ATF7 mediates TNF-α-induced telomere shortening

Abstract Telomeres maintain the integrity of chromosome ends and telomere length is an important marker of aging. The epidemiological studies suggested that many types of stress including psychosocial stress decrease telomere length. However, it remains unknown how various stresses induce telomere s...

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Published in	Nucleic acids research Vol. 46; no. 9; pp. 4487 - 4504
Main Authors	Maekawa, Toshio, Liu, Binbin, Nakai, Daisuke, Yoshida, Keisuke, Nakamura, Ken-ichi, Yasukawa, Mami, Koike, Manabu, Takubo, Kaiyo, Chatton, Bruno, Ishikawa, Fuyuki, Masutomi, Kenkichi, Ishii, Shunsuke
Format	Journal Article
Language	English
Published	England Oxford University Press 18.05.2018
Subjects	Activating Transcription Factors - genetics Activating Transcription Factors - metabolism Activating Transcription Factors - physiology Animals Biochemistry, Molecular Biology Fibroblasts Genome Integrity, Repair and Genomics HeLa Cells Histones - metabolism Humans Ku Autoantigen - metabolism Life Sciences Mice, Inbred C57BL Mice, Knockout Phosphorylation Telomerase - metabolism Telomere - metabolism Telomere Shortening Tumor Necrosis Factor-alpha - physiology
Online Access	Get full text
ISSN	0305-1048 1362-4962 1362-4962
DOI	10.1093/nar/gky155

