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Shoot branching is a pivotal process during plant growth and development, and is antagonistically orchestrated by auxin and sugars. In contrast to extensive investigations on hormonal regulatory networks, our current knowledge on the role of sugar signalling pathways in bud outgrowth is scarce. Based on a comprehensive stepwise strategy, we investigated the role of glycolysis/the tricarboxylic acid (TCA) cycle and the oxidative pentose phosphate pathway (OPPP) in the control of bud outgrowth. We demonstrated that these pathways are necessary for bud outgrowth promotion upon plant decapitation and in response to sugar availability. They are also targets of the antagonistic crosstalk between auxin and sugar availability. The two pathways act synergistically to down-regulate the expression of BRC1, a conserved inhibitor of shoot branching. Using Rosa calluses stably transformed with GFP-fused promoter sequences of RhBRC1 (pRhBRC1), glycolysis/TCA cycle and the OPPP were found to repress the transcriptional activity of pRhBRC1 cooperatively. Glycolysis/TCA cycle- and OPPP-dependent regulations involve the –1973/–1611 bp and –1206/–709 bp regions of pRhBRC1, respectively. Our findings indicate that glycolysis/TCA cycle and the OPPP are integrative parts of shoot branching control and can link endogenous factors to the developmental programme of bud outgrowth, likely through two distinct mechanisms.

Growth at the shoot apical meristem (SAM) is essential for shoot architecture construction. The phytohormones gibberellins (GA) play a pivotal role in coordinating plant growth, but their role in the SAM remains mostly unknown. Here, we developed a ratiometric GA signalling biosensor by engineering one of the DELLA proteins, to suppress its master regulatory function in GA transcriptional responses while preserving its degradation upon GA sensing. We demonstrate that this novel degradation-based biosensor accurately reports on cellular changes in GA levels and perception during development. We used this biosensor to map GA signalling activity in the SAM. We show that high GA signalling is found primarily in cells located between organ primordia that are the precursors of internodes. By gain- and loss-of-function approaches, we further demonstrate that GAs regulate cell division plane orientation to establish the typical cellular organisation of internodes, thus contributing to internode specification in the SAM.

Summary Agrobacterium T‐DNA‐encoded 6B proteins cause remarkable growth effects in plants. Nicotiana otophora carries two cellular T‐DNAs with three slightly divergent 6b genes (TE‐1‐6b‐L, TE‐1‐6b‐R and TE‐2‐6b) originating from a natural transformation event. In Arabidopsis thaliana, expression of 2×35S:TE‐2‐6b, but not 2×35S:TE‐1‐6b‐L or 2×35S:TE‐1‐6b‐R, led to plants with crinkly leaves, which strongly resembled mutants of the miR319a/TCP module. This module is composed of MIR319A and five CIN‐like TCP (TEOSINTHE BRANCHED1, CYCLOIDEA and PROLIFERATING CELL NUCLEAR ANTIGEN BINDING FACTOR) genes (TCP2, TCP3, TCP4, TCP10 and TCP24) targeted by miR319a. The CIN‐like TCP genes encode transcription factors and are required for cell division arrest at leaf margins during development. MIR319A overexpression causes excessive growth and crinkly leaves. TE‐2‐6b plants did not show increased miR319a levels, but the mRNA levels of the TCP4 target gene LOX2 were decreased, as in jaw‐D plants. Co‐expression of green fluorescent protein (GFP)‐tagged TCPs with native or red fluorescent protein (RFP)‐tagged TE‐6B proteins led to an increase in TCP protein levels and formation of numerous cytoplasmic dots containing 6B and TCP proteins. Yeast double‐hybrid experiments confirmed 6B/TCP binding and showed that TE‐1‐6B‐L and TE‐1‐6B‐R bind a smaller set of TCP proteins than TE‐2‐6B. A single nucleotide mutation in TE‐1‐6B‐R enlarged its TCP‐binding repertoire to that of TE‐2‐6B and caused a crinkly phenotype in Arabidopsis. Deletion analysis showed that TE‐2‐6B targets the TCP4 DNA‐binding domain and directly interferes with transcriptional activation. Taken together, these results provide detailed insights into the mechanism of action of the N. otophora TE‐encoded 6b genes., Significance Statement It was found previously that the Agrobacterium‐derived TE‐2‐6b gene from Nicotiana otophora induces strong growth effects in Nicotiana tabacum. However, the molecular mechanism has remained unknown. We show here that TE‐2‐6b induces a jaw‐D‐like phenotype in Arabidopsis – known to result from a decrease in CIN‐like TCPs – and that different TE‐6B proteins interact with different TCP subsets, thus providing insights into the molecular mechanism by which TE‐6B proteins stimulate plant growth.

