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Abstract
To examine the effect of mitochondrial function on photosynthesis, wild-type and transgenic
Nicotiana tabacum with varying amounts of alternative oxidase (AOX) were treated with
different respiratory inhibitors. Initially, each inhibitor increased the reduction
state of the chloroplast electron transport chain, most severely in AOX knockdowns
and least severely in AOX overexpressors. This indicated that the mitochondrion was
a necessary sink for photo-generated reductant, contributing to the 'P700 oxidation
capacity' of photosystem I. Initially, the Complex III inhibitor myxothiazol and the
mitochondrial ATP synthase inhibitor oligomycin caused an increase in photosystem
II regulated non-photochemical quenching not evident with the Complex III inhibitor
antimycin A (AA). This indicated that the increased quenching depended upon AA-sensitive
cyclic electron transport (CET). Following 12 h with oligomycin, the reduction state
of the chloroplast electron transport chain recovered in all plant lines. Recovery
was associated with large increases in the protein amount of chloroplast ATP synthase
and mitochondrial uncoupling protein. This increased the capacity for photophosphorylation
in the absence of oxidative phosphorylation and enabled the mitochondrion to act again
as a sink for photo-generated reductant. Comparing the AA and myxothiazol treatments
at 12 h showed that CET optimized photosystem I quantum yield, depending upon the
P700 oxidation capacity. When this capacity was too high, CET drew electrons away
from other sinks, moderating the P700+ amount. When P700 oxidation capacity was too
low, CET acted as an electron overflow, moderating the amount of reduced P700. This
study reveals flexible chloroplast-mitochondrion interactions able to overcome lesions
in energy metabolism.
[1
]Department of Biological Sciences Department of Cell and Systems Biology University
of Toronto Scarborough 1265 Military Trail Toronto ONM1C1A4Canada