The control of chlorophyll catabolism and the status of yellowing as a biomarker of leaf senescence

Abstract

The pathway of chlorophyll catabolism during leaf senescence is known in a fair amount of biochemical and cell biological detail. In the last few years, genes encoding a number of the catabolic enzymes have been characterized, including the key ring-opening activities, phaeophorbide a oxygenase (PaO) and red chlorophyll catabolite reductase (RCCR). Recently, a gene that modulates disassembly of chlorophyll-protein complexes and activation of pigment ring-opening has been isolated by comparative mapping in monocot species, positional cloning exploiting rice genomics resources and functional testing in Arabidopsis. The corresponding gene in pea has been identified as Mendel's I locus (green/yellow cotyledons). Mutations in this and other chlorophyll catabolic genes have significant consequences, both for the course of leaf senescence and senescence-like stress responses, notably hypersensitivity to pathogen challenge. Loss of chlorophyll can occur via routes other than the PaO/RCCR pathway, resulting in changes that superficially resemble senescence. Such 'pseudosenescence' responses tend to be pathological rather than physiological and may differ from senescence in fundamental aspects of biochemistry and regulation.