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Significance Complex cellular phenotypes are dependent upon a large underlying network of genes. Determining the number of interacting genes, the nature of their interactions, and the robustness of their encompassing network to cellular and genomic perturbations is important for understanding how genotype determines phenotype. Here, we approached these questions in the cyanobacterial circadian gene network by knocking out circadian input kinase A (cikA ), a gene involved in synchronizing and relaying temporal signals within the cell, and screening for second-site suppressor mutations that rescue the severely alteredcikA- null circadian phenotype. We identified two independent mutations insasA (Synechococcus adaptive sensor A), a known clock-associated gene, that restore normal rhythms. These results change our conception of the circadian gene network architecture and show how easily the network can adapt to severe perturbations.

Single mutations in sasA enable a simpler Δ cikA gene network architecture with equivalent circadian properties