Fig. 3.

Model for the functionality of PARP and NAD in stress signaling. Stress provokes an increase of NAD⁺ in hpAtPARP2 plants. By the action of the ADP-ribosyl cyclase, NAD⁺ might be converted to cADPR. Repetitive Ca²⁺ peaks trigger the biosynthesis of ABA, activating ABA-responsive and stress-protective genes. In addition, ABA could positively regulate the activity of ADP-ribosyl cyclase, providing a relay mechanism that might amplify the original cADPR signal. Other pathways possibly involved in mediating stress tolerance are indicated in gray. The relative contribution of each pathway to the final stress tolerance is not known and might depend on the nature and severity of the stress.