About: Epitranscriptomic regulation of the response to the air pollutant naphthalene in mouse lungs: from the perspectives of specialized translation and tolerance linked to the writer ALKBH8

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About: Epitranscriptomic regulation of the response to the air pollutant naphthalene in mouse lungs: from the perspectives of specialized translation and tolerance linked to the writer ALKBH8 Goto Sponge NotDistinct Permalink

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
title	Epitranscriptomic regulation of the response to the air pollutant naphthalene in mouse lungs: from the perspectives of specialized translation and tolerance linked to the writer ALKBH8
Creator	Yin, Lei Zhang, Qing-Yu Leonardi, Andrea Andres Melendez, J Begley, Thomas Dedon, Peter Ding, Xinxin Endres, Lauren Evke, Sara Kovalchuk, Nataliia Martin, Samuel Nevins, Steven Van Winkle, Laura
source	BioRxiv
abstract	Background The epitranscriptomic writer Alkylation Repair Homolog 8 (ALKBH8) is a tRNA methyltransferase that modifies the wobble uridine of selenocysteine tRNA to promote the specialized translation, via stop codon recoding, of proteins that contain selenocysteine. Corresponding selenoproteins play critical roles in protecting against reactive oxygen species and environmental stress. Using a novel animal model deficient in Alkbh8, we have investigated the importance of epitranscriptomic systems in the response to naphthalene (NA), an abundant polycyclic aromatic hydrocarbon, glutathione depleter and lung toxicant found in tobacco smoke, gasoline and mothballs. Objectives Our goal was to define the molecular reprogramming of Alkbh8 deficient (Alkbh8def) mice and evaluate the roles that the epitranscriptomic writer ALKBH8 and selenoproteins play in mitigating NA-induced toxicity and lung dysfunction. Methods We performed basal lung analysis and NA exposure studies using WT, Alkbh8def and Cyp2abfgs-null mice, the latter of which lack the cytochrome P450 enzymes required for NA bioactivation. We characterized gene expression, molecular markers of damage, viability and tolerance to NA. Results Under basal conditions, lungs from Alkbh8def mice have increased oxidation-reduction potential (ORP) and 8-isoprostane levels, and have reprogrammed at the molecular level to display increased stress response transcripts. In addition, the ALKBH8 writer deficient lungs have a decreased GSH/GSSG ratio. Alkbh8def mice are more sensitive to NA than WT, showing higher susceptibility to lung damage both at the cellular and molecular levels. WT mice develop a tolerance to NA after 3 days, defined as resistance to a high challenging dose after repeated exposures, which is absent in Alkbh8def mice, with writer deficient not surviving NA exposure. Discussion We conclude that the epitranscriptomic writer ALKBH8 plays a protective role against NA-induced lung dysfunction and promotes NA tolerance. Our work provides an early example of how epitranscriptomic systems can regulate the response to environmental stress in vivo.
has issue date	2019-08-07(xsd:dateTime)
bibo:doi	10.1101/727909
has license	biorxiv
sha1sum (hex)	bd9bd04c67aa75cf8d66aaec0c11b984f447100f
schema:url	https://doi.org/10.1101/727909
resource representing a document's title	Epitranscriptomic regulation of the response to the air pollutant naphthalene in mouse lungs: from the perspectives of specialized translation and tolerance linked to the writer ALKBH8
schema:publication	bioRxiv
resource representing a document's body	covid:bd9bd04c67aa75cf8d66aaec0c11b984f447100f#body_text
is schema:about of	named entity 'reactive oxygen species' named entity 'animal model' named entity 'air pollutant' named entity 'Homolog' named entity 'selenocysteine' named entity 'critical' named entity 'environmental stress' named entity 'stop codon' named entity 'gasoline' named entity 'animal model' named entity 'Alkylation' named entity 'lung' named entity 'tRNA' named entity 'Homolog' named entity 'ALKBH8' named entity 'specialized translation' named entity 'epitranscriptomic' named entity 'thiol' named entity 'inflammatory response' named entity 'FITC' named entity 'tRNA' named entity 'RNA' named entity 'DDR' named entity 'mRNAs' named entity 'AREs' named entity 'club cells' named entity 'oxidized' named entity 'epitranscriptomic' named entity 'ROS' named entity 'GPX1' named entity 'disulfide bonds' named entity 'selenoprotein' named entity 'ROS' named entity 'BALF' named entity 'lungs' named entity 'ROS' named entity 'TRX2' named entity 'oxidative damage' named entity 'oxidative damage' named entity 'Alkbh8' named entity 'AlkB' named entity 'bronchoalveolar lavage' named entity 'cytokine' named entity 'Alkbh8' named entity 'epitranscriptomic' named entity 'club cells' named entity 'neomycin' named entity 'synthesis inhibitor' named entity 'Alkbh8' named entity 'ORP' named entity 'tRNA' named entity '14,000' named entity 'Glutathione' named entity 'GSH/GSSG' named entity 'erythroid' named entity '3'UTR' named entity 'PBS' named entity 'bacteria' named entity 'protein' named entity 'chemical species' named entity 'TRX2' named entity 'supernatant' named entity 'carbonyl' named entity 'uridine' named entity 'lungs' named entity 'Alkbh8' named entity 'uridine' named entity 'standard error' named entity 'corn oil' named entity 'Alkbh8' named entity 'bronchoalveolar lavage fluid' named entity 'Epitranscriptomic'

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