From the articles:
"Cyanobacteriochrome CcaS is the green light receptor that induces the expression of phycobilisome linker protein"
- A putative cyanobacteriochrome, CcaS, is known to chromatically regulate the expression of the [phycobilisome] linker gene (cpcG2).
- Reversible photoconversion between a green-absorbing form (Pg, λmax = 535 nm) and a red-absorbing form (Pr, λmax = 672 nm).
- Expression of phycobilisome linker gene cpcG2 has been reported to be chromatically regulated by a cyanobacteriochrome gene, ccaS , and a response regulator gene, ccaR ,in Synechocystis sp. PCC 6803 (24). CcaR directly binds to the promoter region of cpcG2.
- The autophosphorylation of CcaS and the phosphotransfer to CcaR are up-regulated by green light.
- These results suggest that CcaS phosphorylates CcaR under green light, which may change the DNA-binding affinity of CcaR. Phosphorylated CcaR would bind to the promoter region of cpcG2 and activate its transcription.
- The green-light-induced expression of cpcG2 can be interpreted as the accumulation of CpcG2-PBS to compensate for the reduced light harvesting by photosystem I chlorophylls because the green light excites PBS more efficiently than chlorophylls. Thus, the chromatic regulation of CpcG2-PBS by CcaS and CcaR enables Synechocystis to coordinate the excitation of the two photosystems to efficiently drive linear electron transport.
"Cyanobacteriochrome CcaS regulates phycoerythrin accumulation in Nostoc punctiforme, a group II
- ccaS green/red-perceiving histidine-kinase gene
- Under green ligth, wild-type cells accumulated a significant amount of PE (phycoerythrin)
- CcaS phosphorylates CcaR under green light and that phosphorylated CcaR then induces cpeC-cpcG2-cpeR1 expression, leading to PE accumulation.
- CcaS enhances phosphorylation activity upon GL irradiation.
- CcaS directly transfers phosphates to the OmpR-class response regulator (CcaR) in vitro
- It should be noted that the PE peak never completely dissapeares under RL, even after full acclimation [N. punctiforme].
- Operon of PE (cpeB-cpeA) was 2.5-fold higher under GL than under RL
- Deletion of ccaR resulted in complete loss of GL-induced cpeC-cpcG2-cpeR1 expression.
- CcaR protein specifically binds upstream of this operon. It directly binds to the G-box [CTTTNCNATTT]x2 in the promoter of cpeC-cpcG2-cpeR1 and regulates its expression.
- CcaS regulates cpeC-cpcG2-cpeR1 expression via phosphorylation of CcaR (transcriptional activator).
- It is speculated that the conserved G-box motif enables the specific interaction between CcaR and the cpeC-cpcG2-cpeR1 promoter.
- The phosphorylated state of CcaR is responsible for activation of cpeC-cpcG2-cpeR1 expression.
- CcaS-independent but CcaR-dependent pathway constitutively activates cpeC-cpcG2-cpeR1. It expression was supressed in wild type under RL.
- CcaS not only phosphorylates CcaR under GL but also dephosphorylates CcaR under RL.