{"id":87323,"date":"2026-01-30T09:42:24","date_gmt":"2026-01-30T08:42:24","guid":{"rendered":"https:\/\/aktuelles.uni-frankfurt.de\/?p=87323"},"modified":"2026-02-02T17:10:27","modified_gmt":"2026-02-02T16:10:27","slug":"a-broken-dna-repair-tool-accelerates-aging","status":"publish","type":"post","link":"https:\/\/aktuelles.uni-frankfurt.de\/en\/english\/a-broken-dna-repair-tool-accelerates-aging\/","title":{"rendered":"A broken DNA repair tool accelerates aging"},"content":{"rendered":"<p><em>Goethe University-led study reveals how mutations in the repair enzyme SPRTN trigger inflammation and premature ageing \u2013 new insight into Ruijs-Aalfs syndrome<\/em><\/p>\n\n\n\n<p><strong>If severe DNA damage is not repaired, the consequences for the health of cells and tissues are dramatic. A study led by researchers at Goethe University Frankfurt, part of the Rhine-Main University Alliance, shows that the failure of a key DNA repair enzyme called SPRTN not only results in genetic damage, but also triggers chronic inflammatory responses that accelerate aging and lead to developmental abnormalities. The findings shed light on the rare hereditary disorder Ruijs-Aalfs syndrome and may open new avenues for therapeutic intervention.<\/strong><\/p>\n\n\n\n<div style=\"height:20px\" aria-hidden=\"true\" class=\"wp-block-spacer\"><\/div>\n\n\n\n<figure class=\"wp-block-image aligncenter size-full\"><img fetchpriority=\"high\" decoding=\"async\" width=\"650\" height=\"450\" src=\"https:\/\/aktuelles.uni-frankfurt.de\/wp-content\/uploads\/2026\/01\/Mitosis_HeLa_w_o_SPRTN_arr_650x450_c_InstituteOfBiochemistry2_GU.jpg\" alt=\"Fatal error: The failure of the repair enzyme SPRTN in these cultured cells leads to fatal errors in cell division, e.g. by distributing the chromosomes (red) to three daughter cell nuclei instead of two (arrow). Green: Cell division apparatus\/cytoskeleton. Photo: Institute of Biochemistry II, Goethe University Frankfurt\" class=\"wp-image-87322\" srcset=\"https:\/\/aktuelles.uni-frankfurt.de\/wp-content\/uploads\/2026\/01\/Mitosis_HeLa_w_o_SPRTN_arr_650x450_c_InstituteOfBiochemistry2_GU.jpg 650w, https:\/\/aktuelles.uni-frankfurt.de\/wp-content\/uploads\/2026\/01\/Mitosis_HeLa_w_o_SPRTN_arr_650x450_c_InstituteOfBiochemistry2_GU-300x208.jpg 300w, https:\/\/aktuelles.uni-frankfurt.de\/wp-content\/uploads\/2026\/01\/Mitosis_HeLa_w_o_SPRTN_arr_650x450_c_InstituteOfBiochemistry2_GU-500x346.jpg 500w, https:\/\/aktuelles.uni-frankfurt.de\/wp-content\/uploads\/2026\/01\/Mitosis_HeLa_w_o_SPRTN_arr_650x450_c_InstituteOfBiochemistry2_GU-18x12.jpg 18w\" sizes=\"(max-width: 650px) 100vw, 650px\" \/><figcaption class=\"wp-element-caption\">Fatal error: The failure of the repair enzyme SPRTN in these cultured cells leads to fatal errors in cell division, e.g. by distributing the chromosomes (red) to three daughter cell nuclei instead of two (arrow). Green: Cell division apparatus\/cytoskeleton. \u00a9 Institute of Biochemistry II, Goethe University Frankfurt<\/figcaption><\/figure>\n\n\n\n<p>Although DNA is tightly packed and protected within the cell nucleus, it is constantly threatened by damage from normal metabolic processes or external stressors such as radiation or chemical substances. To counteract this, cells rely on an elaborate network of repair mechanisms. When these systems fail, DNA damage can accumulate, impair cellular function, and contribute to cancer, aging, and degenerative diseases.