Single mutations in sasA enable a simpler Δ cikA gene network architecture with equivalent circadian properties
Abstract
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 altered cikA- null circadian phenotype. We identified two independent mutations in sasA ( 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.
Document Details
- Document Type
- Pub Defense Publication
- Publication Date
- Nov 10, 2014
- Source ID
- 10.1073/pnas.1419902111
Entities
People
- Joseph S. Boyd
- Ralph J. Greenspan
- Ryan K. Shultzaberger
- Susan Golden
- Takeo Katsuki
Organizations
- Army Research Office
- Office of Extramural Research
- University of California, San Diego
- W. M. Keck Foundation