To better understand host-phage interactions and the genetic bases of phage resistance in a model system relevant to potential phage therapy, we isolated several spontaneous mutants of the USA300 S. aureus clinical isolate NRS384 that were resistant to phage K. Six of these had a single missense mutation in the host rpoC gene, which encodes the RNA polymerase beta prime subunit. To examine the hypothesis that the mutations in the host RNA polymerase affect the transcription of phage genes, we performed RNA-seq analysis on total RNA samples collected from NRS384 wild-type (WT) and rpoC_G26D mutant cultures infected with phage K, at different time points post-infection. Infection of the WT host led to a steady increase of phage transcription relative to the host. Our analysis allowed us to define 55 transcriptional units and to define different early, middle, and late phage genes based on their temporal expression patterns. An examination of predicted promoter sequences revealed that those associated with late gene expression lacked a conserved -35 region, suggesting the involvement of a phage-encoded factor in the transcription of those genes. Infection of the rpoC_G26D mutant host led to a transcriptional pattern that was similar to the WT at early time points. However, beginning at 20 minutes post-infection, transcription of late genes, such as phage structural genes and host lysis genes, was severely reduced. Our data indicate that the rpoC_G26D mutant is deficient in proceeding to late phage gene expression, thus resulting in a failed infection cycle for phage K. In addition to providing a detailed view of the global transcriptional landscape of phage K throughout the infection cycle, these studies can begin to inform our studies into the mechanistic bases of phage K’s control of its transcriptional program.