{"database":"biostudies-literature","file_versions":[],"scores":{"citationCount":0,"reanalysisCount":0,"viewCount":52,"searchCount":0},"additional":{"submitter":["Liu X"],"funding":["National Institute of Diabetes and Digestive and Kidney Diseases","NIDDK NIH HHS","National Institute of General Medical Sciences","NIGMS NIH HHS"],"pagination":["e3000219"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6459490"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["17(4)"],"pubmed_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."],"journal":["PLoS biology"],"pubmed_title":["Dhh1 promotes autophagy-related protein translation during nitrogen starvation."],"pmcid":["PMC6459490"],"funding_grant_id":["P30 DK020572","R01 GM053396","GM053396","DK114131","R01 DK114131"],"pubmed_authors":["Liu X","Yao Z","Jin M","Klionsky DJ","Namkoong S","Yin Z","Lee JH"],"view_count":["52"],"additional_accession":[]},"is_claimable":false,"name":"Dhh1 promotes autophagy-related protein translation during nitrogen starvation.","description":"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.","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019 Apr","modification":"2024-02-15T03:38:14.924Z","creation":"2019-06-06T23:05:29Z"},"accession":"S-EPMC6459490","cross_references":{"pubmed":["30973873"],"doi":["10.1371/journal.pbio.3000219"]}}