<\/p>\n\n\n\n<p>One particularly severe form of DNA damage are the so-called DNA\u2013protein crosslinks (DPCs), in which proteins become attached to DNA. DPCs can arise from alcohol consumption, exposure to substances such as formaldehyde or other aldehydes, or from errors made by enzymes involved in DNA replication and repair. Because DPCs can cause serious errors during cell division by stalling DNA replication, DNA\u2013protein crosslinks pose a serious threat to genome integrity.<\/p>\n\n\n\n<p>The enzyme SPRTN removes DPCs by cleaving the DNA-protein crosslinks. SPRTN malfunctions, for example as a result of mutations, may predispose individuals to develop bone deformities and liver cancer in their teenage years. This rare genetic disorder is known as Ruijs-Aalfs syndrome. Its underlying mechanism remains poorly understood, and there are no specific therapies.<\/p>\n\n\n\n<p>Now a research team led by Prof. Ivan \u00d0iki\u0107 from the Institute of Biochemistry II at Goethe University demonstrated that the loss of a functional SPRTN enzyme not only leads to the accumulation of damaged DNA in the cell nucleus. Using cell culture experiment and genetically modified mice they found out that, in addition, DNA from the nucleus also leaks into the interior of the cell, the cytoplasm.<\/p>\n\n\n\n<div style=\"height:20px\" aria-hidden=\"true\" class=\"wp-block-spacer\"><\/div>\n\n\n\n<figure class=\"wp-block-image aligncenter size-full\"><img decoding=\"async\" width=\"650\" height=\"577\" src=\"https:\/\/aktuelles.uni-frankfurt.de\/wp-content\/uploads\/2026\/01\/sprtn-protection-anne-claire-jacomin.jpg\" alt=\"SPRTN sch\u00fctzt die DNA wie ein Helm, indem es DNA-Protein-Crosslinks repariert. K\u00fcnstlerische Darstellung: Anne-Claire Jacomin, Goethe-Universit\u00e4t Frankfurt\" class=\"wp-image-87324\" srcset=\"https:\/\/aktuelles.uni-frankfurt.de\/wp-content\/uploads\/2026\/01\/sprtn-protection-anne-claire-jacomin.jpg 650w, https:\/\/aktuelles.uni-frankfurt.de\/wp-content\/uploads\/2026\/01\/sprtn-protection-anne-claire-jacomin-300x266.jpg 300w, https:\/\/aktuelles.uni-frankfurt.de\/wp-content\/uploads\/2026\/01\/sprtn-protection-anne-claire-jacomin-500x444.jpg 500w, https:\/\/aktuelles.uni-frankfurt.de\/wp-content\/uploads\/2026\/01\/sprtn-protection-anne-claire-jacomin-14x12.jpg 14w\" sizes=\"(max-width: 650px) 100vw, 650px\" \/><figcaption class=\"wp-element-caption\">SPRTN protects the DNA like a helmet by reparing DNA-protein crosslinks. Artist\u2019s impression: Anne-Claire Jacomin, Goethe University Frankfurt<\/figcaption><\/figure>\n\n\n\n<div style=\"height:20px\" aria-hidden=\"true\" class=\"wp-block-spacer\"><\/div>\n\n\n\n<p>DNA in the cytoplasm is recognized by the cell as a danger signal, as such DNA usually originates from invading viruses or bacteria or from malignant transformation. Cytoplasmic DNA therefore activates defense mechanisms in the cell by initiating the so-called cGAS-STING signaling pathway. Furthermore, the cell releases messenger substances that attract immune cells, leading to chronic inflammation.<\/p>\n\n\n\n<p>The Frankfurt-led research team observed that this chronic inflammatory response is especially pronounced in the mouse embryos and persists in adulthood, particularly in the lung and liver. As a result, the mice died early or showed signs of premature ageing similar to those seen in people with Ruijs-Aalfs syndrome. Blocking the relevant immune response alleviated many of the symptoms.<\/p>\n\n\n\n<p>\u201cUnrepaired DNA-protein crosslinks have broader systemic consequences,\u201d explains \u00d0iki\u0107. \u201cThey not only compromise genome stability but also drive chronic inflammation that can significantly influence lifespan.