Role of Poly(ADP-Ribose) Polymerase (PARP) Enzyme in the Systemic Acquired Acclimation Induced by Light Stress in Phaseolus vulgaris L. Plants

Plants are able to acclimate to environmental constraints through functional modifications that may also occur in tissues that are not directly exposed to stress. This process is termed “systemic acquired acclimation.” The present study aims to evaluate the involvement of PolyADP-ribose) polymerase (PARP) protein in the acclimation process to high light (HL) stress in Phaseolus vulgaris plants. For this purpose, some leaves located at the top of the plant, in the apical position, were directly exposed to HL (“inducing” leaves), while others on the same plant, distal from the top, continued to be exposed to growth light (“receiving” leaves) to verify the hypothesis that an “alert” message may be transferred from injured tissues to distal ones. Biochemical and eco-physiological analyses, namely PARP activity, H(2)O(2) and water- and fat-soluble antioxidants (i.e., ascorbic acid, tocopherol, glutathione (GSH), phenols, carotenoids, etc.) content, and chlorophyll fluorescence measurements were performed on both “inducing” and “receiving” leaves. Even if no change in PARP expression was found, its activity increased in “receiving” unstressed leaves in response to the light stress duration experimented by “inducing” leaves, while antioxidant capacity declined. When the “receiving” leaves were exposed to HL, the PARP activity returned to the control value, while antioxidant capacity photosynthetic electron transport rate (J(f)) decreased and increased, respectively, compared to Control. Our results seem to show an acclimation pathway triggered in remote tissues not yet subjected to stress, likely involving a reactive oxygen species wave activating the PARP enzyme in a mechanism still to be clarified. In addition, the increased tolerance of plants directly exposed to HL could implicate a boosted synthesis of soluble antioxidants accompanied by a reduction of PARP activity to reduce excessive consumption of NAD(P).