<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Emerson JM</submitter><funding>HHS | NIH | National Institute of General Medical Sciences</funding><funding>NIGMS NIH HHS</funding><pagination>15707-12</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4697410</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>112(51)</volume><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</pubmed_abstract><journal>Proceedings of the National Academy of Sciences of the United States of America</journal><pubmed_title>period-1 encodes an ATP-dependent RNA helicase that influences nutritional compensation of the Neurospora circadian clock.</pubmed_title><pmcid>PMC4697410</pmcid><funding_grant_id>R01 GM034985</funding_grant_id><funding_grant_id>R01 GM083336</funding_grant_id><funding_grant_id>GM34985</funding_grant_id><funding_grant_id>GM083336</funding_grant_id><funding_grant_id>R37 GM034985</funding_grant_id><funding_grant_id>R35 GM118021</funding_grant_id><pubmed_authors>Emerson JM</pubmed_authors><pubmed_authors>Dunlap JC</pubmed_authors><pubmed_authors>Ringelberg CS</pubmed_authors><pubmed_authors>Loros JJ</pubmed_authors><pubmed_authors>Bartholomai BM</pubmed_authors><pubmed_authors>Baker SE</pubmed_authors></additional><is_claimable>false</is_claimable><name>period-1 encodes an ATP-dependent RNA helicase that influences nutritional compensation of the Neurospora circadian clock.</name><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</description><dates><release>2015-01-01T00:00:00Z</release><publication>2015 Dec</publication><modification>2025-04-19T17:51:59.398Z</modification><creation>2019-08-04T07:55:56Z</creation></dates><accession>S-EPMC4697410</accession><cross_references><pubmed>26647184</pubmed><doi>10.1073/pnas.1521918112</doi></cross_references></HashMap>