Abstract

Peroxisomes are subcellular organelles with multiple functions mediated by their plasticity and dynamic behavior in plants. Changes in their shape, size, number and enzyme content occur in response to developmental and metabolic cues as well as environmental conditions. The number of peroxisomes per cell is thus mainly determined by its capacity to proliferate. In mammals, peroxisome proliferators such as the hypolipidemic drug clofibrate are perceived by the Peroxisome Proliferator-Activated Receptors (PPARs) nuclear receptors. Therein, activated transcription of the peroxisome biogenesis PEX11 genes and the recruitment of dynamin-related proteins lead to peroxisome proliferation. We recently reported that Arabidopsis thaliana, despite of lacking a PPAR homolog protein, activated the proliferation of peroxisomes in response to clofibrate. Concomitantly, clofibrate activated the expression of wound-responsive genes through the jasmonic acid signaling master regulator COI1 F-box protein. Besides, wounding activated the expression of the peroxisome biogenesis-related PEX1 and PEX14 genes, but not of PEX11 or DRP3A, which analogously to mammals, code for the main regulators of peroxisome proliferation in Arabidopsis. Thus, wounding did not activate peroxisome proliferation. Noteworthy, jasmonic acid-treated plants contained fewer but larger peroxisomes. Despite of the cross-talk between clofibrate- and wound-induced signaling, the proliferation of peroxisomes and the wound-activated defense remained uncoupled.

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