Dynamic Integration of Auxin Transport and Signalling

Recent years have seen rapid progress in our understanding of the mechanism of action of the plant hormone auxin. A major emerging theme is the central importance of the interplay between auxin signalling and the active transport of auxin through the plant to create dynamic patterns of auxin accumulation. Even in tissues where auxin distribution patterns appear stable, they are the product of standing waves, with auxin flowing through the tissue, maintaining local pockets of high and low concentration. The auxin distribution patterns result in changes in gene expression to trigger diverse, context-dependent growth and differentiation responses. Multi-level feedback loops between the signal transduction network and the auxin transport network provide self-stabilising patterns that remain sensitive to the external environment and to the developmental progression of the plant. The full biological implications of the behaviour of this system are only just beginning to be understood through a combination of experimental manipulation and mathematical modelling

Auxin, Self-Organisation, and the Colonial Nature of Plants

Evolution has provided at least two particularly successful independent solutions to the problems of multicellularity — animals and higher plants. An obvious requirement for successful multicellularity is communication between different parts of the organism, both locally, for example between neighbouring cells, and over very long distances. Recent advances in understanding hormone signalling networks in plants are beginning to reveal how co-ordination of activity across the whole plant body can be achieved despite the lack of a control centre, typical of animal systems. Of particular importance in this distributed regulatory approach are the self-organising properties of the transport system for the plant hormone auxin. This review examines the integrative role of the auxin transport network in co-ordinating plant growth and development

The culture of scientific research.

In 2014, the UK-based Nuffield Council on Bioethics carried out a series of engagement activities, including an online survey to which 970 people responded, and 15 discussion events at universities around the UK to explore the culture of research in the UK and its effect on ethical conduct in science and the quality of research. The findings of the project were published in December 2014 and the main points are summarised here. We found that scientists are motivated in their work to find out more about the world and to benefit society, and that they believe collaboration, multidisciplinarity, openness and creativity are important for the production of high quality science. However, in some cases, our findings suggest, the culture of research in higher education institutions does not support or encourage these goals or activities. For example, high levels of competition and perceptions about how scientists are assessed for jobs and funding are reportedly contributing to a loss of creativity in science, less collaboration and poor research practices. The project led to suggestions for action for funding bodies, research institutions, publishers and editors, professional bodies and individual researchers

Cytokinin Targets Auxin Transport to Promote Shoot Branching.

Cytokinin promotes shoot branching by activating axillary buds, but its mechanism of action in Arabidopsis (Arabidopsis thaliana) in this process is unclear. We have shown previously that a hextuple mutant lacking a clade of type-A Arabidopsis Response Regulators (ARRs) known to act in cytokinin signaling has reduced shoot branching compared with the wild type. Since these proteins typically act as negative regulators of cytokinin signaling, this is an unexpected result. To explore this paradox more deeply, we characterized the effects of loss of function of the type-B ARR, ARR1, which positively regulates cytokinin-induced gene expression. The arr1 mutant has increased branching, consistent with a role antagonistic to the type-A ARRs but in apparent conflict with the known positive role for cytokinin in bud activation. We show that the arr branching phenotypes correlate with increases in stem auxin transport and steady-state levels of the auxin export proteins PIN3 and PIN7 on the plasma membrane of xylem-associated cells in the main stem. Cytokinin treatment results in an increased accumulation of PIN3, PIN7, and the closely related PIN4 within several hours, and loss of PIN3, PIN4, and PIN7 can partially rescue the arr1 branching phenotype. This suggests that there are multiple signaling pathways for cytokinin in bud outgrowth; one of these pathways regulates PIN proteins in shoots, independently of the canonical signaling function of the ARR genes tested here. A hypothesis consistent with the arr shoot phenotypes is that feedback control of biosynthesis leads to altered cytokinin accumulation, driving cytokinin signaling via this pathway.European Research Council Gatsby Charitable Foundatio

A plant's diet, surviving in a variable nutrient environment.

As primary producers, plants rely on a large aboveground surface area to collect carbon dioxide and sunlight and a large underground surface area to collect the water and mineral nutrients needed to support their growth and development. Accessibility of the essential nutrients nitrogen (N) and phosphorus (P) in the soil is affected by many factors that create a variable spatiotemporal landscape of their availability both at the local and global scale. Plants optimize uptake of the N and P available through modifications to their growth and development and engagement with microorganisms that facilitate their capture. The sensing of these nutrients, as well as the perception of overall nutrient status, shapes the plant's response to its nutrient environment, coordinating its development with microbial engagement to optimize N and P capture and regulate overall plant growth

Strigolactone can promote or inhibit shoot branching by triggering rapid depletion of the auxin efflux protein PIN1 from the plasma membrane.

Plants continuously extend their root and shoot systems through the action of meristems at their growing tips. By regulating which meristems are active, plants adjust their body plans to suit local environmental conditions. The transport network of the phytohormone auxin has been proposed to mediate this systemic growth coordination, due to its self-organising, environmentally sensitive properties. In particular, a positive feedback mechanism termed auxin transport canalization, which establishes auxin flow from active shoot meristems (auxin sources) to the roots (auxin sinks), has been proposed to mediate competition between shoot meristems and to balance shoot and root growth. Here we provide strong support for this hypothesis by demonstrating that a second hormone, strigolactone, regulates growth redistribution in the shoot by rapidly modulating auxin transport. A computational model in which strigolactone action is represented as an increase in the rate of removal of the auxin export protein, PIN1, from the plasma membrane can reproduce both the auxin transport and shoot branching phenotypes observed in various mutant combinations and strigolactone treatments, including the counterintuitive ability of strigolactones either to promote or inhibit shoot branching, depending on the auxin transport status of the plant. Consistent with this predicted mode of action, strigolactone signalling was found to trigger PIN1 depletion from the plasma membrane of xylem parenchyma cells in the stem. This effect could be detected within 10 minutes of strigolactone treatment and was independent of protein synthesis but dependent on clathrin-mediated membrane trafficking. Together these results support the hypothesis that growth across the plant shoot system is balanced by competition between shoot apices for a common auxin transport path to the root and that strigolactones regulate shoot branching by modulating this competition

Strigolactone regulation of shoot branching in chrysanthemum (Dendranthema grandiflorum).

