Comparison between plant cell death systems

The use of programmed senescence in plants allows it to control the use of nutrients. The nutrients can be removed from areas where they are no longer required, such as in the leaf, to areas that the plant is developing, such as seeds.

The senescence of leaves is age related and controlled and coordinated by many factors, both internal and external. The senescence process itself involves the programmed death of cells. This occurs in a specific order to enable the recovery of nutrients, and as such it differs from the cell death programs of other processes such as those involved when attacked by pathogens or in the the formation of tracheary components. The next section takes a look into the differences that occur between these cell death processes.

Differences in cell death between senescent and non-senescent cells

perhaps the most understood process of programmed cell death involves the hypersensitive response in response to pathogens. It therefore seems reasonable that comparing these responses to those that are involved in leaf senescence will help to further the understanding of the processes involved.

In hypersensitive responses to pathogens many of the same genes are differentially regulated as are seen in senescence; these include the cell hypersensitive response cell death marker HIN1, and many genes that encode pathogenesis related proteins. Defence genes such as ELI3 and the metallothionene encoding LSC54 gene are also upregulated in both pathogen responsive and leaf senescent cell death processes. Took all together it seems that many of the processes involved in cell death use shared mechanisms.

So what overlays the differences between the programmed cell death of pathogen hypersensitive response and the slower, functional cell death seen in senescence? Many different genes are expressed in one of the programs but not the other. For example SAG 12 is expressed in senescence only, whilst HSR203J is expressed in pathogen response only. This suggests selectivity in the roles of these genes, and they are likely to be involved in mechanisms specific to senescence or pathogen hypersensitive response cell death respectively. In comparative transcriptome analysis it was found that over 800 genes are heightened in the senescence process, and that only ~330 of them were highly upregulated in starvation cell death, indicating about 500 differing genes. It is thought that these may be involved in distinctive processes in senescence related programmed cell death.