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Nat Commun. 2017 Mar 23;8:14690. doi: 10.1038/ncomms14690.

Plant cysteine oxidases are dioxygenases that directly enable arginyl transferase-catalysed arginylation of N-end rule targets.

Author information

1
Chemistry Research Laboratory, University of Oxford, 12 Mansfield Road, Oxford OX1 3TA, UK.
2
Independent Junior Research Group on Protein Recognition and Degradation, Leibniz Institute of Plant Biochemistry (IPB), Weinberg 3, D-06120 Halle (Saale), Germany.
3
ScienceCampus Halle Plant - based Bioeconomy, Betty-Heimann-Strasse 3, D-06120 Halle (Saale), Germany.
4
Institute of Biology I, RWTH Aachen University, Worringerweg 1, D-52074 Aachen, Germany.
5
Chemical Genomics Centre of the Max Planck Society, Otto-Hahn-Strasse 15, D-44227 Dortmund, Germany.
6
VU University Amsterdam, De Boelelaan 1083, 1081 HV Amsterdam, The Netherlands.
7
Department of Biochemistry, University of Oxford, South Parks Road, Oxford OX1 3QU, UK.

Abstract

Crop yield loss due to flooding is a threat to food security. Submergence-induced hypoxia in plants results in stabilization of group VII ETHYLENE RESPONSE FACTORs (ERF-VIIs), which aid survival under these adverse conditions. ERF-VII stability is controlled by the N-end rule pathway, which proposes that ERF-VII N-terminal cysteine oxidation in normoxia enables arginylation followed by proteasomal degradation. The PLANT CYSTEINE OXIDASEs (PCOs) have been identified as catalysts of this oxidation. ERF-VII stabilization in hypoxia presumably arises from reduced PCO activity. We directly demonstrate that PCO dioxygenase activity produces Cys-sulfinic acid at the N terminus of an ERF-VII peptide, which then undergoes efficient arginylation by an arginyl transferase (ATE1). This provides molecular evidence of N-terminal Cys-sulfinic acid formation and arginylation by N-end rule pathway components, and a substrate of ATE1 in plants. The PCOs and ATE1 may be viable intervention targets to stabilize N-end rule substrates, including ERF-VIIs, to enhance submergence tolerance in agriculture.

PMID:
28332493
PMCID:
PMC5376641
DOI:
10.1038/ncomms14690
[Indexed for MEDLINE]
Free PMC Article

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