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Circadian clocks in fungi and animals are driven by a functionally conserved transcription–translation feedback loop. In  Neurospora crassa , negative feedback is executed by a complex of Frequency (FRQ), FRQ-interacting RNA helicase (FRH), and casein kinase I (CKI), which inhibits the activity of the clock’s positive arm, the White Collar Complex (WCC). Here, we show that the  prd-2  ( period-2 ) gene, whose mutation is characterized by recessive inheritance of a long 26 hr period phenotype, encodes an RNA-binding protein that stabilizes the  ck-1a  transcript, resulting in CKI protein levels sufficient for normal rhythmicity. Moreover, by examining the molecular basis for the short circadian period of  upf-1 prd-6   mutants, we uncovered a strong influence of the Nonsense-Mediated Decay pathway on CKI levels. The finding that circadian period defects in two classically derived Neurospora clock mutants each arise from disruption of  ck-1a  regulation is consistent with circadian period being exquisitely sensitive to levels of  casein kinase I .

PRD-2 directly regulates casein kinase I and counteracts nonsense-mediated decay in the Neurospora circadian clock