My research focuses on the regulation of the cpeCDESTR operon in the freshwater cyanobacterium Fremyella diplosiphon. Regulation and proper expression of this operon is important for a number of reasons. Under green light conditions the outer rods of phycobilisomes in F. diplosiphon contain phycoerythrin and its associated linker proteins. The cpeC operon encodes these linker proteins that perform structural and energy transfer roles, allowing phycobilisomes to transfer absorbed light energy to the photosynthetic reaction centers. In addition, a small protein encoded at the end of the operon (cpeR) play a critical role in CCA. CpeR is an activator that is both necessary and sufficient for the expression of a number of green-light expressed genes including cpeBA (encoding for phycoerythrin subunits) and pebAB. This suggests a serial model of gene regulation, where cpeC expression in induced in green light conditions, leading to expression of cpeR. CpeR then activates transcription of the other green-light induced genes.
At least two separate photosensory systems, the Rca and the Cgi systems, control the process of CCA and the regulation of cpeC. The Rca system consists of a multistep two-component phosphorelay that controls red light gene induction and has an inhibitory effect on green-light induced genes under red light conditions. My research and the work of others in the lab has shown that the transcription factor at the end of this phosphorelay, RcaC, binds to a DNA element we have called the L-box within promoters of both red-light induced genes and cpeC to simultaneously activate the transcription of red light genes while repressing transcription of cpeC. However, the RcaC-mediated repression of cpeC accounts for only a portion of its fold induction in red and green light; the rest mediated by the Cgi system. The components of the Cgi system remain unknown at this time, but my research indicates that this system functions by further repressing cpeC in red light conditions and acts through the 5’ leader sequence, possibly by post-transcriptional regulation.
I am currently attempting to better define the mechanisms by which both the Rca and Cgi systems repress cpeC expression in red light and to identify components of the Cgi system via a mutant screen. These experiments have and will continue to add to our understanding of CCA and prokaryotic signal transduction in general.