Abstract
Angiosperms developed floral nectaries that reward pollinating insects. Although nectar function and composition have been characterized, the mechanism of nectar secretion has remained unclear. Here we identify SWEET9 as a nectary-specific sugar transporter in three eudicot species: Arabidopsis thaliana, Brassica rapa (extrastaminal nectaries) and Nicotiana attenuata (gynoecial nectaries). We show that SWEET9 is essential for nectar production and can function as an efflux transporter. We also show that sucrose phosphate synthase genes, encoding key enzymes for sucrose biosynthesis, are highly expressed in nectaries and that their expression is also essential for nectar secretion. Together these data are consistent with a model in which sucrose is synthesized in the nectary parenchyma and subsequently secreted into the extracellular space via SWEET9, where sucrose is hydrolysed by an apoplasmic invertase to produce a mixture of sucrose, glucose and fructose. The recruitment of SWEET9 for sucrose export may have been a key innovation, and could have coincided with the evolution of core eudicots and contributed to the evolution of nectar secretion to reward pollinators.
Original language | English (US) |
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Pages (from-to) | 546-549 |
Number of pages | 4 |
Journal | Nature |
Volume | 508 |
Issue number | 7497 |
DOIs | |
State | Published - 2014 |
Bibliographical note
Funding Information:Acknowledgements We are grateful to D. Ehrhardt, H. Cartwright, J. Lindeboom, K. Barton and T. Liu for help with confocal and scanning electron microscopy. We thank D. Ehrhardt for providing specific endomembrane markers and M. Jia for conducting nectar sugar assays. We thank J. Danielson for help with phylogenetic analyses. This work was made possible by support from the Division of Chemical Sciences, Geosciences and Biosciences, Office of Basic Energy Sciences at the US Department of Energy under grant number DE-FG02-04ER15542 to W.B.F. I.W.L. was supported by the fellowship of Department of Biology, Stanford University and Carnegie. X.-Q.Q. was supported by the Carnegie Institution and Scholarship Program of the Chinese Scholarship Council (2009635108). C.J.C.’s work was supported by a grant from the US National Science Foundation (#0820730). I.T.B. was supported by European Research Council advanced grant ClockworkGreen (293926) and the Max Planck Gesellschaft, and thanks C. Diezel for technical assistance.