期刊
BIOCHEMICAL JOURNAL
卷 466, 期 -, 页码 137-145出版社
PORTLAND PRESS LTD
DOI: 10.1042/BJ20141237
关键词
Arabidopsis thaliana; Maillard cascade; metabolite damage; Vibrio vulnificus; vitamin B2; Zea mays
资金
- US National Science Foundation [MCB-1153413, MCB-1153357]
- C.V. Griffin Sr. Foundation
- NSF National High Magnetic Field Laboratory User Program in the Advanced Magnetic Resonance Imaging and Spectroscopy (AMRIS) Facility in the University of Florida McKnight Brain Institute
- Southeast Center for Integrated Metabolomics [NIH 1U24DK097209-01A1]
- National Science Foundation [IOS-1025398]
- Direct For Biological Sciences
- Div Of Molecular and Cellular Bioscience [1052492] Funding Source: National Science Foundation
- Direct For Biological Sciences
- Div Of Molecular and Cellular Bioscience [1153413] Funding Source: National Science Foundation
Plants and bacteria synthesize the essential human micronutrient riboflavin (vitaminB2) via the same multi-step pathway. The early intermediates of this pathway are notoriously reactive and may be overproduced in vivo because riboflavin biosynthesis enzymes lack feedback controls. In the present paper, we demonstrate disposal of riboflavin intermediates by COG3236 (DUF1768), a protein of previously unknown function that is fused to two different riboflavin pathway enzymes in plants and bacteria (RIBR and RibA respectively). We present cheminformatic, biochemical, genetic and genomic evidence to show that: (i) plant and bacterial COG3236 proteins cleave the N-glycosidic bond of the first two intermediates of riboflavin biosynthesis, yielding relatively innocuous products; (ii) certain COG3236 proteins are in a multi-enzyme riboflavin biosynthesis complex that gives them privileged access to riboflavin intermediates; and (iii) COG3236 action in Arabidopsis thaliana and Escherichia coli helps maintain flavin levels. COG3236 proteins thus illustrate two emerging principles in chemical biology: directed overflow metabolism, in which excess flux is diverted out of a pathway, and the pre-emption of damage from reactive metabolites.
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