Universität zu Köln

Ermolaeva, Maria A. and Schumacher, Bjoern (2014). Systemic DNA damage responses: organismal adapatations to genome instability. Trends Genet., 30 (3). S. 95 - 103. LONDON: ELSEVIER SCIENCE LONDON. ISSN 1362-4555

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Abstract

DNA damage checkpoints are important tumor-suppressor mechanisms that halt cell cycle progression to allow time for DNA repair, or induce senescence and apoptosis to remove damaged cells permanently. Non-cell-autonomous DNA damage responses activate the innate immune system in multiple metazoan species. These responses not only enable clearance of damaged cells and contribute to tissue remodeling and regeneration but can also result in chronic inflammation and tissue damage. Germline DNA damage-induced systemic stress resistance (GDISR) is mediated by an ancestral innate immune response and results in organismal adjustments to the presence of damaged cells. We discuss GDISR as an organismal DNA damage checkpoint mechanism through which elevated somatic endurance can extend reproductive lifespan when germ cells require extended time for restoring genome stability.

Item Type:	Journal Article
Creators:	Creators Email ORCID ORCID Put Code Ermolaeva, Maria A. UNSPECIFIED UNSPECIFIED UNSPECIFIED Schumacher, Bjoern UNSPECIFIED UNSPECIFIED UNSPECIFIED
URN:	urn:nbn:de:hbz:38-444604
DOI:	10.1016/j.tig.2013.12.001
Journal or Publication Title:	Trends Genet.
Volume:	30
Number:	3
Page Range:	S. 95 - 103
Date:	2014
Publisher:	ELSEVIER SCIENCE LONDON
Place of Publication:	LONDON
ISSN:	1362-4555
Language:	English
Faculty:	Unspecified
Divisions:	Unspecified
Subjects:	no entry
Uncontrolled Keywords:	Keywords Language INNATE IMMUNE-SYSTEM; CROSS-LINK REPAIR; CAENORHABDITIS-ELEGANS; INDUCED APOPTOSIS; SOMATIC GROWTH; MOUSE MODEL; SENESCENCE; P53; TRIGGERS; CANCER Multiple languages Genetics & Heredity Multiple languages
URI:	http://kups.ub.uni-koeln.de/id/eprint/44460