Sugar efflux transporters are essential for the maintenance of animal blood glucose levels, plant nectar production, and plant seed and pollen development. Despite broad biological importance, the identity of sugar efflux transporters has remained elusive. Using optical glucose sensors, we identified a new class of sugar transporters, named SWEETs, and show that at least six out of seventeen Arabidopsis, two out of over twenty rice and two out of seven homologues in Caenorhabditis elegans, and the single copy human protein, mediate glucose transport. Arabidopsis SWEET8 is essential for pollen viability, and the rice homologues SWEET11 and SWEET14 are specifically exploited by bacterial pathogens for virulence by means of direct binding of a bacterial effector to the SWEET promoter. Bacterial symbionts and fungal and bacterial pathogens induce the expression of different SWEET genes, indicating that the sugar efflux function of SWEET transporters is probably targeted by pathogens and symbionts for nutritional gain. The metazoan homologues may be involved in sugar efflux from intestinal, liver, epididymis and mammary cells.The molecular nature of cellular sugar efflux in both plants and animals is unknown despite the fact that sugar efflux is an essential component for cellular exchange of carbon and energy in multicellular organisms [1][2][3][4] . Sugar efflux from the tapetum or transmitting tract of the style, for example, fuels pollen development and pollen tube growth 5 . Flowers secrete sugars for nectar production to attract pollinators, and plants secrete carbohydrates into the rhizosphere, potentially to feed beneficial microorganisms 6 . Sugar efflux carriers are

The trade-off between growth and immunity is crucial for survival in plants. However, the mechanism underlying growthimmunity balance has remained elusive. The PRE-IBH1-HBI1 tripartite helix-loop-helix/basic helix-loop-helix module is part of a central transcription network that mediates growth regulation by several hormonal and environmental signals. Here, genome-wide analyses of HBI1 target genes show that HBI1 regulates both overlapping and unique targets compared with other DNA binding components of the network in Arabidopsis thaliana, supporting a role in specifying network outputs and fine-tuning feedback regulation. Furthermore, HBI1 negatively regulates a subset of genes involved in immunity, and pathogen-associated molecular pattern (PAMP) signals repress HBI1 transcription. Constitutive overexpression and lossof-function experiments show that HBI1 inhibits PAMP-induced growth arrest, defense gene expression, reactive oxygen species production, and resistance to pathogen. These results show that HBI1, as a component of the central growth regulation circuit, functions as a major node of crosstalk that mediates a trade-off between growth and immunity in plants.

1Among the hundreds of receptor-like kinases (RLKs) in plants, the brassinosteroid (BR) hormone 2 receptor BR-INSENSITIVE 1 (BRI1) and the immunity receptor FLAGELLIN SENSING 2 3 (FLS2) share a common co-receptor kinase, but lead to distinct growth and immunity responses, 4 respectively. Here we show that the BSU1 family of phosphatases, known to mediate BR 5 inactivation of GSK3-like kinases, also mediate flagellin-FLS2 signaling to the MAP kinases, 6 through different phosphocodes. Flagellin treatment induced phosphorylation of BSU1 7 phosphatase at serine-251 (S251) located in the N-terminal kelch-repeat domain. The bsu 8 quadruple mutant (bsu-q), with loss or compromised function of all four BSU family members, 9 showed defects in flagellin-triggered MAP kinase activation. The Botrytis-induced kinase 1 10 (BIK1), a substrate of FLS2, phosphorylated BSU1 at S251 in a flagellin-dependent manner. 11Mutation of S251 to alanine in BSU1 reduced its phosphorylation by BIK1, interaction with 12 MEKK1 and ability to restore flagellin-induced MAP kinase activation of the bsu quadruple 13 mutant, without affecting its ability to activate BR-dependent growth. Our results demonstrate that 14 BSU1 acts as a substrate of BIK1 downstream of FLS2 in the innate immunity pathway, in addition 15 to its role in the BR pathway. Our results suggest that different RLKs sharing downstream 16 components may maintain signaling specificity through phosphocodes in higher plants. 17 18 Text 19The Arabidopsis genome encodes hundreds of receptor-like kinases (RLKs), which perceive 20 diverse extracellular signals and trigger distinct cellular responses such as growth, differentiation, 21 and immunity. The mechanisms that ensure specificity of RLK signal transduction are not fully 22 understood. Among over two hundred leucine-rich repeat receptor-like kinases (LRR-RLK) in Arabidopsis 1 , the brassinosteroid (BR) receptor BR-INSENSITIVE1 (BRI1) and the flagellin 1 receptor FLAGELLIN SENSING 2 (FLS2) have been most extensively studied 2, 3 . BR binding to 2 BRI1 triggers its association with and activation by the co-receptor BRI1-ASSOCIATED 3 KINASE1 (BAK1) 4, 5 . BRI1 in turn phosphorylates the BR-SIGNALING KINASE (BSK) and 4 CONSTITUTIVE DIFFERENTIAL GROWTH 1 (CDG1) family of receptor-like cytoplasmic 5 kinases (RLCKs), to activate the BRI1-SUPRESSOR1 (BSU1) family of phosphatases 6, 7 , which 6 dephosphorylate and inactivate the GSK3-like kinases, leading to PP2A-mediated 7 dephosphorylation of the BZR1 family of transcription factors and activation of growth responses 8, 8 9 . Similarly, flagellin, a pathogen associated molecular pattern (PAMP), activates FLS2 by 9 inducing association with the BAK1 co-receptor 10 , and downstream signal transduction also 10 involves RLCKs 11, 12 . Members of the RLCK VII subfamily such as Botrytis-induced kinase 1 11 (BIK1) and PBS1-LIKE (PBL) kinases lead to activation of MAP kinases 13, 14 . There is evidence 12 that BIK1 plays a role in BR signaling, and BSKs are also involved in FLS2 signaling [15][1...