Programmed cell death is an essential part of the live of any organism; it shapes the body and organs and plays an important role in the response to adverse environmental conditions and attack by a variety of pathogenic organisms. The mechanisms by which PCD is executed are diverse. In animal cells two main types of PCD have been described: apoptosis and autophagy. The question whether apoptosis exists in plants has been addressed by investigating the morphological and biochemical similarities between cell death in animals and plants and by searching for homologies in key apoptosis genes. Here we discusssome similarities between the regulation of animal and plant programmed cell death. We conclude that cell death in plants exhibits morphological and biochemical features that are comparable to those observed in dying animal cells. Although some of these features such as DNA and nuclear degradation are commonly associated with animal apoptosis, in most plant cell death, autophagic features are more abundant. A main distinguishing feature of apoptosis is that the contents of the dying cell is taken up and hydrolysed in the lysosome of another cell. This is in marked contrast to autophagy, where the contents of the dying cell is hydrolysed in the lysosome of the same cell. Engulfment by - and hydrolysis of fragments of the dying cell in - other cells, has not been reported in plants, therefore, the cell death process in plants is not truly apoptotic. Among general apoptosis (PCD) regulators only a few are conserved between animals and plants. We discuss the features of plant Bcl-2-related proteins, Bax inhibitor-1 (BI-1), defender against apoptotic cell death (DAD) and caspase-like proteases. Recent data indicate that both BI-1 and a caspase-like proteolytic network are conserved components of the cell death machinery in both animals and plants, which may explain the observed morphological similarities between dying plant and animal cells.
|Title of host publication||Apoptosis|
|Place of Publication||Kerala|
|Publication status||Published - 2005|