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The long noncoding RNA (lncRNA)AUXIN-REGULATED PROMOTER LOOP(APOLO) recognizes a subset of target loci across theArabidopsis thalianagenome by forming RNA-DNA hybrids (R-loop) and modulating local three-dimensional chromatin conformation. Here we show thatAPOLOis involved in regulating the shade avoidance syndrome (SAS) by dynamically modulating the expression of key factors. In response to far-red (FR) light, the expression ofAPOLOanticorrelates with its targetBRANCHED1(BRC1), a master regulator of shoot branching inArabidopsis thaliana.APOLOderegulation results inBRC1transcriptional repression and an increase in the number of branches.APOLOtranscriptional accumulation fine-tunes the formation of a repressive chromatin loop encompassing theBRC1promoter, which normally occurs only in leaves as well as in a late response to FR treatment in axillary buds. In addition, our data reveal thatAPOLOparticipates in leaf hyponasty, in agreement with its previously reported role in the control of auxin homeostasis through direct modulation ofYUCCA2(auxin synthesis),PIDandWAG2(auxin efflux). We found that direct application ofAPOLORNA to leaves results in a rapid increase in auxin accumulation that is associated with changes in the response of the plants to FR light. Collectively, our data support the view that lncRNAs coordinate the shade avoidance syndrome inArabidopsis thalianaand shed light on the potential of lncRNAs as bioactive exogenous molecules. Deploying exogenous RNAs that modulate plant-environment interactions are important new tools for sustainable agriculture.

The microRNA156 (miR156)/SQUAMOSA PROMOTER-BINDING PROTEIN-LIKE(SPL/SBP) regulatory hub is highly conserved among phylogenetically distinct species, but how it interconnects multiple pathways to converge to common integrators controlling shoot architecture is still unclear. Here, we demonstrated that the miR156/SlSBP15hub modulates tomato shoot branching (SB) by connecting phytohormones with important genetic pathways regulating both axillary bud (AB) development and outgrowth. We verified that plants overexpressing the miR156 (156-OE plants) display high SB, whereas plants overexpressing a miR156-resistant SlSBP15 alelle (rSBP15 plants) display arrested SB and are able to partially restore the wild-type (WT) phenotype in156-OE background. Although rSBP15 plants showed ABs smaller than MT, its activation is dependent on shoot apex-derived auxin transport inhibition. Additionally, hormonal measurements reveal that IAA and ABA concentrations were lower in 156-OE and higher in rSBP15-OE plants. SlSBP15 regulates AB development and outgrowth by inhibiting auxin transport and the activity ofGOBLET(GOB), and by interacting with BRANCHED1b (SlBRC1b) at the protein level to control abscisic acid (ABA) levels within ABs. Our data provide a new mechanism by which the miR156/SPL/SBPhub regulates SB, and suggest thatSlSBP15has potential applications in improving tomato architecture.

Shoot branching is a complex mechanism in which secondary shoots grow from buds that are initiated from meristems established in leaf axils. The model plant Arabidopsis thaliana has a rosette leaf growth pattern in the vegetative stage. After flowering initiation, the main stem starts to elongate with the top leaf primordia developing into cauline leaves. Meristems in arabidopsis are initiated in the axils of rosette or cauline leaves, giving rise to rosette or cauline buds, respectively. Plasticity in the process of shoot branching is regulated by resource and nutrient availability as well as by plant hormones. However, few studies have attempted to test whether cauline and rosette branching are subject to the same plasticity. Here, we addressed this question by phenotyping cauline and rosette branching in three arabidopsis ecotypes and several arabidopsis mutants with varied shoot architectures. Our results show that there is no negative correlation between cauline and rosette branch numbers in arabidopsis, demonstrating that there is no trade-off between cauline and rosette bud outgrowth. Through investigation of the altered branching pattern of flowering pathway mutants and arabidopsis ecotypes grown in various photoperiods and light regimes, we further elucidated that the number of cauline branches is closely related to flowering time. The number or rosette branches has an enormous plasticity compared with cauline branches and is influenced by genetic background, flowering time, light intensity and temperature. Our data reveal different plasticity in the regulation of branching at rosette and cauline nodes and promote a framework for future branching analyses.One sentence summaryDifferent plasticity of branching at cauline and rosette nodes of arabidopsis is revealed through detailed correlative analyses of branching under varied genetic and environmental contexts.

The control of branch outgrowth is critical for plant fitness, stress resilience and crop yield. The Arabidopsis thaliana transcription factor BRANCHED1 (BRC1) plays a pivotal role in this process as it integrates signals that inhibit axillary bud growth to control shoot branching. Despite the remarkable activity of BRC1 as a potent growth inhibitor, the mechanisms by which it promotes and maintains bud dormancy are still largely unknown. Here we combine ChIP-seq, transcriptomic and systems biology approaches to characterise the BRC1-regulated gene network. We identify a group of BRC1 direct target genes encoding transcription factors (BTFs) that orchestrate, together with BRC1, an intricate transcriptional network enriched in abscisic acid signalling components. The BRC1 network is enriched in feed-forward loops and feed-back loops, robust against noise and mutation, reversible in response to stimuli, and stable once established. This knowledge is fundamental to adapt plant architecture and crop production to ever-changing environmental conditions. Dutch Scientific Organization NWO-JSTP 833.13.008 Ministerio de Economía y Competitividad BIO2014-57011-R Ministerio de Economía y Competitividad BIO2017-84363-R Ministerio de Economía y Competitividad BIO2017-84066-R