Abscission Zones

The deliberate shedding of plant parts—the abscission process—results when specific cells exercise a genetic program to separate (Sexton and Roberts, 1982; Osborne, 1989). Attention has focused on the mechanism of detachment rather than the fate of the abscission zone cells. Extensive evidence indicates that zone cells synthesize and secrete hydrolases including proteases and nucleases; some of these enzymes act to separate and destroy cell walls (Sexton and Roberts, 1982; Osborne, 1989). It has been shown that any band of cells in a petiole can differentiate into abscission zone cells (McManus et al., 1998). The process is a true transdifferentiation which does not require cell division. Cell death certainly occurs during abscission. Many cells in the zone disintegrate or detach during the separation process. Cells on the separation surface of the organ being removed die, along with all others in the organ. On the proximal side of the abscission zone, cells enlarge and eventually form scar or wound tissue. This tissue is composed of dead cells, presumably some of the very zone cells which enlarged and aided the separation process. The abscission process shares features with PCD in response to pathogens; they include ethylene-induction of pathogenesis-related proteins and involvement of reactive oxygen species (González-Carranza et al., 1998). In abscission, H2O2 has not been implicated, but induction of peroxidases and accumulation of a metallothionen-like protein specifically in the zone cells could indicate the involvement of reactive oxygen species. A matrix metal-loproteinase gene, expressed late in senescence but before appearance of DNA laddering, has been identified in cucumber cotyledons and suggested to have a role in breakdown of the extracellular matrix and PCD (Delorme et al., 2000). Despite the evidence available, it remains to be determined if the cells in the zone separate and die as the result of detachment or if cells enter a programmed death process during which they separate and fragment so that abscission occurs. These questions highlight the need to identify more of the genes involved in initiating PCD.

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