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Abstract
Reactive oxygen species (ROS) production increases in plants under stress. ROS can
damage cellular components, but they can also act in signal transduction to help the
cell counteract the oxidative damage in the stressed compartment. H(2)O(2) might induce
a general stress response, but it does not have the required specificity to selectively
regulate nuclear genes required for dealing with localized stress, e.g. in chloroplasts
or mitochondria. Here we argue that peptides deriving from proteolytic breakdown of
oxidatively damaged proteins have the requisite specificity to act as secondary ROS
messengers and regulate source-specific genes and in this way contribute to retrograde
ROS signalling during oxidative stress. Likewise, unmodified peptides deriving from
the breakdown of redundant proteins could help coordinate organellar and nuclear gene
expression.