Organ bending through differential growth represents a major mechanism by which plants are able to adaptively alter their morphology in response to local changes in the environment. Two plant hormones, auxin and ethylene, have been implicated as regulators of differential growth responses; however, the mechanisms by which they elicit their effects remain largely unknown. Here, we describe isolation of the NPH4 gene of Arabidopsis, which is conditionally required for differential growth responses of aerial tissues, and we report that NPH4 encodes the auxin-regulated transcriptional activator ARF7. The phenotypes of nph4 mutants, which include multiple differential growth defects associated with reduced auxin responsiveness, including impaired auxin-induced gene expression, are consistent with the predicted loss of function of a transcriptional activator, and these phenotypes indicate that auxin-dependent changes in gene transcription are prerequisite for proper organ bending responses. Although NPH4/ARF7 appears to be a major regulator of differential growth, it is not the sole regulator because phenotypes of nph4 null mutants were suppressed by application of ethylene. This latter finding illustrates the intimate connection between auxin and ethylene in the control of growth in higher plants. INTRODUCTIONPlants have evolved movement strategies that involve organ bending to respond adaptively to environmental signals. Dramatic and rapid changes in plant morphology can result from differential growth, that is, unequal cellular growth in one position of an organ relative to an opposing position. Examples of differential growth responses include stem and root tropisms, modification of apical hook structures, and nastic movements of leaves (reviewed in Darwin and Darwin, 1896;Palmer, 1985). Each of these examples of stimulusdriven organ bending represents a process by which plants maximize the positive attributes of their environment while minimizing the negatives.Two plant hormones, auxin and ethylene, have been implicated as regulators of differential growth responses (Went and Thimann, 1937; Davies, 1987; Kaufman et al., 1995). Although each of these hormones is capable of modulating growth when applied externally, the relative contribution of each in response to changes in their endogenous concentrations, and the sensitivities to either, has been difficult to reconcile (Davies, 1987). Much of this ambiguity stems from functional overlap between the auxin and ethylene signal and response, as well as their biosynthetic, pathways. For example, auxin stimulates ethylene production (Yang and Hoffman, 1984), which in turn stimulates the expression of genes, such as HOOKLESS 1 ( HLS1 ; Lehman et al., 1996), that are involved in auxin homeostatic processes. Results from recent genetic and molecular studies suggest that auxin may be the major regulator of differential growth responses, with ethylene modifying the auxin responses (Romano et al., 1993; Lehman et al., 1996; Chen et al., 1998;Luschnig et al., 1998;Madlung ...

Organ bending through differential growth represents a major mechanism by which plants are able to adaptively alter their morphology in response to local changes in the environment. Two plant hormones, auxin and ethylene, have been implicated as regulators of differential growth responses; however, the mechanisms by which they elicit their effects remain largely unknown. Here, we describe isolation of the NPH4 gene of Arabidopsis, which is conditionally required for differential growth responses of aerial tissues, and we report that NPH4 encodes the auxin-regulated transcriptional activator ARF7. The phenotypes of nph4 mutants, which include multiple differential growth defects associated with reduced auxin responsiveness, including impaired auxin-induced gene expression, are consistent with the predicted loss of function of a transcriptional activator, and these phenotypes indicate that auxin-dependent changes in gene transcription are prerequisite for proper organ bending responses. Although NPH4/ARF7 appears to be a major regulator of differential growth, it is not the sole regulator because phenotypes of nph4 null mutants were suppressed by application of ethylene. This latter finding illustrates the intimate connection between auxin and ethylene in the control of growth in higher plants. INTRODUCTIONPlants have evolved movement strategies that involve organ bending to respond adaptively to environmental signals. Dramatic and rapid changes in plant morphology can result from differential growth, that is, unequal cellular growth in one position of an organ relative to an opposing position. Examples of differential growth responses include stem and root tropisms, modification of apical hook structures, and nastic movements of leaves (reviewed in Darwin and Darwin, 1896;Palmer, 1985). Each of these examples of stimulusdriven organ bending represents a process by which plants maximize the positive attributes of their environment while minimizing the negatives.Two plant hormones, auxin and ethylene, have been implicated as regulators of differential growth responses (Went and Thimann, 1937; Davies, 1987; Kaufman et al., 1995). Although each of these hormones is capable of modulating growth when applied externally, the relative contribution of each in response to changes in their endogenous concentrations, and the sensitivities to either, has been difficult to reconcile (Davies, 1987). Much of this ambiguity stems from functional overlap between the auxin and ethylene signal and response, as well as their biosynthetic, pathways. For example, auxin stimulates ethylene production (Yang and Hoffman, 1984), which in turn stimulates the expression of genes, such as HOOKLESS 1 ( HLS1 ; Lehman et al., 1996), that are involved in auxin homeostatic processes. Results from recent genetic and molecular studies suggest that auxin may be the major regulator of differential growth responses, with ethylene modifying the auxin responses (Romano et al., 1993; Lehman et al., 1996; Chen et al., 1998;Luschnig et al., 1998;Madlung ...

