</scope><scope>7TA</scope><scope>7TB</scope><scope>7TK</scope><scope>7TM</scope><scope>7U5</scope><scope>7U9</scope><scope>8BQ</scope><scope>8FD</scope><scope>C1K</scope><scope>F28</scope><scope>FR3</scope><scope>H8D</scope><scope>H8G</scope><scope>H94</scope><scope>JG9</scope><scope>JQ2</scope><scope>K9.</scope><scope>KR7</scope><scope>L7M</scope><scope>L~C</scope><scope>L~D</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0003-1556-0820</orcidid><orcidid>https://orcid.org/0000-0002-3066-7071</orcidid><orcidid>https://orcid.org/0000-0001-6495-3482</orcidid><orcidid>https://orcid.org/0009-0004-7664-212X</orcidid><orcidid>https://orcid.org/0000-0002-2848-2473</orcidid><orcidid>https://orcid.org/0000-0002-1656-8480</orcidid><orcidid>https://orcid.org/0009-0009-5328-2543</orcidid><orcidid>https://orcid.org/0009-0007-9631-1012</orcidid><orcidid>https://orcid.org/0000-0002-9964-234X</orcidid><orcidid>https://orcid.org/0000-0001-9680-2304</orcidid><orcidid>https://orcid.org/0000-0002-1656-6995</orcidid><orcidid>https://orcid.org/0000-0002-6274-1942</orcidid><orcidid>https://orcid.org/0000-0003-1398-8970</orcidid><orcidid>https://orcid.org/0000-0003-0517-8804</orcidid></search><sort><creationdate>20240517</creationdate><title>DNA damage induces p53-independent apoptosis through ribosome stalling</title><author>Boon, Nicolaas J ; Oliveira, Rafaela A ; Körner, Pierré-René ; Kochavi, Adva ; Mertens, Sander ; Malka, Yuval ; Voogd, Rhianne ; van der Horst, Suzanne E M ; Huismans, Maarten A ; Smabers, Lidwien P ; Draper, Jonne M ; Wessels, Lodewyk F A ; Haahr, Peter ; Roodhart, Jeanine M L ; Schumacher, Ton N M ; Snippert, Hugo J ; Agami, Reuven ; Brummelkamp, Thijn R</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c325t-808ac2a09024d9ce36fd0ae162acbd5f03cd703ab3a6b556b50aa94c962ffd4e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Apoptosis</topic><topic>Cell death</topic><topic>Cell Line, Tumor</topic><topic>Chemotherapy</topic><topic>Codon - 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Cells lacking p53 can still undergo apoptosis upon DNA damage, yet the responsible pathways are unknown. We observed that p53-independent apoptosis in response to DNA damage coincided with translation inhibition, which was characterized by ribosome stalling on rare leucine-encoding UUA codons and globally curtailed translation initiation. A genetic screen identified the transfer RNAse SLFN11 and the kinase GCN2 as factors required for UUA stalling and global translation inhibition, respectively. Stalled ribosomes activated a ribotoxic stress signal conveyed by the ribosome sensor ZAKα to the apoptosis machinery. 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| identifier | ISSN: 0036-8075 |
| ispartof | Science (American Association for the Advancement of Science), 2024-05, Vol.384 (6697), p.785-792 |
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| source | American Association for the Advancement of Science; Alma/SFX Local Collection |
| subjects | Apoptosis Cell death Cell Line, Tumor Chemotherapy Codon - genetics Damage Deoxyribonucleic acid DNA DNA Damage Endonuclease Genetic screening Humans Leucine - genetics MAP Kinase Kinase Kinases - genetics MAP Kinase Kinase Kinases - metabolism Nuclear Proteins - genetics Nuclear Proteins - metabolism p53 Protein Protein Biosynthesis Protein Serine-Threonine Kinases - genetics Protein Serine-Threonine Kinases - metabolism Ribosomes - metabolism Signal Transduction Stalling Tumor Suppressor Protein p53 - genetics Tumor Suppressor Protein p53 - metabolism |
| title | DNA damage induces p53-independent apoptosis through ribosome stalling |
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