Nitrate, one of the main nitrogen (N) sources for crops, acts as a nutrient and key signaling molecule coordinating gene expression, metabolism and various growth processes throughout the plant life cycle. It is widely accepted that nitrate-triggered developmental programs cooperate with hormone synthesis and transport, to finely adapt plant architecture to N availability. Here, we report that nitrate, acting through its signaling pathway, promotes growth in Arabidopsis and wheat, in part by modulating the accumulation of gibberellin (GA)-regulated DELLA growth repressors. We show that nitrate reduces the abundance of DELLAs by increasing GA contents through activation of GA metabolism gene expression. Consistently, the growth restraint conferred by nitrate deficiency is partially rescued in global-DELLA mutant that lacks all DELLAs. At the cellular level, we show that nitrate enhances both cell proliferation and elongation in a DELLA-dependent and -independent manner, respectively. Our findings establish a connection between nitrate and GA signaling pathways that allow plants to adapt their growth to nitrate availability.

Nitrate, one of the main nitrogen (N) sources for crops, acts as a nutrient and key signaling molecule coordinating gene expression, metabolism, and various growth processes throughout the plant life cycle. It is widely accepted that nitrate-triggered developmental programs cooperate with hormone synthesis and transport to finely adapt plant architecture to N availability. Here, we report that nitrate, acting through its signaling pathway, promotes growth in Arabidopsis and wheat, in part by modulating the accumulation of gibberellin (GA)-regulated DELLA growth repressors. We show that nitrate reduces the abundance of DELLAs by increasing GA contents through activation of GA metabolism gene expression. Consistently, the growth restraint conferred by nitrate deficiency is partially rescued in global-DELLA mutant that lacks all DELLAs. At the cellular level, we show that nitrate enhances both cell proliferation and elongation in a DELLA dependent and independent manner, respectively. Our findings establish a connection between nitrate and GA signaling pathways that allow plants to adapt their growth to nitrate availability plants to adapt their growth to nitrate availability

International audience; Plants are able to sense a rise in temperature of several degrees, and appropriately adapt their metabolic and growth processes. To this end, plants produce various signalling molecules that act throughout the plant body. Here, we report that root-derived GA$_{12}$, a precursor of the bioactive gibberellins, mediates thermo-responsive shoot growth in $Arabidopsis$. Our data suggest that root-to-shoot translocation of GA$_{12}$ enables a flexible growth response to ambient temperature changes.

INDETERMINATE DOMAIN (IDD)/ BIRD proteins are a highly conserved plant-specific family of transcription factors which play multiple roles in plant development and physiology. Here, we show that mutation in IDD4/IMPERIAL EAGLE increases resistance to the hemi-biotrophic pathogen Pseudomonas syringae, indicating that IDD4 may act as a repressor of basal immune response and PAMP-triggered immunity. Furthermore, the idd4 mutant exhibits enhanced plant-growth indicating IDD4 as suppressor of growth and development. Transcriptome comparison of idd4 mutants and IDD4ox lines aligned to genome-wide IDD4 DNA-binding studies revealed major target genes related to defense and developmental-biological processes. IDD4 is a phospho-protein that interacts and becomes phosphorylated on two conserved sites by the MAP kinase MPK6. DNA-binding studies of IDD4 after flg22 treatment and with IDD4 phosphosite mutants show enhanced binding affinity to ID1 motif-containing promoters and its function as a transcriptional regulator. In contrast to the IDD4-phospho-dead mutant, the IDD4 phospho-mimicking mutant shows altered susceptibility to PstDC3000, salicylic acid levels and transcriptome reprogramming. In summary, we found that IDD4 regulates various hormonal pathways thereby coordinating growth and development with basal immunity., Author summary This work illustrates the involvement of the IDD family member 4 in the regulation of defense responses against hemibiotrophic pathogens and in processes governing plant growth. IDD4 is embedded in widely-ramified regulatory pathways and exerts transcriptional control of key factors that shape and balance growth with defense. Mutation in IDD4 and overexpression affect the plant shoot and root growth. At the same time, IDD4 acts as a repressor of innate immunity against the hemi-biotrophic pathogen Pst DC3000. IDD4 interacts with and is in vitro phosphorylated by the immune MAP kinase MPK6. Genome-wide IDD4 DNA-binding studies revealed subsets of direct targets contributing to various developmental processes and immunity. Chromatin-immunoprecipitation and DNA-shift experiments identified the ID1 motif as the prime target site of IDD4 and revealed that phospho-modifed IDD4 shows altered DNA binding ability and thereby gene expression and pathogen resistance. Overall, these results indicate that IDD4 links signal transduction to gene expression of genes involved in basal immunity and growth and development.

