American Society of Plant Biologists 
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Minisymposium 4: Oxidative stress

Abs # 14004: Poly(ADP-ribosyl)ation activity in plants affects energy homeostasis, cell death and stress tolerance

Presenter: De Block, Marc , marc.deblock@bayercropscience.com
AuthorsDe Block, Marc  (A)   Verduyn, Christoph  (A)   De Brouwer, Dirk  (A)   Cornelissen, Marc  (A)  
Affiliations: (A): Bayer BioScience N.V.

As animals plants metabolize polymers of ADP-ribose by means of the enzymes poly(ADP-ribose) polymerase (PARP) and poly(ADP-ribose) glycohydrolase (PARG). In plants two parp genes have been identified: parp1 and parp2. Most plant species, as corn, rice and potato, have only one parg gene. Both PARP1 and PARP2 are activated at the transcriptional and enzymatic level by DNA strand breaks caused by e.g. stress-induced radicals. By activation they synthesize polymers of ADP-ribose on a range of nuclear proteins using NAD+ as substrate. The negatively charged ADP-ribose polymers alter the properties of the proteins. In animals it has been shown that both PARP1 and PARP2 contain an automodification domain and that poly(ADP-ribosyl)ation blocks the enzyme activity. However, the ADP-ribose polymers have a very short lifetime. They are quickly hydrolysed by PARG. This has as consequence that the proteins and enzymes are restored in their original state, but also that PARP is re-activated and can restart the process. Numerous reports in the animal field indicate that over-activation of PARP in combination with PARG-activity causes a rapid breakdown of the NAD+ pool. This results in a stimulation of resynthesis of NAD+ using three to five molecules of ATP for each molecule of NAD+. In this way the cellular ATP reserves are depleted and leads to necrotic cell death. Here we show that in plants strong stresses activate PARP and cause cell death. Moreover, when the PARP-activity is reduced by means of chemical inhibitors or by silencing of the parp or parg genes, explants and whole plants become tolerant to a broad range of abiotic stresses. Our data indicate that the basis of this stress tolerance is the maintenance of energy homeostasis without enhancement of the mitochondrial respiration, minimizing the production of reactive oxygen species. Based on the obtained results the following conclusions and statements can be made. First, plants with reduced poly(ADP-ribosyl)ation-activity are tolerant to a broad range of stresses. Second, stress tolerance is obtained by maintaining energy homeostasis. Third, energy homeostasis is maintained by reducing stress-induced energy consumption by preventing NAD+ breakdown. This results in higher energy-use efficiency. Fourth, reducing stress-induced energy consumption avoids a too intense mitochondrial respiration and consequently prevents the formation of reactive oxygen species.

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