Universität zu Köln

Totska, Khrystyna, Barata, João C. V. V., Sandt, Walter, Meyer, David H. ORCID: 0000-0002-5667-4720 and Schumacher, Björn ORCID: 0000-0001-6097-5238 (2025). Age Deceleration and Reversal Gene Patterns in Dauer Diapause. Aging Cell, 24 (12). Wiley. ISSN 1474-9718

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Abstract

[Artikel-Nr. e70253] The aging process is characterized by a general decrease in physical functionality and poses the biggest risk factor for a variety of diseases such as cancer, cardiovascular diseases, and neurodegenerative disorders among others. Understanding the naturally evolved mechanisms that slow aging and rejuvenate an animal could reveal important concepts on how to prevent age‐associated diseases and even revert aging. The C. elegans dauer stage is a robust and long‐lived alternative developmental state that, after dauer exit, has a normal adult lifespan with fully retained fecundity. To understand how longevity during dauer and rejuvenation following dauer exit is mediated, we characterized the gene expression changes during dauer and upon exit. We assessed how biological age, as determined via BiT Age, a transcriptome aging clock, is affected during dauer and upon dauer exit. During the dauer stage, we measured a decelerated increase in age compared to the chronological age and an age reversal following dauer exit. Transcriptomic analyses revealed major metabolic shifts and enhanced biomolecular degradation that are reversed during exit. Moreover, we show that transcription‐blocking lesions can induce lasting transcription stress in dauers that is rapidly resolved by transcription‐coupled nucleotide excision repair during dauer exit. Our data provide new insights into the underlying mechanisms of naturally occurring age deceleration and rejuvenation. [Funding: This work was supported by Deutsche Forschungsgemeinschaft, Reinhart Koselleck project 524088035, FOR 5504 project 496650118, FOR 5762 project 531902955, SFB 1678, SFB 1607, CECAD EXC 2030-390661388, ANR-DFG project 545378328, and the DFG projects 570621149, 558166204, 540136447, 496914708, 437825591, 437407415, and 418036758; European Research Council, ERC-2023- SyG, 101118919; Hevolution Foundation, HF- GRO-23-1199212-35; José Carreras Leukämie- Stiftung, DJCLS 04 R/2023; Deutsche Krebshilfe, 70114555; John Templeton Foundation, 61734].

Item Type:	Article
Creators:	Creators Email ORCID ORCID Put Code Totska, Khrystyna UNSPECIFIED UNSPECIFIED UNSPECIFIED Barata, João C. V. V. UNSPECIFIED UNSPECIFIED UNSPECIFIED Sandt, Walter UNSPECIFIED UNSPECIFIED UNSPECIFIED Meyer, David H. UNSPECIFIED https://orcid.org/0000-0002-5667-4720 UNSPECIFIED Schumacher, Björn UNSPECIFIED https://orcid.org/0000-0001-6097-5238 UNSPECIFIED
URN:	urn:nbn:de:hbz:38-800982
Identification Number:	10.1111/acel.70253
Journal or Publication Title:	Aging Cell
Volume:	24
Number:	12
Number of Pages:	17
Date:	17 December 2025
Publisher:	Wiley
ISSN:	1474-9718
Language:	English
Faculty:	Central Institutions / Interdisciplinary Research Centers Collaborative Research Centers Faculty of Medicine
Divisions:	CECAD - Cluster of Excellence Cellular Stress Responses in Aging-Associated Diseases Zentrum für Molekulare Medizin
Subjects:	Medical sciences Medicine
['eprint_fieldname_oa_funders' not defined]:	Publikationsfonds UzK
Refereed:	Yes
URI:	http://kups.ub.uni-koeln.de/id/eprint/80098