FIG. 4.—

The proposed chloroplast signal transduction pathway coupling the redox state of the photosynthetic electron carrier plastoquinone in the chloroplast thylakoid membrane with initiation of transcription of chloroplast DNA at the promoter regions of the genes psa (encoding reaction center proteins of photosystem I) and psb (encoding reaction center proteins of photosystem II). (A) Under light 1, a rate-limiting low light selective for photosystem I, electron flow through photosystem I (PS I) has a greater potential than that through photosystem II (PS II), and so PQ pool is maintained in its oxidized form. CSK is autophosphorylated and active as a protein kinase using both SIG-1 and PTK as substrates: SIG-1 and PTK are thus maintained in their phosphorylated forms. Phospho-SIG-1 represses transcription at the psa promoter while allowing transcription of psb genes. Phospho-PTK is inactive; therefore, it cannot suppress chloroplast transcription nonspecifically, and under this circumstance, only CSK-mediated—via phospho-SIG-1—specific repression of psa genes occurs. This differential reaction center gene transcription increases the stoichiometry of photosystem II relative to photosystem I. (B) Under light 2, a rate-limiting low light selective for photosystem II, electron flow through photosystem I (PS I) has a lower potential than that through photosystem II (PS II), and so PQ pool is maintained in its reduced form (PQH₂). CSK is inactive as a protein kinase. The repression of psa genes, occurred during light 1, is now relieved by the action of a PEP phosphatase that catalyzes dephosphorylation of phospho-SIG-1. As a result, PS I transcription increases. Under this light condition, PTK is active as a protein kinase acting on subunits of PEP. However, the action of PEP phosphatase overrides PTK activity by dephosphorylating both SIG-1 as well as PEP subunits so that nonspecific repression of reaction center genes is counteracted. The increase in photosystem I transcription in light 2, therefore, leads to an increase in photosystem I units relative to photosystem II.