Amino acid catabolism in plants

Abstract

Amino acids are among the most versatile compounds in plants performing diverse functions within proteins as well as individually. The publications constituting this habilitation thesis focus on different aspects of amino acid catabolism. Not all of the biochemical pathways catalyzing degradation of the twenty proteinogenic amino acids in plants are known, and annotation of amino acid catabolic enzymes in databases and pathway maps is still insufficient for comprehensive evaluation of proteomics or transcriptomics datasets. Thus, a manually assembled pathway map covering 136 reactions involved in amino acid related pathways is presented and used for reevaluation of already published as well as interpretation of new omics datasets. This approach clearly defines gaps in the present knowledge and at the same time postulates candidate proteins for unknown reactions as a starting point for further investigation. In addition, it provides insight into the different metabolic functions of amino acid catabolism and their significance during abiotic and biotic stress response. A major topic of the work presented here is cysteine catabolism. Cysteine in addition to the amino group also contains a thiol moiety and therefore represents an intersection of carbon, nitrogen and sulfur metabolism. The degradation of cysteine via different enzymatic routes releases reduced sulfur in the form of sulfide or persulfide, which act as signaling molecules and can be further metabolized either by reincorporation into cysteine or by oxidation. This thesis describes a mitochondrial cysteine catabolic pathway that oxidizes the thiol group catalyzed by the sulfur dioxygenase ETHE1. In plants, this pathway is essential during early embryo development and also required for energy metabolism during low light availability. Mutations in the ETHE1 gene in humans cause the metabolic disease ethylmalonic encephalopathy, which is characterized by rapidly progressive encephalopathy, chronic diarrhea, and peripheral microangio¬pathy caused by accumulation of toxic sulfide levels. These symptoms can be relieved by combined treatment with a bactericide that represses sulfide production by intestinal anaerobes and N-acetylcysteine as a precursor for glutathione, which can act as a buffer for reduced sulfur.