Shoot branching is a key process for plant growth and fitness. Newly produced axes result from axillary bud outgrowth, which is at least partly mediated through the regulation of BRANCHED1 gene expression (BRC1/TB1/FC1). BRC1 encodes a pivotal bud-outgrowth-inhibiting transcription factor belonging to the TCP family. As the regulation of BRC1 expression is a hub for many shoot-branching-related mechanisms, it is influenced by endogenous (phytohormones and nutrients) and exogenous (light) inputs, which involve so-far only partly identified molecular networks. This review highlights the central role of BRC1 in shoot branching and its responsiveness to different stimuli, and emphasizes the different knowledge gaps that should be addressed in the near future.

International audience; Plant phenotypic plasticity is controlled by diverse hormone pathways, which integrate and convey information from multiple developmental and environmental signals. Moreover, in plants many processes such as growth, development, and defense are regulated in similar ways by multiple hormones. Among them, gibberellins (GAs) are phytohormones with pleiotropic actions, regulating various growth processes throughout the plant life cycle. Previous work has revealed extensive interplay between GAs and other hormones, but the molecular mechanism became apparent only recently. Molecular and physiological studies have demonstrated that DELLA proteins, considered as master negative regulators of GA signaling, integrate multiple hormone signaling pathways through physical interactions with transcription factors or regulatory proteins from different families. In this review, we summarize the latest progress in GA signaling and its direct crosstalk with the main phytohormone signaling, emphasizing the multifaceted role of DELLA proteins with key components of major hormone signaling pathways.

