SCFSAP controls organ size by targeting PPD proteins for degradation in Arabidopsis thaliana

Zhibiao Wang, Na Li, Shan Jiang, Nathalie Gonzalez, Xiahe Huang, Yingchun Wang, Dirk Inzé and Yunhai Li ()
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Zhibiao Wang: State Key Laboratory of Plant Cell and Chromosome Engineering, CAS Center for Excellence in Molecular Plant Sciences, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences
Na Li: State Key Laboratory of Plant Cell and Chromosome Engineering, CAS Center for Excellence in Molecular Plant Sciences, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences
Shan Jiang: State Key Laboratory of Plant Cell and Chromosome Engineering, CAS Center for Excellence in Molecular Plant Sciences, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences
Nathalie Gonzalez: VIB
Xiahe Huang: State Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences
Yingchun Wang: State Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences
Dirk Inzé: VIB
Yunhai Li: State Key Laboratory of Plant Cell and Chromosome Engineering, CAS Center for Excellence in Molecular Plant Sciences, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences

Nature Communications, 2016, vol. 7, issue 1, 1-11

Abstract: Abstract Control of organ size by cell proliferation and growth is a fundamental process, but the mechanisms that determine the final size of organs are largely elusive in plants. We have previously revealed that the ubiquitin receptor DA1 regulates organ size by repressing cell proliferation in Arabidopsis. Here we report that a mutant allele of STERILE APETALA (SAP) suppresses the da1-1 mutant phenotype. We show that SAP is an F-box protein that forms part of a SKP1/Cullin/F-box E3 ubiquitin ligase complex and controls organ size by promoting the proliferation of meristemoid cells. Genetic analyses suggest that SAP may act in the same pathway with PEAPOD1 and PEAPOD2, which are negative regulators of meristemoid proliferation, to control organ size, but does so independently of DA1. Further results reveal that SAP physically associates with PEAPOD1 and PEAPOD2, and targets them for degradation. These findings define a molecular mechanism by which SAP and PEAPOD control organ size.

Date: 2016
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DOI: 10.1038/ncomms11192

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