Plant Physiol. Journal of Pharmacology and Experimental Therapeutics
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Published on May 28, 2008; 10.1104/pp.108.122598

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Received May 5, 2008
Accepted May 22, 2008

The level of free intracellular zinc mediates programmed cell death/cell survival decisions in plant embryos

Andreas Helmersson , Sara von Arnold , and Peter V. Bozhkov *

Department of Plant Biology and Forest Genetics, Uppsala BioCenter, Swedish University of Agricultural Sciences, P.O. Box 7080, SE-750 07 Uppsala, Sweden

* Corresponding author; email: peter.bozhkov{at}vbsg.slu.se.

Zinc is a potent regulator of programmed cell death (PCD) in animals. While certain, cell type-specific concentrations of intracellular free zinc are required to protect cells from death, zinc depletion commits cells to death in diverse systems. As in animals, PCD has a fundamental role in plant biology, but its molecular regulation is poorly understood. In particular, the involvement of zinc in the control of plant PCD remains unknown. Here we used somatic embryos of Norway spruce (Picea abies) to investigate the role of zinc in developmental PCD, which is crucial for correct embryonic patterning. Staining of the early embryos with zinc-specific molecular probes (Zinquin-ethyl-ester and Dansylaminoethyl-cyclen) has revealed high accumulation of zinc in the proliferating cells of the embryonal masses and abrupt decrease of zinc content in the dying terminally-differentiated suspensor cells. Exposure of early embryos to a membrane-permeable zinc chelator N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine led to embryonic lethality, as it induced ectopic cell death affecting embryonal masses. This cell death involved the loss of plasma membrane integrity, metacaspase-like proteolytic activity and nuclear DNA fragmentation. To verify the anti-cell death effect of zinc, we incubated early embryos with increased concentrations of zinc sulphate. Zinc supplementation inhibited developmental PCD and led to suppression of terminal differentiation and elimination of the embryo-suspensors, causing inhibition of embryo maturation. Our data demonstrate that perturbation of zinc homeostasis disrupts the balance between cell proliferation and PCD required for plant embryogenesis. This establishes zinc as an important cue governing cell-fate decisions in plants.






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