\u201d<\/p>\n\n\n\n<p>The physician and molecular biologist sees potential for the development of therapies: \u201cIn addition to Ruijs-Aalfs syndrome, there are other rare genetic diseases in which DNA-protein crosslinks play an important role. With our work, we have laid an important foundation for future therapeutic approaches to these diseases as well. By studying the underlying mechanisms of these rare diseases, we discovered a new link between DNA damage, inflammatory responses, and the lifespan of an organism. This also contributes to the understanding of the biology of ageing.\u201d<\/p>\n\n\n\n<p>Partners in the research project included Goethe University and Johannes Gutenberg University Mainz (Institute of Molecular Biology\/Professor Petra Beli and Institute of Transfusion Medicine\/Professor Daniela Krause) within the Rhine-Main Universities alliance (RMU), the German Consortium for Translational Cancer Research (DKTK), the German Cancer Research Center (DKFZ), EPFL Lausanne, Charit\u00e9 Berlin and the Universities of Cologne and Split (Croatia).<\/p>\n\n\n\n<div style=\"height:20px\" aria-hidden=\"true\" class=\"wp-block-spacer\"><\/div>\n\n\n\n<p class=\"has-background\" style=\"background-color:#eeeeee\"><strong>Publication: <\/strong>Ines Tomaskovic, Cristian Prieto-Garcia, Maria Boskovic, Mateo Glumac, Tsung-Lin Tsai, Thorsten Mosler, Rubina Kazi, Rajeshwari Rathore, Jorge Andrade, Marina Hoffmann, Giulio Giuliani, Anne-Claire Jacomin, Raquel S. Pereira, Elias Knop, Laurens Wachsmuth, Petra Beli, Koraljka Husnjak, Manolis Pasparakis, Andrea Ablasser, Daniela S. Krause, Michael Potente, Stamatis Papathanasiou, Janos Terzic, Ivan Dikic. <strong>DNA-Protein crosslinks promote cGAS-STING-driven premature aging and embryonic lethality. Science (2026)<\/strong> <a href=\"https:\/\/doi.org\/10.1126\/science.adx9445\" target=\"_blank\" rel=\"noreferrer noopener\">https:\/\/doi.org\/10.1126\/science.adx9445<\/a><\/p>\n\n\n\n<div style=\"height:20px\" aria-hidden=\"true\" class=\"wp-block-spacer\"><\/div>\n\n\n\n<p class=\"has-background\" style=\"background-color:#eeeeee\"><strong>Contact:<\/strong><br>Professor Ivan \u00d0iki\u0107<br>Institute of Biochemistry II<br>and Buchmann Institute for Molecular Life Sciences<br>Goethe University Frankfurt<br>Tel: +49 (0)69 6301-5964<br><a href=\"mailto:dikic@biochem2.uni-frankfurt.de\" target=\"_blank\" rel=\"noreferrer noopener\">dikic@biochem2.uni-frankfurt.de<\/a><br><a href=\"https:\/\/biochem2.com\/research-group\/molecular-signaling\" target=\"_blank\" rel=\"noreferrer noopener\">https:\/\/biochem2.com\/research-group\/molecular-signaling<\/a><\/p>","protected":false},"excerpt":{"rendered":"<p>Goethe University-led study reveals how mutations in the repair enzyme SPRTN trigger inflammation and premature ageing \u2013 new insight into Ruijs-Aalfs syndrome If severe DNA damage is not repaired, the [&hellip;]<\/p>\n","protected":false},"author":23,"featured_media":87322,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"_eb_attr":"","_price":"","_stock":"","_tribe_ticket_header":"","_tribe_default_ticket_provider":"","_ticket_start_date":"","_ticket_end_date":"","_tribe_ticket_show_description":"","_tribe_ticket_show_not_going":false,"_tribe_ticket_use_global_stock":"","_tribe_ticket_global_stock_level":"","_global_stock_mode":"","_global_stock_cap":"","_tribe_rsvp_for_event":"","_tribe_ticket_going_count":"","_tribe_ticket_not_going_count":"","_tribe_tickets_list":"[]","_tribe_ticket_has_attendee_info_fields":false,"footnotes":""},"categories":[126,254],"tags":[243],"post_folder":[],"class_list":["post-87323","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-english","category-research","tag-biochemistry"],"yoast_head":"<!