Dhh1 promotes autophagy-related protein translation during nitrogen starvation.
Identifieur interne : 000364 ( Main/Exploration ); précédent : 000363; suivant : 000365Dhh1 promotes autophagy-related protein translation during nitrogen starvation.
Auteurs : Xu Liu [États-Unis] ; Zhiyuan Yao [États-Unis] ; Meiyan Jin [États-Unis] ; Sim Namkoong [États-Unis] ; Zhangyuan Yin [États-Unis] ; Jun Hee Lee [États-Unis] ; Daniel J. Klionsky [États-Unis]Source :
- PLoS biology [ 1545-7885 ] ; 2019.
Descripteurs français
- KwdFr :
- Autophagie (physiologie), Azote (déficit), Azote (métabolisme), Cellules HEK293 (MeSH), DEAD-box RNA helicases (génétique), DEAD-box RNA helicases (métabolisme), Facteurs de transcription (métabolisme), Humains (MeSH), Liaison aux protéines (MeSH), Phosphorylation (MeSH), Protein kinases (génétique), Protein kinases (métabolisme), Protein-Serine-Threonine Kinases (métabolisme), Protéines adaptatrices de la transduction du signal (génétique), Protéines adaptatrices de la transduction du signal (métabolisme), Protéines associées à l'autophagie (génétique), Protéines associées à l'autophagie (métabolisme), Protéines de Saccharomyces cerevisiae (génétique), Protéines de Saccharomyces cerevisiae (métabolisme), Protéines proto-oncogènes (génétique), Protéines proto-oncogènes (métabolisme), Saccharomyces cerevisiae (métabolisme).
- MESH :
- déficit : Azote.
- génétique : DEAD-box RNA helicases, Protein kinases, Protéines adaptatrices de la transduction du signal, Protéines associées à l'autophagie, Protéines de Saccharomyces cerevisiae, Protéines proto-oncogènes.
- métabolisme : Azote, DEAD-box RNA helicases, Facteurs de transcription, Protein kinases, Protein-Serine-Threonine Kinases, Protéines adaptatrices de la transduction du signal, Protéines associées à l'autophagie, Protéines de Saccharomyces cerevisiae, Protéines proto-oncogènes, Saccharomyces cerevisiae.
- physiologie : Autophagie.
- Cellules HEK293, Humains, Liaison aux protéines, Phosphorylation.
English descriptors
- KwdEn :
- Adaptor Proteins, Signal Transducing (genetics), Adaptor Proteins, Signal Transducing (metabolism), Autophagy (physiology), Autophagy-Related Proteins (genetics), Autophagy-Related Proteins (metabolism), DEAD-box RNA Helicases (genetics), DEAD-box RNA Helicases (metabolism), HEK293 Cells (MeSH), Humans (MeSH), Nitrogen (deficiency), Nitrogen (metabolism), Phosphorylation (MeSH), Protein Binding (MeSH), Protein Kinases (genetics), Protein Kinases (metabolism), Protein-Serine-Threonine Kinases (metabolism), Proto-Oncogene Proteins (genetics), Proto-Oncogene Proteins (metabolism), Saccharomyces cerevisiae (metabolism), Saccharomyces cerevisiae Proteins (genetics), Saccharomyces cerevisiae Proteins (metabolism), Transcription Factors (metabolism).
- MESH :
- chemical , deficiency : Nitrogen.
- chemical , genetics : Adaptor Proteins, Signal Transducing, Autophagy-Related Proteins, DEAD-box RNA Helicases, Protein Kinases, Proto-Oncogene Proteins, Saccharomyces cerevisiae Proteins.
- chemical , metabolism : Adaptor Proteins, Signal Transducing, Autophagy-Related Proteins, DEAD-box RNA Helicases, Nitrogen, Protein Kinases, Protein-Serine-Threonine Kinases, Proto-Oncogene Proteins, Saccharomyces cerevisiae Proteins, Transcription Factors.
- metabolism : Saccharomyces cerevisiae.
- physiology : Autophagy.
- HEK293 Cells, Humans, Phosphorylation, Protein Binding.
