In plants, the hormone auxin shapes gene expression to regulate growth and development. Despite the detailed characterization of auxin-inducible genes, a comprehensive overview of the temporal and spatial dynamics of auxin-regulated gene expression is lacking. Here, we analyze transcriptome data from many publicly available Arabidopsis profiling experiments and assess tissue-specific gene expression both in response to auxin concentration and exposure time and in relation to other plant growth regulators. Our analysis shows that the primary response to auxin over a wide range of auxin application conditions and in specific tissues comprises almost exclusively the up-regulation of genes and identifies the most robust auxin marker genes. Tissue-specific auxin responses correlate with differential expression of Aux/IAA genes and the subsequent regulation of context- and sequence-specific patterns of gene expression. Changes in transcript levels were consistent with a distinct sequence of conjugation, increased transport capacity and down-regulation of biosynthesis in the temperance of high cellular auxin concentrations. Our data show that auxin regulates genes associated with the biosynthesis, catabolism and signaling pathways of other phytohormones. We present a transcriptional overview of the auxin response. Specific interactions between auxin and other phytohormones are highlighted, particularly the regulation of their metabolism. Our analysis provides a roadmap for auxin-dependent processes that underpins the concept of an 'auxin code'--a tissue-specific fingerprint of gene expression that initiates specific developmental processes.
Background: The plant hormone auxin directs many aspects of plant growth and development. To understand the evolution of auxin signalling, we compared the genes encoding two families of crucial transcriptional regulators, AUXIN RESPONSE FACTOR (ARF) and AUXIN/INDOLE-3-ACETIC ACID (Aux/IAA), among flowering plants and two non-seed plants, Physcomitrella patens and Selaginella moellendorffii.
We investigated the effect of supplemental LED inter-lighting (80% red, 20% blue; 70 W m −2 ; light period 04:00-22:00) on the productivity and physiological traits of tomato plants (Flavance F1) grown in an industrial greenhouse with high pressure sodium (HPS) lamps (235 W m −2 , 420 µmol m −2 s −1 at canopy). Physiological trait measurements included diurnal photosynthesis and fruit relative growth rates, fruit weight at specific positions in the truss, root pressure, xylem sap hormone and ion compositions, and fruit quality. In the control treatment with HPS lamps alone, the ratio of far-red to red light (FR:R) was 1.2 at the top of the canopy and increased to 5.4 at the bottom. The supplemental LED interlighting decreased the FR:R ratio at the middle and low positions in the canopy and was associated with greener leaves and higher photosynthetic light use efficiency (PLUE) in the leaves in the lower canopy. The use of LED inter-lighting increased the biomass and yield by increasing the fruit weight and enhancing plant growth. The PLUE of plants receiving supplemental LED light decreased at the end of the light period, indicating that photosynthesis of the supplemented plants at the end of the day might be limited by sink capacity. The supplemental LED lighting increased the size of fruits in the middle and distal positions of the truss, resulting in a more even size for each fruit in the truss. Diurnal analysis of fruit growth showed that fruits grew more quickly during the night on the plants receiving LED light than on unsupplemented control plants. This faster fruit growth during the night was related to an increased root pressure. The LED treatment also increased the xylem levels of the phytohormone jasmonate. Supplemental LED inter-lighting increased tomato fruit weight without affecting the total soluble solid contents in fruits by increasing the total assimilates available for fruit growth and by enhancing root activity through an increase in root pressure and water supply to support fruit growth during the night.
The vesicle trafficking inhibitor Brefeldin A (BFA) changes the localization of plasma membrane localized PINs, proteins that function as polar auxin efflux carriers, by inducing their accumulation within cells. Pretreatment with the synthetic auxin 1-NAA reduces this BFA-induced PIN internalization, suggesting that auxinic compounds inhibit the endocytosis of PIN proteins. However, the most important natural auxin, IAA, did not substantially inhibit PIN internalization unless a supplementary antioxidant, butylated hydroxytoluene (BHT), was also included in the incubation medium. We asked whether the relatively small inhibition caused by IAA alone could be explained by its instability in the incubation solution or whether IAA might interact with BHT to inhibit endocytosis. Analysis of the IAA concentration in the incubation solution and of DR5 reporter activity in the roots showed that IAA is both stable and active in the medium. Therefore, IAA degradation was not able to explain the inability of IAA to inhibit endocytosis. Furthermore, when applied in the absence of auxin, BHT caused a strong increase in the rate of PIN1 internalization and a weaker increase in the rate of PIN2 internalization. These increases were unaffected by the simultaneous application of IAA, further indicating that endocytosis is not inhibited by the natural auxin IAA under physiologically relevant conditions. Endocytosis was inhibited at the same rate with 2-NAA, an inactive auxin analog, as was observed with 1-NAA and more strongly than with natural auxins, supporting the idea that this inhibition is not auxin specific.
Auxin is a molecule, which controls many aspects of plant development through both transcriptional and non-transcriptional signaling responses. AUXIN BINDING PROTEIN1 (ABP1) is a putative receptor for rapid non-transcriptional auxin-induced changes in plasma membrane depolarization and endocytosis rates. However, the mechanism of ABP1-mediated signaling is poorly understood. Here we show that membrane depolarization and endocytosis inhibition are ABP1-independent responses and that auxin-induced plasma membrane depolarization is instead dependent on the auxin influx carrier AUX1. AUX1 was itself not involved in the regulation of endocytosis. Auxin-dependent depolarization of the plasma membrane was also modulated by the auxin efflux carrier PIN2. These data establish a new connection between auxin transport and non-transcriptional auxin signaling.
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