植物铝毒害及遗传育种研究进展

本文简单概述了目前植物铝毒害及遗传育种方面的研究进展。Al3+可以通过与细胞骨架的作用,影响根的正常生理功能和形态建成。 植物可以通过根尖分泌有机酸或磷酸等将离子态的铝变成螯合态的铝,通过吸收H+提高根尖周围的pH,将Al3+变成难溶性的 Al(OH)3或磷酸铝从而解除铝毒害, 也可以通过在细胞内与Al3+形成无毒害的复合结构从而解除铝毒害。国外通过基因工程和突变体筛选已经获得了一批耐铝的植物材料,国内一些研究者通过突变体筛选也获得了一些耐铝的植物材料。 对植物耐铝性的遗传研究表明, 植物的耐铝性既可以是受单基因控制的,也可以是受多基因控制的。     

Alterations of crossbridge angle induced by beta, gamma-imido-adenosine-triphosphate. Electron microscope and optical diffraction studies on myofibrillar fragments of abdominal muscles of the crayfish Orconectes limosus.

The molecular basis of muscle contraction is thought to consist of cyclic movements of parts of the myosin molecules (crossbridges). Unitl now different states of the proposed crossbridge cycle could be stablilized and demonstrated by electron microscopy only in the case of highly specialized insect flight muscles. In this paper evidence is presented that it is also possible to induce crossbridge positions corresponding to the rigor [16] and the pseudorelaxed state [3] in non-insect muscles. Homogenization of myofibrils of the abdominal flexors of the crayfish Orconectes limosus in rigor or AMP.PNP-containing solutions brings about two different crossbridge patterns: The formation of crossbridges attached to the actin filaments in a mainly acute (rigor) or in a mainly perpendicular angle (pseudo-relaxed). Optical diffraction patterns taken from electron micrographs of sarcomere fragments are likewise compatible with those taken from sarcomeres of insect flight muscles fixed in comparable conditions [2,3].     

植物铝毒害及遗传育种研究进展

本文简单概述了目前植物铝毒害及遗传育方面的研究进展,Al^3 可以通过与细胞骨架的作用,影响根的正常生理功能和形态建成,植物可以通过根尖分泌有机酸或磷酸等将离子态的为成螯合态的铝,通过吸收H^ 提高根尖周围的pH,将Al^3 变成难溶性的Al(OH)3或磷酸铝从而解 除铝毒害,也可以通过在细胞内与Ａl^3 形成无毒害的复合结构从而解除铝毒害,国外通过基因工程和突变体筛选已经获得了一批耐铝的植物材料,国内一些研究者通过变体筛选也获得了一些耐铝的植物材料,对植物耐铝性的遗传研究表明,植物的耐铝性既可以是受单基因控制的,也可以是受多基因控制的。     

The PPAR-gamma activator, Rosiglitazone, inhibits actin polymerisation in monocytes: involvement of Akt and intracellular calcium

Monocyte hyperactivation as seen in diabetes results in increased cytoskeletal rigidity and reduced cell deformability leading to microchannel occlusions and microvascular complications. The thiazolidinediones (TZDs) are PPAR-gamma agonists that have been reported to exert beneficial non-metabolic effects on the vasculature. This study demonstrates that the TZD, Rosiglitazone, significantly reduces f-MLP-induced actin polymerisation in human monocytic cells (p < 0.05). Two of the key signalling processes known to be involved in the regulation of cytoskeletal remodelling were investigated: PI(3)K-dependent Akt phosphorylation and intracellular calcium concentration [Ca(2+)](i). The PI(3)K inhibitor, Wortmannin, ameliorated f-MLP-induced actin polymerisation (p < 0.05), while the Ca(2+) sequestration inhibitor, thapsigargin, induced actin depolymerisation (p < 0.05), confirming the involvement of both processes in cytoskeletal remodelling. Rosiglitazone significantly reduced f-MLP activation of Akt (p < 0.05), and significantly increased [Ca(2+)](i) in both resting and f-MLP-stimulated cells (p < 0.05). Therefore, Rosiglitazone interacts with signalling events downstream of occupancy of the f-MLP receptor, to modulate cytoskeletal remodelling in a PPAR-gamma-independent manner. To our knowledge, these results are the first to present evidence that a PPAR-gamma agonist can modulate actin remodelling in monocytes, and may therefore be protective against microvascular damage in diabetes.     