Departamento Gene´tica Molecular de Plantas, CentroNacional de Biotecnologi´a (CSIC), Campus de Cantoblanco,Darwin 3, 28049 Madrid, SpainSummaryThe circadian clock plays a pivotal role in the control ofArabidopsis hypocotyl elongation by regulating rhythmicexpression of the bHLH factors PHYTOCHROME INTERACT-ING FACTOR 4 and 5 (PIF4 and 5). Coincidence of increasedPIF4/PIF5transcriptlevelswiththedarkperiodallowsnuclearaccumulation of these factors, and in short days it phasesmaximal hypocotyl growth at dawn [1–3]. During early night,PIF4andPIF5transcriptionisrepressedbytheEveningCom-plex (EC) proteins EARLY FLOWERING3 (ELF3), EARLYFLOWERING4(ELF4),andLUXARRHYTHMO(LUX)[4].WhileELF3 has an essential role in EC complex assembly, severallines of evidence indicate that this protein controls plantgrowth via other mechanisms that are presently unknown.Here, we show that the ELF3 and PIF4 proteins interact inan EC-independent manner, and that this interaction pre-vents PIF4 from activating its transcriptional targets. Wealso show that PIF4 overexpression leads to ELF3 proteindestabilization, and that this effect is mediated indirectly bynegativefeedbackregulationofphotoactivePHYTOCHROMEB(phyB).PhysicalinteractionofthephyBphotoreceptorwithELF3hasbeenreported,butitsfunctionalrelevanceremainspoorly understood. Our findings establish that phyB isneeded for ELF3 accumulation in the light, most likely bycompeting for CONSTITUTIVELY PHOTOMORPHOGENIC1(COP1)-mediated ubiquitination and the proteasomal degra-dation of ELF3. Our results explain the short hypocotylphenotype of ELF3 overexpressors, despite their normalclockfunction,andprovideamolecularframeworkforunder-standinghowwarmtemperaturespromotehypocotylelonga-tion and affect the endogenous clock.Results and DiscussionELF3 Binds the PIF4 bHLH Domain and Suppresses PIF4Protein Transcriptional ActivityThe PIF4 and PIF5 bHLH factors control plant growth bydirectly activating the expression of genes involved in cellwall loosening and directional cell expansion [5–7]. The circa-dian clock regulates PIF4 and PIF5 gene expression, whereaslight-activatedphytochromessignalphosphorylationandspe-cific destruction of the PIF4/PIF5 proteins in the light [8–10].Such control at both the gene expression and protein levelsiscriticalformodulationofPIF4andPIF5nuclearaccumulationin diurnal light/dark cycles, and in short days phases maximalhypocotyl growth at dawn [1–3, 11, 12]. Rhythmic PIF4 andPIF5 expression is regulated by the Evening Complex (EC),formed by interaction of the ELF3, ELF4, and LUX proteins,whichbindthePIF4andPIF5promotersviatheLUXtranscrip-tionfactorandrepressPIF4/PIF5expressionduringearlynight[4]. Assembly of thismultiprotein complexrequiresELF3 func-tion, which acts as an interaction scaffold between the ELF4and LUX proteins. Mutations in the elf3, elf4,orlux geneslead to a tall hypocotyl and early flowering phenotype [13, 14]that is suppressed by loss-of-function mutations in the pif4and pif5 genes [4]. Loss of pif4pif5 function, however, doesnot rescue the arrhythmic clock function of these mutants[15–17], with more recent data showing that the ELF4-ELF3-LUX complex functions as an integral part of the core oscil-lator, as it mediates nighttime repression of the clock PRR9,PRR7, GI, and LUX genes [18–21].ELF3 also has an essential function in modulating light inputto the clock and in resetting the oscillator [15, 17, 22–24]through a poorly understood mechanism. Besides the ELF4and LUX proteins [4, 16], yeast interaction studies showedthat ELF3 binds a number of protein partners, including thered light photoreceptor phyB [15], the ubiquitin E3 ligaseCOP1 [25], the floral repressor SHORT VEGETATIVE PHASE(SVP), and the clock proteins GIGANTEA (GI) and CIRCADIANCLOCK ASSOCIATED 1 (CCA1) [25–27]. It was thus proposedthatELF3is amultifunctional protein,withtwoseparablerolesas acomponent of theEC complex,and in gating light input tothe oscillator by modulation of phyB signaling [23].In a yeast two-hybrid screen using the PIF4 protein as bait,weidentifiedELF3asadirectPIF4interactor(Figure1A).Inter-action studies using deleted versions of the ELF3 and PIF4proteins confirmed this interaction, and mapped the bindingdomainstothePIF4bHLH(Figure1A)andtheELF3C-terminalregions (Figures S1A and S1B available online). The ELF3C-terminal domain is necessary for nuclear localization [16]andprotein homodimerization [15],but PIF4is thefirst partneridentified in this conserved region.We confirmed this interaction in living plant cells usingbimolecular fluorescence complementation (BiFC) assays inNicotiana benthamiana leaves. Nuclear fluorescence of the re-constitutedsplitYFP(yellowfluorescentprotein)wasobservedin leaves cotransfected with the ELF3-YFP

For multicellular organisms, long-distance communication is essential for coordination of organ growth and development. In higher plants, a dual root-to-shoot cytokinin signalling system plays a key role in adapting the growth of distant shoot organs to fluctuating environments.

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Gibberellins (GAs) affect several growth and developmental responses during the plant life cycle. Components essential for GA perception and GA signaling have been identified in rice and Arabidopsis and are conserved among vascular plants but not in Physcomitrella patens. The recent observation that DELLAs bind in nuclei to different members of the phytochrome interacting factor family, to block their transcriptional activity, is an important breakthrough to the understanding of the functional mechanism of these repressors. Beyond its role in GA-signaling repression, DELLAs were found to regulate GA homeostasis and to represent a convergence point for other hormone-signaling pathways. These repressors impose a growth restraint under environmental adverse conditions, allowing land plants to adapt their life cycle to the changing environment.

Cell elongation during seedling development is antagonistically regulated by light and gibberellins (GAs). Light induces photomorphogenesis, leading to inhibition of hypocotyl growth, whereas GAs promote etiolated growth, characterized by increased hypocotyl elongation. The mechanism underlying this antagonistic interaction remains unclear. Here we report on the central role of the Arabidopsis thaliana nuclear transcription factor PIF4 (encoded by PHYTOCHROME INTERACTING FACTOR 4) in the positive control of genes mediating cell elongation and show that this factor is negatively regulated by the light photoreceptor phyB (ref. 4) and by DELLA proteins that have a key repressor function in GA signalling. Our results demonstrate that PIF4 is destabilized by phyB in the light and that DELLAs block PIF4 transcriptional activity by binding the DNA-recognition domain of this factor. We show that GAs abrogate such repression by promoting DELLA destabilization, and therefore cause a concomitant accumulation of free PIF4 in the nucleus. Consistent with this model, intermediate hypocotyl lengths were observed in transgenic plants over-accumulating both DELLAs and PIF4. Destabilization of this factor by phyB, together with its inactivation by DELLAs, constitutes a protein interaction framework that explains how plants integrate both light and GA signals to optimize growth and development in response to changing environments.

