Oxygen-dependent proteolysis regulates the stability of angiosperm polycomb repressive complex 2 subunit VERNALIZATION 2

Daniel J. Gibbs (), Hannah M. Tedds, Anne-Marie Labandera, Mark Bailey, Mark D. White, Sjon Hartman, Colleen Sprigg, Sophie L. Mogg, Rory Osborne, Charlene Dambire, Tinne Boeckx, Zachary Paling, Laurentius A. C. J. Voesenek, Emily Flashman and Michael J. Holdsworth ()
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Daniel J. Gibbs: University of Birmingham
Hannah M. Tedds: University of Birmingham
Anne-Marie Labandera: University of Birmingham
Mark Bailey: University of Birmingham
Mark D. White: University of Oxford
Sjon Hartman: Utrecht University
Colleen Sprigg: University of Birmingham
Sophie L. Mogg: University of Birmingham
Rory Osborne: University of Birmingham
Charlene Dambire: University of Nottingham
Tinne Boeckx: University of Nottingham
Zachary Paling: University of Birmingham
Laurentius A. C. J. Voesenek: Utrecht University
Emily Flashman: University of Oxford
Michael J. Holdsworth: University of Nottingham

Nature Communications, 2018, vol. 9, issue 1, 1-11

Abstract: Abstract The polycomb repressive complex 2 (PRC2) regulates epigenetic gene repression in eukaryotes. Mechanisms controlling its developmental specificity and signal-responsiveness are poorly understood. Here, we identify an oxygen-sensitive N-terminal (N-) degron in the plant PRC2 subunit VERNALIZATION(VRN) 2, a homolog of animal Su(z)12, that promotes its degradation via the N-end rule pathway. We provide evidence that this N-degron arose early during angiosperm evolution via gene duplication and N-terminal truncation, facilitating expansion of PRC2 function in flowering plants. We show that proteolysis via the N-end rule pathway prevents ectopic VRN2 accumulation, and that hypoxia and long-term cold exposure lead to increased VRN2 abundance, which we propose may be due to inhibition of VRN2 turnover via its N-degron. Furthermore, we identify an overlap in the transcriptional responses to hypoxia and prolonged cold, and show that VRN2 promotes tolerance to hypoxia. Our work reveals a mechanism for post-translational regulation of VRN2 stability that could potentially link environmental inputs to the epigenetic control of plant development.

Date: 2018
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DOI: 10.1038/s41467-018-07875-7

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