Abstract

Nonfluorescent chlorophyll catabolites (NCCs) have been described as end products of chlorophyll breakdown in Arabidopsis [1]. NCCs are open tetrapyrroles formed from respective fluorescent precursors, termed FCCs, through acid-catalyzed isomerization after import of FCCs into the vacuoles of senescing cells.

I present an overview on the current knowledge of the pathway of chlorophyll degradation. In addition, I provide evidence for physical interaction at the thylakoid membrane between the enzymes required for conversion of chlorophyll to a primary FCC . This interaction infers that metabolic channeling of breakdown intermediates occurs, most likely to minimize the risk of toxicity of these potentially photodynamic intermediates.

In Arabidopsis, quantification of NCCs in senescent leaves had implied that their amount might correspond to the pool of chlorophyll present in green leaves. I present genetic and biochemical evidence for a cytochrome P450 monooxygenase to be involved in the formation of a new type of chlorophyll catabolites in Arabidopsis. Mutants of this P450 (cyp-1) accumulate much more NCCs than wild-type plants. Analysis of chlorophyll catabolite profiles of wild-type and cyp-1 mutants identified novel catabolites in wild-type that are absent in the mutants; these new catabolites, tentatively named urobilinogenoidic nonfluorescent chlorophyll catabolites (uNCCs), account for more than 90% of broken-down chlorophyll, while NCCs only represent a minor fraction. In summary, I propose that a cytochrom P450 monoxygenase is involved in chlorophyll breakdown in Arabidopsis. Moreover, due to the 10-fold increase of NCCs in cyp-1 mutants, I propose, in contrast to earlier finding, that uNCCs not NCCs represent the majority of the chlorophyll catabolites that accumulate in Arabidopsis.

[1] Hörtensteiner, S.; Kräutler, B. (2011) Chlorophyll breakdown in higher plants. Biochim. Biophys. Acta 1807: 977-988