International audience; Iron is an essential element for most living organisms. Plants acquire iron from the rhizosphere and have evolved different biochemical and developmental responses to adapt to a low-iron environment. In Arabidopsis, FIT encodes a basic helix-loop-helix transcription factor that activates the expression of iron-uptake genes in root epidermis upon iron deficiency. Here, we report that the gibberellin (GA) signaling DELLA repressors contribute substantially in the adaptive responses to iron-deficient conditions. When iron availability decreases, DELLAs accumulate in the root meristem, thereby restraining root growth, while being progressively excluded from epidermal cells in the root differentiation zone. Such DELLA exclusion from the site of iron acquisition relieves FIT from DELLA-dependent inhibition and therefore promotes iron uptake. Consistent with this mechanism, expression of a non-GA-degradable DELLA mutant protein in root epidermis interferes with iron acquisition. Hence, spatial distribution of DELLAs in roots is essential to fine-tune the adaptive responses to iron availability.

The gibberellin (GA) phytohormones play important roles in plant growth and development, promoting seed germination, elongation growth and reproductive development(1). Over the years, substantial progress has been made in understanding the regulation of GA signalling and metabolism, which ensures appropriate levels of GAs for growth and development(2). Moreover, an additional level of regulation may reside in the transport of GAs from production sites to recipient tissues that require GAs for growth. Although there is considerable evidence suggesting the existence of short- and long-distance movement of GAs in plants(3-8), the nature and the biological properties of this transport are not yet understood. Here, we combine biochemical and conventional micrografting experiments in Arabidopsis thaliana to show that the GA precursor GA12, although biologically inactive by itself, is the major mobile GA signal over long distances. Quantitative analysis of endogenous GAs in xylem and phloem exudates further indicates that GA12 moves through the plant vascular system. Finally, we demonstrate that GA12 is functional in recipient tissues, supporting growth via the activation of the GA signalling cascade. Collectively, these results reveal the existence of long-range transport of endogenous GA12 in plants that may have implications for the control of developmental phase transitions and the adaptation to adverse environments.

Ent-kaurenoic acid oxidase (KAO), a class of cytochrome P450 monooxygenases of the subfamily CYP88A, catalyzes the conversion of ent-kaurenoic acid (KA) to gibberellin (GA) GA12 , the precursor of all GAs, thereby playing an important role in determining GA concentration in plants. Past work has demonstrated the importance of KAO activity for growth in various plant species. In Arabidopsis, this enzyme is encoded by two genes designated KAO1 and KAO2. In this study, we used various approaches to determine the physiological roles of KAO1 and KAO2 throughout plant development. Analysis of gene expression pattern reveals that both genes are mainly expressed in germinating seeds and young developing organs, thus suggesting functional redundancy. Consistent with this, kao1 and kao2 single mutants are indistinguishable from wild-type plants. By contrast, the kao1 kao2 double mutant exhibits typical non-germinating GA-dwarf phenotypes, similar to those observed in the severely GA-deficient ga1-3 mutant. Phenotypic characterization and quantitative analysis of endogenous GA contents of single and double kao mutants further confirm an overlapping role of KAO1 and KAO2 throughout Arabidopsis development.

SummaryRegulation of plant height, one of the most important agronomic traits, is the focus of intensive research for improving crop performance [1]. Stem elongation takes place as a result of repeated cell divisions and subsequent elongation of cells produced by apical and intercalary meristems. The gibberellin (GA) phytohormones have long been known to control stem and internodal elongation by stimulating the degradation of nuclear growth-repressing DELLA proteins; however, the mechanism allowing GA-responsive growth is only slowly emerging [2]. Here, we show that DELLAs directly regulate the activity of the plant-specific class I TCP transcription factor family, key regulators of cell proliferation [3]. Our results demonstrate that class I TCP factors directly bind the promoters of core cell-cycle genes in Arabidopsis inflorescence shoot apices while DELLAs block TCP function by binding to their DNA-recognition domain. GAs antagonize such repression by promoting DELLA destruction and therefore cause a concomitant accumulation of TCP factors on promoters of cell-cycle genes. Consistent with this model, the quadruple mutant tcp8 tcp14 tcp15 tcp22 exhibits severe dwarfism and reduced responsiveness to GA action. Altogether, we conclude that GA-regulated DELLA-TCP interactions in inflorescence shoot apex provide a novel mechanism to control plant height.

