{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Emerson JM"],"funding":["HHS | NIH | National Institute of General Medical Sciences","NIGMS NIH HHS"],"pagination":["15707-12"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4697410"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["112(51)"],"pubmed_abstract":["Mutants in the period-1 (prd-1) gene, characterized by a recessive allele, display a reduced growth rate and period lengthening of the developmental cycle controlled by the circadian clock. We refined the genetic location of prd-1 and used whole genome sequencing to find the mutation defining it, confirming the identity of prd-1 by rescuing the mutant circadian phenotype via transformation. PRD-1 is an RNA helicase whose orthologs, DDX5 [DEAD (Asp-Glu-Ala-Asp) Box Helicase 5] and DDX17 in humans and DBP2 (Dead Box Protein 2) in yeast, are implicated in various processes, including transcriptional regulation, elongation, and termination, ribosome biogenesis, and mRNA decay. Although prd-1 mutants display a long period (∼25 h) circadian developmental cycle, they interestingly display a WT pe"],"journal":["Proceedings of the National Academy of Sciences of the United States of America"],"pubmed_title":["period-1 encodes an ATP-dependent RNA helicase that influences nutritional compensation of the Neurospora circadian clock."],"pmcid":["PMC4697410"],"funding_grant_id":["R01 GM034985","R01 GM083336","GM34985","GM083336","R37 GM034985","R35 GM118021"],"pubmed_authors":["Emerson JM","Dunlap JC","Ringelberg CS","Loros JJ","Bartholomai BM","Baker SE"],"additional_accession":[]},"is_claimable":false,"name":"period-1 encodes an ATP-dependent RNA helicase that influences nutritional compensation of the Neurospora circadian clock.","description":"Mutants in the period-1 (prd-1) gene, characterized by a recessive allele, display a reduced growth rate and period lengthening of the developmental cycle controlled by the circadian clock. We refined the genetic location of prd-1 and used whole genome sequencing to find the mutation defining it, confirming the identity of prd-1 by rescuing the mutant circadian phenotype via transformation. PRD-1 is an RNA helicase whose orthologs, DDX5 [DEAD (Asp-Glu-Ala-Asp) Box Helicase 5] and DDX17 in humans and DBP2 (Dead Box Protein 2) in yeast, are implicated in various processes, including transcriptional regulation, elongation, and termination, ribosome biogenesis, and mRNA decay. Although prd-1 mutants display a long period (∼25 h) circadian developmental cycle, they interestingly display a WT pe","dates":{"release":"2015-01-01T00:00:00Z","publication":"2015 Dec","modification":"2025-04-19T17:51:59.398Z","creation":"2019-08-04T07:55:56Z"},"accession":"S-EPMC4697410","cross_references":{"pubmed":["26647184"],"doi":["10.1073/pnas.1521918112"]}}