interferon and immune responses
Open access
Peer reviewed
Scollr summary
What this paper is about
Results show that cGAS functions to maintain heterochromatin organization in the nucleus, independent of its cytoplasmic role as a DNA sensor or its catalytic activity, with implications for geroprotective strategies targeting this pathway.
Full abstract
Read the full abstract
Aging-associated inflammation, or 'inflammaging" is a driver of multiple age-associated diseases. Cyclic GMP-AMP Synthase (cGAS) is a cytosolic DNA sensor that functions to activate interferon response upon detecting viral DNA in the cytoplasm. cGAS contributes to inflammaging by responding to endogenous signals such as damaged DNA or LINE1 (L1) cDNA which forms in aged cells. While cGAS knockout mice are viable their aging has not been examined. Unexpectedly, we found that cGAS knockout mice exhibit accelerated aging phenotype associated with induction of inflammation. Transcription of L1 elements was increased in both cGAS knockout mice and in cGAS siRNA knockdown cells associated with high levels of cytoplasmic L1 DNA and expression of ORF1 protein. Cells from cGAS knockout mice showed increased chromatin accessibility and decreased DNA methylation on L1 transposons. Stimulated emission depletion microscopy (STED) showed that cGAS forms nuclear condensates that co-localize with H3K9me3 heterochromatin marks, and H3K9me3 pattern is disrupted in cGAS knockout cells. Taken together these results suggest a previously undescribed role for cGAS in maintaining heterochromatin on transposable elements. We propose that loss of cGAS leads to loss of chromatin organization, de-repression of transposable elements and induction of inflammation resulting in accelerated aging.
Direct answer
What can I do from this paper page?
Use this page to scan "cGAS-deficient mice display premature aging associated with derepression of LINE1 elements and inflammation" quickly: start with the summary and abstract, then check the authors, source, topics, and related papers. From here, open Scollr to follow interferon and immune responses research, save the paper, or map adjacent work.
Research areas
Follow related topics
Citation
BibTeX
@article{Martinez2026cGAS,
title = {cGAS-deficient mice display premature aging associated with derepression of LINE1 elements and inflammation},
author = {John C. Martinez and Francesco Morandini and Cheyenne Rechsteiner and Lucinda Fitzgibbons and Natasha Sieczkiewicz and Xiaoyan Liao and Weijie He and Sung Jae Bae and Michael E. Meadow and Eric Hillpot and Joseph Cutting and Victoria Paige and Max Zacher and Seyed Ali Biashad and Matthew Simon and Inés Muela-Zarzuela and Mario D. Cordero and Martin S. Taylor and John M. Sedivy and Andrei Seluanov and Vera Gorbunova},
journal = {Nature Aging},
year = {2026},
doi = {10.1038/s43587-026-01206-y},
url = {https://doi.org/10.1038/s43587-026-01206-y}
}FAQ
Using this paper in a discovery workflow
How do I find related work for this paper?
Use the related papers and topic links on this page as starting points. In Scollr, you can also open the paper and build a literature map around its references, citing papers, and related work.
How can I keep up with new interferon and immune responses research papers?
Follow interferon and immune responses research in Scollr. New papers from the topic flow into a personalized feed, and you can save useful studies to revisit later.
Can I cite this paper from this page?
This page includes a static BibTeX block for cGAS-deficient mice display premature aging associated with derepression of LINE1 elements and inflammation. Always verify the DOI, source, and publication details against the publisher record before submitting a manuscript.
Follow this research in Scollr
Follow the topics and authors behind this paper, save useful studies, and build a literature map when you are ready to go deeper.
Get the app