The induction of phototropism in etiolated (dark-grown) seedlings exposed to an unidirectional pulse or extended irradiation with low fluence rate blue light (BL) requires the action of the phototropin (nph1) BL receptor. Although cryptochromes and phytochromes are not required for phototropic induction, these photoreceptors do modulate the magnitude of curvature resulting from phototropin activation. Modulatory increases in the magnitude of phototropic curvature have been termed "enhancement." Here, we show that phototropic enhancement is primarily a phytochrome A (phyA)-dependent red/far-red-reversible low fluence response. This phyA-dependent response is genetically separable from the basal phototropin-dependent response, as demonstrated by its retention under extended irradiation conditions in the nph4 mutant background, which normally lacks the basal BL-induced response. It is interesting that the nph4 mutants fail to exhibit the basal phototropin-dependent and phyA-dependent enhancement responses under limiting light conditions. Given that NPH4 encodes a transcriptional activator, auxin response factor 7 (ARF7), we hypothesize that the ultimate target(s) of phyA action during the phototropic enhancement response is a rate-limiting ARF-containing transcriptional complex in which the constituent ARFs can vary in identity or activity depending upon the irradiation condition.

Background: Understanding of gravity sensing and response is critical to long-term human habitation in space and can provide new advantages for terrestrial agriculture. To this end, the altered gene expression profile induced by microgravity has been repeatedly queried by microarray and RNA-seq experiments to understand gravitropism. However, the quantification of altered protein abundance in space has been minimally investigated. Results: Proteomic (iTRAQ-labelled LC-MS/MS) and transcriptomic (RNA-seq) analyses simultaneously quantified protein and transcript differential expression of three-day old, etiolated Arabidopsis thaliana seedlings grown aboard the International Space Station along with their ground control counterparts. Protein extracts were fractionated to isolate soluble and membrane proteins and analyzed to detect differentially phosphorylated peptides. In total, 968 RNAs, 107 soluble proteins, and 103 membrane proteins were identified as differentially expressed. In addition, the proteomic analyses identified 16 differential phosphorylation events. Proteomic data delivered novel insights and simultaneously provided new context to previously made observations of gene expression in microgravity. There is a sweeping shift in post-transcriptional mechanisms of gene regulation including RNA-decapping protein DCP5, the splicing factors GRP7 and GRP8, and AGO4,. These data also indicate AHA2 and FERONIA as well as CESA1 and SHOU4 as central to the cell wall adaptations seen in spaceflight. Patterns of tubulin-α 1, 3,4 and 6 phosphorylation further reveal an interaction of microtubule and redox homeostasis that mirrors osmotic response signaling elements. The absence of gravity also results in a seemingly wasteful dysregulation of plastid gene transcription.

Chloroplasts move in a light-dependent manner that can modulate the photosynthetic potential of plant cells. Identification of genes required for light-induced chloroplast movement is beginning to define the molecular machinery that controls these movements. In this work, we describe plastid movement impaired 2 (pmi2), a mutant in Arabidopsis (Arabidopsis thaliana) that displays attenuated chloroplast movements under intermediate and high light intensities while maintaining a normal movement response under low light intensities. In wild-type plants, fluence rates below 20 mmol m 22 s 21 of blue light lead to chloroplast accumulation on the periclinal cell walls, whereas light intensities over 20 mmol m 22 s 21 caused chloroplasts to move toward the anticlinal cell walls (avoidance response). However, at light intensities below 75 mmol m 22 s 21 , chloroplasts in pmi2 leaves move to the periclinal walls; 100 mmol m 22 s 21 of blue light is required for chloroplasts in pmi2 to move to the anticlinal cell walls, indicating a shift in the light threshold for the avoidance response in the mutant. The pmi2 mutation has been mapped to a gene that encodes a protein of unknown function with a large coiled-coil domain in the N terminus and a putative P loop. PMI2 shares sequence and structural similarity with PMI15, another unknown protein in Arabidopsis that, when mutated, causes a defect in chloroplast avoidance under high-light intensities.