The novel Rho-family GTPase rif regulates coordinated actin-based membrane rearrangements

Small GTPases of the Rho family have a critical role in controlling cell morphology, motility and adhesion through dynamic regulation of the actin cytoskeleton [1,2]. Individual Rho GTPases have been shown to regulate distinct components of the cytoskeletal architecture; RhoA stimulates the bundling of actin filaments into stress fibres [3], Rac reorganises actin to produce membrane sheets or lamellipodia [4] and Cdc42 causes the formation of thin, actin-rich surface projections called filopodia [5]. We have isolated a new Rho-family GTPase, Rif (Rho in filopodia), and shown that it represents an alternative signalling route to the generation of filopodial structures. Coordinated regulation of Rho-family GTPases can be used to generate more complicated actin rearrangements, such as those underlying cell migration [6]. In addition to inducing filopodia, Rif functions cooperatively with Cdc42 and Rac to generate additional structures, increasing the diversity of actin-based morphology.     

Action of cytochalasin D on cytoskeletal networks

Extraction of SC-1 cells (African green monkey kidney) with the detergent Triton X-100 in combination with stereo high-voltage electron microscopy of whole mount preparations has been used as an approach to determine the mode of action of cytochalasin D on cells. The cytoskeleton of extracted BSC-1 cells consists of substrate-associated filament bundles (stress fibers) and a highly cross-linked network of four major filament types extending throughout the cell body; 10-nm filaments, actin microfilaments, microtubules, and 2- to 3-nm filaments. Actin filaments and 2- to 3-nm filaments form numerous end- to-side contacts with other cytoskeletal filaments. Cytochalasin D treatment severely disrupts network organization, increases the number of actin filament ends, and leads to the formation of filamentous aggregates or foci composed mainly of actin filaments. Metabolic inhibitors prevent filament redistribution, foci formation, and cell arborization, but not disorganization of the three-dimensional filament network. In cells first extracted and then treated with cytochalasin D, network organization is disrupted, and the number of free filament ends is increased. Supernates of preparations treated in this way contain both short actin filaments and network fragments (i.e., actin filaments in end-to-side contact with other actin filaments). It is proposed that the dramatic effects of cytochalasin D on cells result from both a direct interaction of the drug with the actin filament component of cytoskeletal networks and a secondary cellular response. The former leads to an immediate disruption of the ordered cytoskeletal network that appears to involve breaking of actin filaments, rather than inhibition of actin filament-filament interactions (i.e., disruption of end-to-side contacts). The latter engages network fragments in an energy-dependent (contractile) event that leads to the formation of filament foci.     

The control of cytoskeletal actin and exocytosis in intact and permeabilized adrenal chromaffin cells: role of calcium and protein kinase C

The control of cytoskeletal actin and exocytosis was examined in intact and digitonin-permeabilized chromaffin cells. Cytoskeletal actin was assayed by determining the actin content of Triton-insoluble cytoskeletons. The secretagogues nicotine, high K+ and Ba2+ resulted in a rapid reduction in the amount of actin associated with the cytoskeleton. The effect of nicotine but not high K+ on cytoskeletal actin was independent of external Ca2+ and the reduction in cytoskeletal actin was mimicked by the phorbol ester 12-O-tetradecanoylphorbol-13-acetate suggesting a role for protein kinase C. In digitonin-permeabilized cells micromolar calcium produced both catecholamine secretion and a reduction in cytoskeletal actin. The reduction in cytoskeletal actin was transient. Secretion was enhanced by the GTP analogue guanosine 5'-(3-O-thio)triphosphate and the analogue also reduced cytoskeletal actin at low calcium levels. The effects of guanosine 5'-(3-O-thio)triphosphate were inhibited by the phospholipase C inhibitor neomycin and were mimicked by 12-O-tetradecanoylphorbol-13-acetate. An additional GTP analogue, guanyl-5'-yl imidodiphosphate, had no effect on cytoskeletal actin. These results provide further evidence for a requirement for reorganisation of cortical actin in the secretory processes and suggest that the reduction in actin associated with the cytoskeleton may be mediated by protein kinase C and/or calcium in intact and permeabilized chromaffin cells.     

Actin cytoskeletal network in aging and cancer.

The cytoskeleton is being recognized as an important modulator of metabolic functions of the cell. The actin cytoskeletal network, in particular, is involved in events regulating cell proliferation and differentiation. The state of actin in a variety of cell types is regulated by signals arising from the cell surface through a wide spectrum of interactions. In this review, we explore the role of actin cytoskeletal network in a series of events which are known to influence cell proliferation and differentiation. These include interaction of actin network with extracellular matrix proteins, cell surface membranes, second messengers, cytoplasmic enzymes and the nucleus. Because of the involvement of the actin network in such diverse interactions, we propose that alterations in the actin cytoskeletal function may be an important aspect of generalized decrease in cellular functions associated with aging. Preliminary data indicate that alterations in the cytoskeletal network do occur in cells obtained from older individuals. Alterations in actin state are also reported during malignant transformation of cells in culture, and in naturally occurring tumors. Taken together, the existing data seem to suggest that changes in the actin cytoskeletal network may be a part of the aging process as well as malignant transformation. Therefore, the study of the actin cytoskeletal network and its regulation has the potential to yield important information regarding cellular senescence and neoplastic transformation.     

