Abstract
A transient in chlorophyll fluorescence after cessation of actinic light illumination was re-investigated in Arabidopsis. It has been ascribed to electron donation from stromal reductants to plastoquinone (PQ) by the NAD(P)H dehydrogenase (NDH) complex, because the transient was absent in tobacco transformants with an inactivated plastid-encoded ndh gene. By using mutants lacking either the NDH complex (ndhM) or a PGR5 protein being proposed to mediate electron donation from stromal reductants to PQ via the ferredoxin (Fd)-dependent pathway (pgr5), it was shown that the PGR5- or Fd-dependent electron donation is also capable of inducing transient increase in the post-illumination chlorophyll fluorescence. The transient increase was found to be enhanced in a mutant impaired in plastid fructose-1,6-bisphosphate aldolase (FBA) activity. Analyses of the mutant, termed fba3-1, reveaed that the transient signal in the wild type can be ascribed to imbalance between activities of electron transport in the thylakoid and the Calvin cycle.
