AUX1-mediated root hair auxin influx governs SCFTIR1/AFB-type Ca2+ signaling.
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ABSTRACT:
SUBMITTER: Dindas J
PROVIDER: S-EPMC5862985 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Asymmetric root growth (ARG) on tilted plates, or root coiling on horizontally placed plates, is proposed to be a combination of gravitropism, mechanical sensing, and "circumnutation," a word designated by Charles Darwin to describe the helical movement that all plant organs make around the growth direction. ARG is developmentally controlled in which microtubule-regulating proteins and the phytohormone auxin participates. Nutrient deficiency influences ARG. However, it is unclear which nutrients play key roles in regulating ARG, what endogenous components are involved in responding to nutrient deficiency for ARG, and how nutrient deficiency is translated into endogenous responses. We report here that nitrate deficiency resulted in a strong ARG in Arabidopsis. Nitrate deficiency caused root coiling on horizontal plates, which is inhibited by an auxin transport inhibitor, and by mutations in PIN-FORMED2 (PIN2) and AUXIN RESISTANT 1 (AUX1). We further show that suppression of ARG by nitrate is mediated by the nitrate transporter/sensor NRT1.1. In addition, PIN2- and AUX1-mediated auxin transports are epistatic to NRT1.1 in nitrate deficiency-induced ARG. This study reveals a signaling pathway in root growth by responding to exogenous nitrate and relaying it into altered auxin transport.
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Project description:Plant survival depends on vascular tissues, which originate in a self-organizing manner as strands of cells co-directionally transporting the plant hormone auxin. The latter phenomenon (also known as auxin canalization) is classically hypothesized to be regulated by auxin itself via the effect of this hormone on the polarity of its own intercellular transport. Correlative observations supported this concept, but molecular insights remain limited. In the current study, we established an experimental system based on the model Arabidopsis thaliana, which exhibits auxin transport channels and formation of vasculature strands in response to local auxin application. Our methodology permits the genetic analysis of auxin canalization under controllable experimental conditions. By utilizing this opportunity, we confirmed the dependence of auxin canalization on a PIN-dependent auxin transport and nuclear, TIR1/AFB-mediated auxin signaling. We also show that leaf venation and auxin-mediated PIN repolarization in the root require TIR1/AFB signaling. Further studies based on this experimental system are likely to yield better understanding of the mechanisms underlying auxin transport polarization in other developmental contexts.
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Project description:Root traits such as root angle and hair length influence resource acquisition particularly for immobile nutrients like phosphorus (P). Here, we attempted to modify root angle in rice by disrupting the OsAUX1 auxin influx transporter gene in an effort to improve rice P acquisition efficiency. We show by X-ray microCT imaging that root angle is altered in the osaux1 mutant, causing preferential foraging in the top soil where P normally accumulates, yet surprisingly, P acquisition efficiency does not improve. Through closer investigation, we reveal that OsAUX1 also promotes root hair elongation in response to P limitation. Reporter studies reveal that auxin response increases in the root hair zone in low P environments. We demonstrate that OsAUX1 functions to mobilize auxin from the root apex to the differentiation zone where this signal promotes hair elongation when roots encounter low external P. We conclude that auxin and OsAUX1 play key roles in promoting root foraging for P in rice.
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Project description:The plant hormone auxin controls root epidermal cell development in a concentration-dependent manner. Root hairs are produced on a subset of epidermal cells as they increase in distance from the root tip. Auxin is required for their initiation and continued growth, but little is known about its distribution in this region of the root. Contrary to the expectation that hair cells might require active auxin influx to ensure auxin supply, we did not detect the auxin-influx transporter AUX1 in root-hair cells. A high level of AUX1 expression was detected in adjacent non-hair cell files. Non-hair cells were necessary to achieve wild-type root-hair length, although an auxin response was not required in these cells. Three-dimensional modelling of auxin flow in the root tip suggests that AUX1-dependent transport through non-hair cells maintains an auxin supply to developing hair cells as they increase in distance from the root tip, and sustains root-hair outgrowth. Experimental data support the hypothesis that instead of moving uniformly though the epidermal cell layer, auxin is mainly transported through canals that extend longitudinally into the tissue.
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Project description:The actin cytoskeleton is required for cell expansion and implicated in cellular responses to the phytohormone auxin. However, the mechanisms that coordinate auxin signaling, cytoskeletal remodeling and cell expansion are poorly understood. Previous studies examined long-term actin cytoskeleton responses to auxin, but plants respond to auxin within minutes. Before this work, an extracellular auxin receptor - rather than the auxin transporter AUXIN RESISTANT 1 (AUX1) - was considered to precede auxin-induced cytoskeleton reorganization. In order to correlate actin array organization and dynamics with degree of cell expansion, quantitative imaging tools established baseline actin organization and illuminated individual filament behaviors in root epidermal cells under control conditions and after indole-3-acetic acid (IAA) application. We evaluated aux1 mutant actin organization responses to IAA and the membrane-permeable auxin 1-naphthylacetic acid (NAA). Cell length predicted actin organization and dynamics in control roots; short-term IAA treatments stimulated denser and more parallel, longitudinal arrays by inducing filament unbundling within minutes. Although AUX1 is necessary for full actin rearrangements in response to auxin, cytoplasmic auxin (i.e. NAA) stimulated a lesser response. Actin filaments became more 'organized' after IAA stopped elongation, refuting the hypothesis that 'more organized' actin arrays universally correlate with rapid growth. Short-term actin cytoskeleton response to auxin requires AUX1 and/or cytoplasmic auxin.
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