Aluminum Inhibition of the Inositol 1,4,5-Trisphosphate Signal Transduction Pathway in Wheat Roots: A Role in Aluminum Toxicity?

In crop plants, aluminum (Al) rhizotoxicity is a major problem worldwide; however, the cause of Al toxicity remains elusive. The effects of Al on the inositol 1,4,5-trisphosphate (Ins[1,4,5]P3)-mediated signal transduction pathway were investigated in wheat roots. Exogenously applied Al (50 [mu]M) rapidly inhibited root growth (<2 hr) but did not affect general root metabolism. An Ins(1,4,5)P3 transient was generated in root tips, either before or after exposure to Al for 1 hr, by treating the roots with H2O2 (10 mM). Background (unstimulated) levels of Ins(1,4,5)P3 were similar in both Al-treated and Al-untreated root apices. However, H2O2-stimulated levels of Ins(1,4,5)P3 in root apices showed a significant (>50%) reduction after Al exposure in comparison with untreated controls, indicating that Al may be interfering with the phosphoinositide signaling pathway. When phospholipase C (PLC) was assayed directly in the presence of Al or other metal cations in microsomal membranes, AlCl3 and Al-citrate specifically inhibited PLC action in a dose-dependent manner and at physiologically relevant Al levels. Al exposure had no effect on inositol trisphosphate dephosphorylation or on a range of enzymes isolated from wheat roots, suggesting that Al exposure may specifically target PLC. Possible mechanisms of PLC inhibition by Al and the role of Ins(1,4,5)P3 in Al toxicity and growth are discussed. This study provides compelling evidence that the phytotoxic metal cation Al has an intracellular target site that may be integrally involved in root growth.     

有机酸在植物解铝毒中的作用及生理机制

酸性土壤上铝毒是限制作物产量的一个重要障碍因子,具有螯合能力的有机酸在植物铝的外部排斥机制和内部耐受机制均具有重要作用,在铝的外部排斥解毒过程中,植物通过根系分泌有机酸进入根际,如柠檬酸,草酸,苹果酸等与铝形成稳定的复合体,阻止铝进入共质体,从而达到植物体外解除铝毒害效应的目的,且分泌的有机酸对铝的胁迫诱导表现出高度的专一性,分泌的关键点位于根尖,不同的物种间分泌的有机酸种类,分泌的模式及生理机理存在差异,在铝积累型植物的内部解毒过程中,有机酸与铝形成稳定的化合物,降低植物体内铝离子的生理活性,从而降低细胞内铝离子的毒害效应,如绣球花中铝与柠檬酸形成1：1的复合体,荞麦内铝与草酸形成1：3的复合体,本文就有机酸在植物忍耐和积累铝中的作用及生理机制作一简要综述。     

Role of Cyclic Nucleotide-Dependent Actin Cytoskeletal Dynamics: [Ca2+]i and Force Suppression in Forskolin-Pretreated Porcine Coronary Arteries

Initiation of force generation during vascular smooth muscle contraction involves a rise in intracellular calcium ([Ca²⁺]_i) and phosphorylation of myosin light chains (MLC). However, reversal of these two processes alone does not account for the force inhibition that occurs during relaxation or inhibition of contraction, implicating that other mechanisms, such as actin cytoskeletal rearrangement, play a role in the suppression of force. In this study, we hypothesize that forskolin-induced force suppression is dependent upon changes in actin cytoskeletal dynamics. To focus on the actin cytoskeletal changes, a physiological model was developed in which forskolin treatment of intact porcine coronary arteries (PCA) prior to treatment with a contractile agonist resulted in complete suppression of force. Pretreatment of PCA with forskolin suppressed histamine-induced force generation but did not abolish [Ca²⁺]_i rise or MLC phosphorylation. Additionally, forskolin pretreatment reduced filamentous actin in histamine-treated tissues, and prevented histamine-induced changes in the phosphorylation of the actin-regulatory proteins HSP20, VASP, cofilin, and paxillin. Taken together, these results suggest that forskolin-induced complete force suppression is dependent upon the actin cytoskeletal regulation initiated by the phosphorylation changes of the actin regulatory proteins and not on the MLC dephosphorylation. This model of complete force suppression can be employed to further elucidate the mechanisms responsible for smooth muscle tone, and may offer cues to pathological situations, such as hypertension and vasospasm.     

