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Plant Physiology Preview Published on May 5, 2006; 10.1104/pp.106.081059
Received March 28, 2006 Defects in the cytochrome b6/f complex prevent light-induced expression of nuclear genes involved in chlorophyll biosynthesis
Institut fuer Biologie III, Universitaet Freiburg, Schaenzlestrasse 1, D-79104 Freiburg, Germany * Corresponding author; email: beck{at}uni-freiburg.de.
Mutants with defects in the cytb6/f complex were analyzed for their effect on the expression of a subgroup of nuclear genes encoding plastid localized enzymes participating in chlorophyll biosynthesis. Their defects ranged from complete loss of the cytb6/f complex to point mutations affecting specifically the quinone-binding QO site. In these 7 mutants, light induction of the tetrapyrrole biosynthetic genes was either abolished or strongly reduced. In contrast, a normal induction of chlorophyll biosynthesis genes was observed in mutants with defects in photosystem II, photosystem I or plastocyanin, or in wild-type cells treated with DCMU or DBMIB. We conclude that the redox state of the plastoquinone pool does not control light induction of these chlorophyll biosynthetic genes. The signal that affects expression of the nuclear genes appears to solely depend on the integrity of the cytb6/f complex QO site. Since light induction of these genes in Chlamydomonas has recently been shown to involve the blue light receptor phototropin, the results suggest that cytochrome b6/f activity regulates a plastid-derived factor required for their expression. This signaling pathway differs from that which regulates state transitions, since mutant stt7, lacking a protein kinase involved in phosphorylation of the light harvesting complex II, was not altered in the expression of the chlorophyll biosynthetic genes.
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