Previous studies of highly branched mutants in pea (rms1-rms5), Arabidopsis thaliana (max1-max4), petunia (dad1-dad3), and rice (d3, d10, htd1/d17, d14, d27) identified strigolactones or their derivates (SLs), as shoot branching inhibitors. This recent discovery offers the possibility of using SLs to regulate branching commercially, for example, in chrysanthemum, an important cut flower crop. To investigate this option, SL physiology and molecular biology were studied in chrysanthemum (Dendranthema grandiflorum), focusing on the CCD8/MAX4/DAD1/RMS1/D10 gene. Our results suggest that, as has been proposed for Arabidopsis, the ability of SLs to inhibit bud activity depends on the presence of a competing auxin source. The chrysanthemum SL biosynthesis gene, CCD8 was cloned, and found to be regulated in a similar, but not identical way to known CCD8s. Expression analyses revealed that DgCCD8 is predominantly expressed in roots and stems, and is up-regulated by exogenous auxin. Exogenous SL can down-regulate DgCCD8 expression, but this effect can be overridden by apical auxin application. This study provides evidence that SLs are promising candidates to alter the shoot branching habit of chrysanthemum

Root system architecture determines fitness in an Arabidopsis mutant in competition for immobile phosphate ions but not for nitrate ions

Plant root systems often have complex branching patterns. Models indicate that a complex architecture is only required for the acquisition of immobile resources, such as phosphate; mobile ions, notably nitrate, can be effectively taken up by very restricted root systems. We have tested this prediction using the axr4 mutation of Arabidopsis thaliana, the principal phenotypic effect of which is to reduce the number of lateral roots. Arabidopsis thaliana is not a host for mycorrhizal fungi and so acquires all its nutrients through the root system. In both a pot experiment and a field experiment conducted under natural conditions for A. thaliana, we found that only phosphate, and not nitrate, affected the fitness of the mutant relative to the isogenic wild-type line, Columbia. These results confirm model predictions and have implications both for the evolution of complex root systems and for the design of efficient root systems for crops

Mutation of the cytosolic ribosomal protein-encoding RPS10B gene affects shoot meristematic function in Arabidopsis.

BACKGROUND: Plant cytosolic ribosomal proteins are encoded by small gene families. Mutants affecting these genes are often viable, but show growth and developmental defects, suggesting incomplete functional redundancy within the families. Dormancy to growth transitions, such as the activation of axillary buds in the shoot, are characterised by co-ordinated upregulation of ribosomal protein genes. RESULTS: A recessive mutation in RPS10B, one of three Arabidopsis genes encoding the eukaryote-specific cytoplasmic ribosomal protein S10e, was found to suppress the excessive shoot branching mutant max2-1. rps10b-1 mildly affects the formation and separation of shoot lateral organs, including the shoot axillary meristems. Axillary meristem defects are enhanced when rps10b-1 is combined with mutations in REVOLUTA, AUXIN-RESISTANT1, PINOID or another suppressor of max2-1, FAR-RED ELONGATED HYPOCOTYL3. In some of these double mutants, the maintenance of the primary shoot meristem is also affected. In contrast, mutation of ALTERED MERISTEM PROGRAMME1 suppresses the rps10b-1axillary shoot defect. Defects in both axillary shoot formation and organ separation were enhanced by combining rps10b-1 with cuc3, a mutation affecting one of three Arabidopsis NAC transcription factor genes with partially redundant roles in these processes. To assess the effect of rps10b-1 on bud activation independently from bud formation, axillary bud outgrowth on excised cauline nodes was analysed. The outgrowth rate of untreated buds was reduced only slightly by rps10b-1 in both wild-type and max2-1 backgrounds. However, rps10b-1 strongly suppressed the auxin resistant outgrowth of max2-1 buds. A developmental phenotype of rps10b-1, reduced stamen number, was complemented by the cDNA of another family member, RPS10C, under the RPS10B promoter. CONCLUSIONS: RPS10B promotes shoot branching mainly by promoting axillary shoot development. It contributes to organ boundary formation and leaf polarity, and sustains max2-1 bud outgrowth in the presence of auxin. These processes require the auxin response machinery and precise spatial distribution of auxin. The correct dosage of protein(s) involved in auxin-mediated patterning may be RPS10B-dependent. Inability of other RPS10 gene family members to maintain fully S10e levels might cause the rps10b-1 phenotype, as we found no evidence for unique functional specialisation of either RPS10B promoter or RPS10B protein.RIGHTS : This article is licensed under the BioMed Central licence at http://www.biomedcentral.com/about/license which is similar to the 'Creative Commons Attribution Licence'. In brief you may : copy, distribute, and display the work; make derivative works; or make commercial use of the work - under the following conditions: the original author must be given credit; for any reuse or distribution, it must be made clear to others what the license terms of this work are