Mutants in theperiod-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 ofprd-1 and used whole genome sequencing to find the mutation defining it, confirming the identity ofprd-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. Althoughprd-1 mutants display a long period (∼25 h) circadian developmental cycle, they interestingly display a WT period when the core circadian oscillator is tracked using afrq-luciferase transcriptional fusion under conditions of limiting nutritional carbon; the core oscillator in theprd-1 mutant strain runs with a long period under glucose-sufficient conditions. Thus, PRD-1 clearly impacts the circadian oscillator and is not only part of a metabolic oscillator ancillary to the core clock. PRD-1 is an essential protein, and its expression is neither light-regulated nor clock-regulated. However, it is transiently induced by glucose; in the presence of sufficient glucose, PRD-1 is in the nucleus until glucose runs out, which elicits its disappearance fromthe nucleus. Because circadian period length is carbon concentration-dependent,prd-1 may be formally viewed as a clock mutant with defective nutritional compensation of circadian period length.