-- This site is optimized with the Yoast SEO plugin v27.3 - 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Fehler: Der Ausfall des Reparaturenzyms SPRTN in diesen kultivierten Zellen f\u00fchrt zu t\u00f6dlichen Pannen bei der Zellteilung, indem zum Beispiel die Chromosomen (rot) auf drei statt auf zwei Tochterzellkerne verteilt werden (Pfeil). Gr\u00fcn: Zellteilungsapparat\/Zytoskelett. Foto: Institut f\u00fcr Biochemie II, Goethe-Universit\u00e4t Frankfurt"},{"@type":"BreadcrumbList","@id":"https:\/\/aktuelles.uni-frankfurt.de\/english\/a-broken-dna-repair-tool-accelerates-aging\/#breadcrumb","itemListElement":[{"@type":"ListItem","position":1,"name":"Startseite","item":"https:\/\/aktuelles.uni-frankfurt.de\/"},{"@type":"ListItem","position":2,"name":"A broken DNA repair tool accelerates aging"}]},{"@type":"WebSite","@id":"https:\/\/aktuelles.uni-frankfurt.de\/#website","url":"https:\/\/aktuelles.uni-frankfurt.de\/","name":"Aktuelles aus der Goethe-Universit\u00e4t Frankfurt","description":"Aktuelles aus der Goethe-Universit\u00e4t | Neues aus Forschung, Lehre, Studium","publisher":{"@id":"https:\/\/aktuelles.uni-frankfurt.de\/#organization"},"potentialAction":[{"@type":"SearchAction","target":{"@type":"EntryPoint","urlTemplate":"https:\/\/aktuelles.uni-frankfurt.de\/?s={search_term_string}"},"query-input":{"@type":"PropertyValueSpecification","valueRequired":true,"valueName":"search_term_string"}}],"inLanguage":"en-GB"},{"@type":"Organization","@id":"https:\/\/aktuelles.uni-frankfurt.de\/#organization","name":"Goethe University Frankfurt","url":"https:\/\/aktuelles.uni-frankfurt.de\/","logo":{"@type":"ImageObject","inLanguage":"en-GB","@id":"https:\/\/aktuelles.uni-frankfurt.de\/#\/schema\/logo\/image\/","url":"https:\/\/aktuelles.uni-frankfurt.de\/wp-content\/uploads\/2022\/03\/800px-Goethe-Logo.png","contentUrl":"https:\/\/aktuelles.uni-frankfurt.de\/wp-content\/uploads\/2022\/03\/800px-Goethe-Logo.png","width":800,"height":436,"caption":"Goethe-Universit\u00e4t"},"image":{"@id":"https:\/\/aktuelles.uni-frankfurt.de\/#\/schema\/logo\/image\/"}},{"@type":"Person","@id":"https:\/\/aktuelles.uni-frankfurt.de\/#\/schema\/person\/47afd8b2c02023a0f1eee09d035f73e8","name":"Dr. Markus Bernards","url":"https:\/\/aktuelles.uni-frankfurt.de\/en\/author\/markus-bernards\/"}]}},"_links":{"self":[{"href":"https:\/\/aktuelles.uni-frankfurt.de\/en\/wp-json\/wp\/v2\/posts\/87323","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/aktuelles.uni-frankfurt.de\/en\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/aktuelles.uni-frankfurt.de\/en\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/aktuelles.uni-frankfurt.de\/en\/wp-json\/wp\/v2\/users\/23"}],"replies":[{"embeddable":true,"href":"https:\/\/aktuelles.uni-frankfurt.de\/en\/wp-json\/wp\/v2\/comments?post=87323"}],"version-history":[{"count":0,"href":"https:\/\/aktuelles.uni-frankfurt.de\/en\/wp-json\/wp\/v2\/posts\/87323\/revisions"}],"wp:featuredmedia":[{"embeddable":true,"href":"https:\/\/aktuelles.uni-frankfurt.de\/en\/wp-json\/wp\/v2\/media\/87322"}],"wp:attachment":[{"href":"https:\/\/aktuelles.uni-frankfurt.de\/en\/wp-json\/wp\/v2\/media?parent=87323"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/aktuelles.uni-frankfurt.de\/en\/wp-json\/wp\/v2\/categories?post=87323"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/aktuelles.uni-frankfurt.de\/en\/wp-json\/wp\/v2\/tags?post=87323"},{"taxonomy":"post_folder","embeddable":true,"href":"https:\/\/aktuelles.uni-frankfurt.de\/en\/wp-json\/wp\/v2\/post_folder?post=87323"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}