The Neurospora crassa circadian clock is based on a highly regulated molecular negative feedback loop, similar to molecular clocks in all eukaryotes. A core component of the N. crassa molecular clock is the White Collar complex (WCC), composed of the blue light photoreceptor WC-1 and its partner WC-2. The WCC serves as a master regulator that controls light signaling, and the precise timing of target gene expression. Up to 40% of the eukaryote genome is under the control of the clock at the level of transcript abundance, but the molecular links between the core oscillator and downstream target genes, as well as the mechanisms controlling the phase of rhythmic gene expression, are not understood. Using chromatin immunoprecipitation coupled to high-throughput sequencing (ChIP-seq), about 400 binding sites for the WCC were identified throughout the N. crassa genome. We found that 24 transcription factors (TFs) were significantly enriched among the direct WCC target genes. As expected for genes that are controlled by the WCC, the first-tier TFs are both clock- and light-regulated. These data led to the hypothesis that the WCC functions to control rhythms in TFs, which in turn control rhythmicity and phase of downstream target genes and processes. To test this hypothesis, the first-tier TF ADV-1 (Arrested Development-1) was investigated in detail to characterize the downstream circadian genetic network. ADV-1 target genes were identified using ChIP- and RNA-seq, and as expected many ADV-1 downstream target genes were light-responsive and/or clock-controlled. An enrichment for ADV-1 target genes involved in cell fusion, a process that is critical for normal vegetative and sexual development in N. crassa, provided a rationale for the observed developmental defects in ADV-1 deletion cells, and suggested that cell fusion is clock-controlled. Importantly, this work revealed that the transduction of time-of-day information through ADV-1 to its downstream targets is more complex than anticipated. Specifically, I show that deletion of ADV-1 does not always lead to predicted changes in rhythmic gene expression and/or phase, suggesting that ADV-1 functions in combination with other first-tier TFs to control rhythmicity. In support of this idea, genome-wide binding profiles of all of the first-tier TFs uncovered complex feedback and feed forward regulation involving ADV-1. Thus, my data revealed that in order to fully understand how the clock signals phase information to downstream targets, we need to go beyond the candidate gene approach, and instead develop computational models from our TF ChIP-seq and rhythmic transcriptome data to model how time of day information is transduced in the molecular circadian output gene network. Predictions of the model can then be validated using ADV-1 deletion cells alone, or in combination with deletion of other first-tier TFs in the network, with the goal of deriving design principles that define conserved aspects of the circadian output network in all eukaryotes, and important in human health. To test this hypothesis, the first-tier TF ADV-1 (Arrested Development-1) was investigated in detail to characterize the downstream circadian genetic network. ADV-1 target genes were identified using ChIP- and RNA-seq, and as expected many ADV-1 downstream target genes were light-responsive and/or clock-controlled. An enrichment for ADV-1 target genes involved in cell fusion, a process that is critical for normal vegetative and sexual development in N. crassa, provided a rationale for the observed developmental defects in ADV-1 deletion cells, and suggested that cell fusion is clock- controlled. Importantly, this work revealed that the transduction of time-of-day information through ADV-1 to its downstream targets is more complex than anticipated. Specifically, I show that deletion of ADV-1 does not always lead to predicted changes in rhythmic gene expression and/or phase, suggesting that ADV-1 functions in combination with other first-tier TFs to control rhythmicity. In support of this idea, genome-wide binding profiles of all of the first-tier TFs uncovered complex feedback and feed forward regulation involving ADV-1. Thus, my data revealed that in order to fully understand how the clock signals phase information to downstream targets, we need to go beyond the candidate gene approach, and instead develop computational models from our TF ChIP-seq and rhythmic transcriptome data to model how time of day information is transduced in the molecular circadian output gene network. Predictions of the model can then be validated using ADV-1 deletion cells alone, or in combination with deletion of other first-tier TFs in the network, with the goal of deriving design principles that define conserved aspects of the circadian output network in all eukaryotes, and important in human health. The electronic version of this dissertation is accessible from http://hdl.handle.net/1969.1/155195