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Abstract	Abstract Telomeres maintain the integrity of chromosome ends and telomere length is an important marker of aging. The epidemiological studies suggested that many types of stress including psychosocial stress decrease telomere length. However, it remains unknown how various stresses induce telomere shortening. Here, we report that the stress-responsive transcription factor ATF7 mediates TNF-α-induced telomere shortening. ATF7 and telomerase, an enzyme that elongates telomeres, are localized on telomeres via interactions with the Ku complex. In response to TNF-α, which is induced by various stresses including psychological stress, ATF7 was phosphorylated by p38, leading to the release of ATF7 and telomerase from telomeres. Thus, a decrease of ATF7 and telomerase on telomeres in response to stress causes telomere shortening, as observed in ATF7-deficient mice. These findings give credence to the idea that various types of stress might shorten telomere.
AbstractList	Telomeres maintain the integrity of chromosome ends and telomere length is an important marker of aging. The epidemiological studies suggested that many types of stress including psychosocial stress decrease telomere length. However, it remains unknown how various stresses induce telomere shortening. Here, we report that the stress-responsive transcription factor ATF7 mediates TNF-α-induced telomere shortening. ATF7 and telomerase, an enzyme that elongates telomeres, are localized on telomeres via interactions with the Ku complex. In response to TNF-α, which is induced by various stresses including psychological stress, ATF7 was phosphorylated by p38, leading to the release of ATF7 and telomerase from telomeres. Thus, a decrease of ATF7 and telomerase on telomeres in response to stress causes telomere shortening, as observed in ATF7-deficient mice. These findings give credence to the idea that various types of stress might shorten telomere.Telomeres maintain the integrity of chromosome ends and telomere length is an important marker of aging. The epidemiological studies suggested that many types of stress including psychosocial stress decrease telomere length. However, it remains unknown how various stresses induce telomere shortening. Here, we report that the stress-responsive transcription factor ATF7 mediates TNF-α-induced telomere shortening. ATF7 and telomerase, an enzyme that elongates telomeres, are localized on telomeres via interactions with the Ku complex. In response to TNF-α, which is induced by various stresses including psychological stress, ATF7 was phosphorylated by p38, leading to the release of ATF7 and telomerase from telomeres. Thus, a decrease of ATF7 and telomerase on telomeres in response to stress causes telomere shortening, as observed in ATF7-deficient mice. These findings give credence to the idea that various types of stress might shorten telomere. Telomeres maintain the integrity of chromosome ends and telomere length is an important marker of aging. The epidemiological studies suggested that many types of stress including psychosocial stress decrease telomere length. However, it remains unknown how various stresses induce telomere shortening. Here, we report that the stress-responsive transcription factor ATF7 mediates TNF-α-induced telomere shortening. ATF7 and telomerase, an enzyme that elongates telomeres, are localized on telomeres via interactions with the Ku complex. In response to TNF-α, which is induced by various stresses including psychological stress, ATF7 was phosphorylated by p38, leading to the release of ATF7 and telomerase from telomeres. Thus, a decrease of ATF7 and telomerase on telomeres in response to stress causes telomere shortening, as observed in ATF7-deficient mice. These findings give credence to the idea that various types of stress might shorten telomere. Abstract Telomeres maintain the integrity of chromosome ends and telomere length is an important marker of aging. The epidemiological studies suggested that many types of stress including psychosocial stress decrease telomere length. However, it remains unknown how various stresses induce telomere shortening. Here, we report that the stress-responsive transcription factor ATF7 mediates TNF-α-induced telomere shortening. ATF7 and telomerase, an enzyme that elongates telomeres, are localized on telomeres via interactions with the Ku complex. In response to TNF-α, which is induced by various stresses including psychological stress, ATF7 was phosphorylated by p38, leading to the release of ATF7 and telomerase from telomeres. Thus, a decrease of ATF7 and telomerase on telomeres in response to stress causes telomere shortening, as observed in ATF7-deficient mice. These findings give credence to the idea that various types of stress might shorten telomere.
Author	Nakai, Daisuke Nakamura, Ken-ichi Masutomi, Kenkichi Yoshida, Keisuke Takubo, Kaiyo Ishii, Shunsuke Yasukawa, Mami Chatton, Bruno Ishikawa, Fuyuki Maekawa, Toshio Liu, Binbin Koike, Manabu
AuthorAffiliation	6 Université de Strasbourg, UMR7242 Biotechnologie et Signalisation Cellulaire, Ecole Supérieure de Biotechnologie de Strasbourg, BP10413, Illkirch, France 4 Division of Cancer Stem Cell, National Cancer Center Research Institute, Tokyo, Japan 3 Research Team for Geriatric Diseases, Tokyo Metropolitan Institute of Gerontology, Sakaecho 35-2, Itabashi-ku, Tokyo 173-0015, Japan 7 Department of Gene Mechanisms, Graduate School of Biostudies, Kyoto University, Yoshida-Konoe-cho, Sakyo-ku, Kyoto 606-8501, Japan 1 Laboratory of Molecular Genetics, RIKEN Tsukuba Institute, 3-1-1 Koyadai, Tsukuba, Ibaraki 305-0074, Japan 2 Graduate School of Comprehensive Human Sciences, University of Tsukuba, 1-1-1 Tennoudai, Tsukuba, Ibaraki 305-8577, Japan 5 National Institute of Radiological Sciences, National Institutes for Quantum and Radiological Science and Technology, 4-9-1 Anagawa, Inage-ku, Chiba 263-8555, Japan
AuthorAffiliation_xml	– name: 6 Université de Strasbourg, UMR7242 Biotechnologie et Signalisation Cellulaire, Ecole Supérieure de Biotechnologie de Strasbourg, BP10413, Illkirch, France – name: 7 Department of Gene Mechanisms, Graduate School of Biostudies, Kyoto University, Yoshida-Konoe-cho, Sakyo-ku, Kyoto 606-8501, Japan – name: 4 Division of Cancer Stem Cell, National Cancer Center Research Institute, Tokyo, Japan – name: 1 Laboratory of Molecular Genetics, RIKEN Tsukuba Institute, 3-1-1 Koyadai, Tsukuba, Ibaraki 305-0074, Japan – name: 2 Graduate School of Comprehensive Human Sciences, University of Tsukuba, 1-1-1 Tennoudai, Tsukuba, Ibaraki 305-8577, Japan – name: 3 Research Team for Geriatric Diseases, Tokyo Metropolitan Institute of Gerontology, Sakaecho 35-2, Itabashi-ku, Tokyo 173-0015, Japan – name: 5 National Institute of Radiological Sciences, National Institutes for Quantum and Radiological Science and Technology, 4-9-1 Anagawa, Inage-ku, Chiba 263-8555, Japan
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Snippet	Abstract Telomeres maintain the integrity of chromosome ends and telomere length is an important marker of aging. The epidemiological studies suggested that... Telomeres maintain the integrity of chromosome ends and telomere length is an important marker of aging. The epidemiological studies suggested that many types...
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SubjectTerms	Activating Transcription Factors - genetics Activating Transcription Factors - metabolism Activating Transcription Factors - physiology Animals Biochemistry, Molecular Biology Fibroblasts Genome Integrity, Repair and Genomics HeLa Cells Histones - metabolism Humans Ku Autoantigen - metabolism Life Sciences Mice, Inbred C57BL Mice, Knockout Phosphorylation Telomerase - metabolism Telomere - metabolism Telomere Shortening Tumor Necrosis Factor-alpha - physiology
Title	ATF7 mediates TNF-α-induced telomere shortening
URI	https://www.ncbi.nlm.nih.gov/pubmed/29490055 https://www.proquest.com/docview/2009570381 https://hal.science/hal-03344344 https://pubmed.ncbi.nlm.nih.gov/PMC5961373
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