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from singlet oxygen is observed in a mutant that is not able to quickly degrade
the D1 protein. On the contrary, in a mutant strain in which degradation of
D1 takes place quickly, chlorophylls bleaching is very little, if any. On the
basis of these and other experimental evidences, it is proposed that triggering
of D1 degradation is not necessarily associated to an oxidative damage, which
makes it a substrate for the proteolytic activity but, provided that the D1
subunit is maintained in the right conformation, the protein is simply turned
over and replaced by the so-called “repair cycle” at a rate which is regulated
by the redox state of the chloroplast. When the excitation supply exceeds
the rate at which carbon dioxide can be fixed by the Calvin-Benson cycle,
the reduction level increases and the DegP-FtsH proteases are activated to
degrade D1. This mechanism ensure a protection to PSII before the oxidative
damage by activated species of oxygen takes place.
It is like the case of a prudent car driver who decides to substitute its
car tires after a given number of kilometers rather than waiting for them to
blow up.
In this view, continuous degradation and resynthesis of D1 is the price
the chloroplast must pay to preserve a very complex and delicate machinery,
which is able to perform the redox chemistry that is fundamental for all forms
of life on the biosphere.
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