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Abstract
<p class="first" id="d9820413e67">The plant mitochondrial electron transport chain
(ETC) is bifurcated such that electrons
from ubiquinol are passed to oxygen via the usual cytochrome path or through alternative
oxidase (AOX). We previously showed that knockdown of AOX in transgenic tobacco increased
leaf concentrations of nitric oxide (NO), implying that an activity capable of generating
NO had been effected. Here, we identify the potential source of this NO. Treatment
of leaves with antimycin A (AA, Qi -site inhibitor of Complex III) increased NO amount
more than treatment with myxothiazol (Myxo, Qo -site inhibitor) despite both being
equally effective at inhibiting respiration. Comparison of nitrate-grown wild-type
with AOX knockdown and overexpression plants showed a negative correlation between
AOX amount and NO amount following AA. Further, Myxo fully negated the ability of
AA to increase NO amount. With ammonium-grown plants, neither AA nor Myxo strongly
increased NO amount in any plant line. When these leaves were supplied with nitrite
alongside the AA or Myxo, then the inhibitor effects across lines mirrored that of
nitrate-grown plants. Hence the ETC, likely the Q-cycle of Complex III generates NO
from nitrite, and AOX reduces this activity by acting as a non-energy-conserving electron
sink upstream of Complex III.
</p>
[1
]Department of Biological Sciences and Department of Cell and Systems Biology; University
of Toronto Scarborough; 1265 Military Trail Toronto Ontario M1C1A4 Canada