These findings suggested to us that the process of photodamage might not depend on the rate of electron transport.
We also examined the effects of the synthesis of ATP on photodamage in Synechocystis by monitoring such damage in the presence of lincomycin [44]. We found that the rate of photodamage, which was proportional to light intensity, was
unaffected by the inhibition of ATP synthesis by N,N-dicyclohexylcarbodiimide
(DCCD) or by a combination of nigericin and valinomycin (Nig/Val). All these findings suggested that the process of photodamage depended neither on the rate of electron
transport nor on the intracellular level of ATP [44].
Several approaches have been used in attempts to characterize
the roles of electron transport and the synthesis of ATP in the
synthesis of the D1 protein. However, the results have been
controversial. Mattoo et al. [45] suggested that both electron
transport and the synthesis of ATP are important for the
synthesis of D1 in Spirodela oligorrhiza. In Chlamydomonas
reinhardtii, Trebitsh and Danon [46] showed that the redox
signal associated with electron transport in PSI, as well as
reduction of the plastoquinone pool, activated the initiation of
translation of psbA transcripts. Studies in intact chloroplasts
from spinach showed that the level of stromal ATP was
correlated with the light-dependent synthesis of the D1 protein
in intact chloroplasts [47]. Furthermore, Kuroda et al. [48]
further demonstrated that electron transport via PSI was
essential for the light-dependent translational elongation of
the D1 protein. By contrast, Mühlbauer and Eichacker [49]
suggested that a proton gradient, formed as a result of electron
transport, might be important for the light-dependent translational
elongation of the D1 protein in intact chloroplasts from
barley. Thus, it seemed likely that electron transport and/or the
synthesis of ATP might be required for the light-induced
synthesis of the D1 protein. However, the direct effects of
electron transport and the synthesis of ATP on the repair of PSII
remained to be investigated.
We examined the effects of electron transport and the
synthesis of ATP on the initial rate of repair of PSII in Synechocystis
[44]. The rate of repair was diminished upon inhibition
of the synthesis of ATP regardless of the type of electron
transport involved, namely, that in PSI, which was accelerated
by PMS, and that in PSII, which was inhibited by DCMU. It is
likely that an adequate intracellular level of ATP is essential for
repair [44]. Mühlbauer and Eichacker [49] reported that the
stimulation by light of translational elongation depended on the
formation of a proton gradient across the thylakoid membrane.
However, our observation that DCCD abolished the repair of
PSII suggested that it is the level of ATP, rather than a proton
gradient, that is essential for the repair of PSII.
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