Abstract
Macroautophagy (hereafter autophagy) is a well-conserved cellular process through which cytoplasmic components are delivered to the vacuole/lysosome for degradation and recycling. Studies have revealed the molecular mechanism of transcriptional regulation of autophagy-related (ATG) genes upon nutrient deprivation. However, little is known about their translational regulation. Here, we found that Dhh1, a DExD/H-box RNA helicase, is required for efficient translation of Atg1 and Atg13, two proteins essential for autophagy induction. Dhh1 directly associates with ATG1 and ATG13 mRNAs under nitrogen-starvation conditions. The structured regions shortly after the start codons of the two ATG mRNAs are necessary for their translational regulation by Dhh1. Both the RNA-binding ability and helicase activity of Dhh1 are indispensable to promote Atg1 translation and autophagy. Moreover, eukaryotic translation initiation factor 4E (EIF4E)-associated protein 1 (Eap1), a target of rapamycin (TOR)-regulated EIF4E binding protein, physically interacts with Dhh1 after nitrogen starvation and facilitates the translation of Atg1 and Atg13. These results suggest a model for how some ATG genes bypass the general translational suppression that occurs during nitrogen starvation to maintain a proper level of autophagy.
DOI: 10.1371/journal.pbio.3000219
PubMed: 30973873
PubMed Central: PMC6459490
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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<front><div type="abstract" xml:lang="en">Macroautophagy (hereafter autophagy) is a well-conserved cellular process through which cytoplasmic components are delivered to the vacuole/lysosome for degradation and recycling. Studies have revealed the molecular mechanism of transcriptional regulation of autophagy-related (ATG) genes upon nutrient deprivation. However, little is known about their translational regulation. Here, we found that Dhh1, a DExD/H-box RNA helicase, is required for efficient translation of Atg1 and Atg13, two proteins essential for autophagy induction. Dhh1 directly associates with ATG1 and ATG13 mRNAs under nitrogen-starvation conditions. The structured regions shortly after the start codons of the two ATG mRNAs are necessary for their translational regulation by Dhh1. Both the RNA-binding ability and helicase activity of Dhh1 are indispensable to promote Atg1 translation and autophagy. Moreover, eukaryotic translation initiation factor 4E (EIF4E)-associated protein 1 (Eap1), a target of rapamycin (TOR)-regulated EIF4E binding protein, physically interacts with Dhh1 after nitrogen starvation and facilitates the translation of Atg1 and Atg13. These results suggest a model for how some ATG genes bypass the general translational suppression that occurs during nitrogen starvation to maintain a proper level of autophagy.</div>
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<Abstract><AbstractText>Macroautophagy (hereafter autophagy) is a well-conserved cellular process through which cytoplasmic components are delivered to the vacuole/lysosome for degradation and recycling. Studies have revealed the molecular mechanism of transcriptional regulation of autophagy-related (ATG) genes upon nutrient deprivation. However, little is known about their translational regulation. Here, we found that Dhh1, a DExD/H-box RNA helicase, is required for efficient translation of Atg1 and Atg13, two proteins essential for autophagy induction. Dhh1 directly associates with ATG1 and ATG13 mRNAs under nitrogen-starvation conditions. The structured regions shortly after the start codons of the two ATG mRNAs are necessary for their translational regulation by Dhh1. Both the RNA-binding ability and helicase activity of Dhh1 are indispensable to promote Atg1 translation and autophagy. Moreover, eukaryotic translation initiation factor 4E (EIF4E)-associated protein 1 (Eap1), a target of rapamycin (TOR)-regulated EIF4E binding protein, physically interacts with Dhh1 after nitrogen starvation and facilitates the translation of Atg1 and Atg13. These results suggest a model for how some ATG genes bypass the general translational suppression that occurs during nitrogen starvation to maintain a proper level of autophagy.</AbstractText>
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<name sortKey="Lee, Jun Hee" sort="Lee, Jun Hee" uniqKey="Lee J" first="Jun Hee" last="Lee">Jun Hee Lee</name>
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