Signaling by the hormones brassinosteroid (BR) and gibberellin (GA) is critical to normal plant growth and development and is required for hypocotyl elongation in response to dark and elevated temperatures. Active BR signaling is essential for GA promotion of hypocotyl growth and suppresses the dwarf phenotype of GA mutants. Cross-talk between these hormones occurs downstream from the DELLAs, as GA-induced destabilization of these GA signaling repressors is not affected by BRs. Here we show that the light-regulated PIF4 (phytochrome-interacting factor 4) factor is a phosphorylation target of the BR signaling kinase BRASSINOSTEROID-INSENSITIVE 2 (BIN2), which marks this transcriptional regulator for proteasome degradation. Expression of a mutated PIF41A protein lacking a conserved BIN2 phosphorylation consensus causes a severe elongated phenotype and strongly up-regulated expression of the gene targets. However, PIF41A is not able to suppress the dwarf phenotype of the bin2-1 mutant with constitutive activation of this kinase. PIFs were shown to be required for the constitutive BR response of bes1-D and bzr1-1D mutants, these factors acting in an interdependent manner to promote cell elongation. Here, we show that bes1-D seedlings are still repressed by the inhibitor BRZ in the light and that expression of the nonphosphorylatable PIF41A protein makes this mutant fully insensitive to brassinazole (BRZ). PIF41A is preferentially stabilized at dawn, coinciding with the diurnal time of maximal growth. These results uncover a main role of BRs in antagonizing light signaling by inhibiting BIN2-mediated destabilization of the PIF4 factor. This regulation plays a prevalent role in timing hypocotyl elongation to late night, before light activation of phytochrome B (PHYB) and accumulation of DELLAs restricts PIF4 transcriptional activity.

Gibberellins (GAs) are plant hormones involved in the regulation of plant growth in response to endogenous and environmental signals. GA promotes growth by stimulating the degradation of nuclear growth–repressing DELLA proteins. In Arabidopsis thaliana, DELLAs consist of a small family of five proteins that display distinct but also overlapping functions in repressing GA responses. This study reveals that DELLA RGA-LIKE3 (RGL3) protein is essential to fully enhance the jasmonate (JA)-mediated responses. We show that JA rapidly induces RGL3 expression in a CORONATINE INSENSITIVE1 (COI1)– and JASMONATE INSENSITIVE1 (JIN1/MYC2)–dependent manner. In addition, we demonstrate that MYC2 binds directly to RGL3 promoter. Furthermore, we show that RGL3 (like the other DELLAs) interacts with JA ZIM-domain (JAZ) proteins, key repressors of JA signaling. These findings suggest that JA/MYC2-dependent accumulation of RGL3 represses JAZ activity, which in turn enhances the expression of JA-responsive genes. Accordingly, we show that induction of primary JA-responsive genes is reduced in the rgl3-5 mutant and enhanced in transgenic lines overexpressing RGL3. Hence, RGL3 positively regulates JA-mediated resistance to the necrotroph Botrytis cinerea and susceptibility to the hemibiotroph Pseudomonas syringae. We propose that JA-mediated induction of RGL3 expression is of adaptive significance and might represent a recent functional diversification of the DELLAs.

Gibberellins (GAs) are phytohormones controlling major aspects of plant growth and development. Although previous studies suggested the existence of a transport of GAs in plants, the nature and properties associated with this transport were unknown. We recently showed through micrografting and biochemical approaches that the GA12 precursor is the chemical form of GA undergoing long-distance transport across plant organs in Arabidopsis. Endogenous GA12 moves through the plant vascular system from production sites to recipient tissues, in which GA12 can be converted to bioactive forms to support growth via the activation of GA-dependent processes. GAs are also essential to promote seed germination; hence GA biosynthesis mutants do not germinate without exogenous GA treatment. Our results suggest that endogenous GAs are not (or not sufficiently) transmitted to the offspring to successfully complete the germination under permissive conditions.