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 ...

Although sessile in nature, plants are able to use a number of mechanisms to modify their morphology in response to changing environmental conditions. Differential growth is one such mechanism. Despite its importance in plant development, little is known about the molecular events regulating the establishment of differential growth. Here we report analyses of the nph4 ( nonphototropic hypocotyl) mutants of Arabidopsis that suggest that the NPH4 protein plays a central role in the modulation of auxin-dependent differential growth. Results from physiological studies demonstrate that NPH4 activity is conditionally required for a number of differential growth responses, including phototropism, gravitropism, phytochrome-dependent hypocotyl curvature, apical hook maintenance, and abaxial/adaxial leaf-blade expansion. The nph4 mutants exhibited auxin resistance and severely impaired auxin-dependent gene expression, indicating that the defects associated with differential growth likely arise because of altered auxin responsiveness. Moreover, the auxin signaling events mediating phototropism are genetically correlated with the abundance of the NPH4 protein.

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.

Phototropism represents a differential growth response by which plant organs can respond adaptively to changes in the direction of incident light to optimize leaf/stem positioning for photosynthetic light capture and root growth orientation for water/nutrient acquisition. Studies over the past few years have identified a number of components in the signaling pathway(s) leading to development of phototropic curvatures in hypocotyls. These include the phototropin photoreceptors (phot1 and phot2) that perceive directional blue-light (BL) cues and then stimulate signaling, leading to relocalization of the plant hormone auxin, as well as the auxin response factor NPH4/ARF7 that responds to changes in local auxin concentrations to directly mediate expression of genes likely encoding proteins necessary for development of phototropic curvatures. While null mutations in NPH4/ARF7 condition an aphototropic response to unidirectional BL, seedlings carrying the same mutations recover BL-dependent phototropic responsiveness if co-irradiated with red light (RL) or pre-treated with either ethylene. In the present study, we identify second-site enhancer mutations in the nph4 background that abrogate these recovery responses. One of these mutations--map1 (modifier of arf7 phenotypes 1)--was found to represent a missense allele of AUX1--a gene encoding a high-affinity auxin influx carrier previously associated with a number of root responses. Pharmacological studies and analyses of additional aux1 mutants confirmed that AUX1 functions as a modulator of hypocotyl phototropism. Moreover, we have found that the strength of dependence of hypocotyl phototropism on AUX1-mediated auxin influx is directly related to the auxin responsiveness of the seedling in question.