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Duox-generated reactive oxygen species activate ATR/Chk1 to induce G2 arrest in Drosophila tracheoblasts

التفاصيل البيبلوغرافية
العنوان: Duox-generated reactive oxygen species activate ATR/Chk1 to induce G2 arrest in Drosophila tracheoblasts
المؤلفون: Amrutha Kizhedathu, Piyush Chhajed, Lahari Yeramala, Deblina Sain Basu, Tina Mukherjee, Kutti R Vinothkumar, Arjun Guha
المصدر: eLife, Vol 10 (2021)
بيانات النشر: eLife Sciences Publications Ltd, 2021.
سنة النشر: 2021
المجموعة: LCC:Medicine
LCC:Science
LCC:Biology (General)
مصطلحات موضوعية: Drosophila tracheoblasts, G2 arrest, ATR, Chk1/grapes, ROS, Duox, Medicine, Science, Biology (General), QH301-705.5
الوصف: Progenitors of the thoracic tracheal system of adult Drosophila (tracheoblasts) arrest in G2 during larval life and rekindle a mitotic program subsequently. G2 arrest is dependent on ataxia telangiectasia mutated and rad3-related kinase (ATR)-dependent phosphorylation of checkpoint kinase 1 (Chk1) that is actuated in the absence of detectable DNA damage. We are interested in the mechanisms that activate ATR/Chk1 (Kizhedathu et al., 2018; Kizhedathu et al., 2020). Here we report that levels of reactive oxygen species (ROS) are high in arrested tracheoblasts and decrease upon mitotic re-entry. High ROS is dependent on expression of Duox, an H2O2 generating dual oxidase. ROS quenching by overexpression of superoxide dismutase 1, or by knockdown of Duox, abolishes Chk1 phosphorylation and results in precocious proliferation. Tracheae deficient in Duox, or deficient in both Duox and regulators of DNA damage-dependent ATR/Chk1 activation (ATRIP/TOPBP1/claspin), can induce phosphorylation of Chk1 in response to micromolar concentrations of H2O2 in minutes. The findings presented reveal that H2O2 activates ATR/Chk1 in tracheoblasts by a non-canonical, potentially direct, mechanism.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 2050-084X
Relation: https://elifesciences.org/articles/68636; https://doaj.org/toc/2050-084X
DOI: 10.7554/eLife.68636
URL الوصول: https://doaj.org/article/c6a6fa25a40c4c62b5490fb4d24957bd
رقم الأكسشن: edsdoj.6a6fa25a40c4c62b5490fb4d24957bd
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:2050084X
DOI:10.7554/eLife.68636