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In recent years, it has become increasingly apparent that antisense transcription plays an important role in the regulation of gene expression. The circadian clock is no exception: an antisense transcript of the mammalian core-clock gene  PERIOD2 (PER2) , which we shall refer to as  Per2AS  RNA, oscillates with a circadian period and a nearly 12 h phase shift from the peak expression of  Per2  mRNA. In this paper, we ask whether  Per2AS  plays a regulatory role in the mammalian circadian clock by studying  in silico  the potential effects of interactions between  Per2  and  Per2AS  RNAs on circadian rhythms. Based on the antiphasic expression pattern, we consider two hypotheses about how  Per2  and  Per2AS  mutually interfere with each other's expression. In our  pre-transcriptional  model, the transcription of  Per2AS  RNA from the non-coding strand represses the transcription of  Per2  mRNA from the coding strand and  vice versa . In our  post-transcriptional  model,  Per2  and  Per2AS  transcripts form a double-stranded RNA duplex, which is rapidly degraded. To study these two possible mechanisms, we have added terms describing our alternative hypotheses to a published mathematical model of the molecular regulatory network of the mammalian circadian clock. Our  pre-transcriptional  model predicts that transcriptional interference between  Per2  and  Per2AS  can generate alternative modes of circadian oscillations, which we characterize in terms of the amplitude and phase of oscillation of core clock genes. In our  post-transcriptional  model,  Per2 / Per2AS  duplex formation dampens the circadian rhythm. In a model that combines  pre-  and  post-transcriptional  controls, the period, amplitude and phase of circadian proteins exhibit non-monotonic dependencies on the rate of expression of  Per2AS . All three models provide potential explanations of the observed antiphasic, circadian oscillations of  Per2  and  Per2AS  RNAs. They make discordant predictions that can be tested experimentally in order to distinguish among these alternative hypotheses.

Modeling the interactions of sense and antisense Period transcripts in the mammalian circadian clock network