An In Vitro Study of the Effect of Aluminum and the Combined Effect of Strontium, Aluminum, and Fluoride Elements on Early Enamel Carious Lesions

The purpose of this in vitro study was to evaluate the effect of aluminum and of combined strontium, aluminum, and fluoride treatments on enamel demineralization and remineralization. During a 6-day pH-cycling protocol, pre-softened bovine enamel slabs were immersed twice daily for 1 min in the following experimental solutions: (a) distilled water [W] (negative control); (b) 1,000 ppm F [F] (positive control); (c) 1,000 ppm Al [Al]; (d) 1,000 ppm Al,1,000 ppm F applied interchangeably [Al-F]; (e) 1,000 ppm Al, 1,000 ppm F, applied in sequential order [Al+F]; (f) combined 1,000 ppm Al and 150 ppm Sr [Al+Sr]; and (g) combined 150 ppm Sr and 1,000 ppm F [Sr+F]. Subsequently, the specimens were subjected to a 5-day acid resistance test. Lesions were evaluated quantitatively by performing surface microhardness and qualitatively by using polarized light microscopy. According to the results, solutions [Sr+F] and [Al-F] enhanced remineralization and inhibited demineralization as effectively as the [F] solution and significantly superiorly compared to [Al+Sr] and [Al] solutions. All tested solution groups, except for the [Al+Sr] group, presented significantly increased resistance to acidic attack, compared to [W]. PLM examination revealed that all solution groups, except for the [W] group, developed an acid-resistant zone at lesion surfaces. In conclusion, under the present experimental conditions, the combined strontium-fluoride and aluminum-fluoride treatments presented similar anti-caries efficacy compared to fluoride treatment alone, but they did not show evidence of synergistic activity on pre-softened enamel.     

A Highlights from MBoC Selection: Calcineurin-dependent cofilin activation and increased retrograde actin flow drive 5-HT–dependent neurite outgrowth in Aplysia bag cell neurons

Neurite outgrowth in response to soluble growth factors often involves changes in intracellular Ca²⁺; however, mechanistic roles for Ca²⁺ in controlling the underlying dynamic cytoskeletal processes have remained enigmatic. Bag cell neurons exposed to serotonin (5-hydroxytryptamine [5-HT]) respond with a threefold increase in neurite outgrowth rates. Outgrowth depends on phospholipase C (PLC) → inositol trisphosphate → Ca²⁺ → calcineurin signaling and is accompanied by increased rates of retrograde actin network flow in the growth cone P domain. Calcineurin inhibitors had no effect on Ca²⁺ release or basal levels of retrograde actin flow; however, they completely suppressed 5-HT–dependent outgrowth and F-actin flow acceleration. 5-HT treatments were accompanied by calcineurin-dependent increases in cofilin activity in the growth cone P domain. 5-HT effects were mimicked by direct activation of PLC, suggesting that increased actin network treadmilling may be a widespread mechanism for promoting neurite outgrowth in response to neurotrophic factors.     

Cytoskeletal scaffolds regulate riboflavin endocytosis and recycling in placental trophoblasts

Microfilaments and microtubules (MT) play a vital role in cellular endocytic processes. The present study evaluates the role of these cytoskeletal elements in the apical internalization and postendocytic fate of riboflavin (RF) in placental trophoblasts (BeWo cells). Biochemical modification of the actin and microtubule network by (1) okadaic acid (OA), which disrupts MT-based vesicular trafficking; (2) cytochalasin D and latrunculin B, which promote actin depolymerization; and (3) 2,3-butanedione monoxime (BDM), which inhibits myosin–actin interaction, was confirmed by immunofluorescence microscopy using actin- and tubulin-specific antibodies. Furthermore, involvement of the molecular motors dynein and kinesin was assessed in the presence of (1) sodium orthovanadate, which inhibits dynein-ATPase activity and (2) adenosine 5′-(β,γ-imido)triphosphate tetralithium salt hydrate, a non-hydrolyzable ATP analog, which results in defective kinesin-driven processes. RF internalization consequent to cytoskeletal alterations was compared with that of a clathrin-dependent endocytic marker ([¹²⁵I]-transferrin [TF]), a caveolae-mediated endocytic substrate ([³H]-folic acid [FA]), and a fluid-phase endocytic marker ([¹²⁵I]-horse radish peroxidase [HRP]). Apical recycling and bidirectional transport of RF and TF was measured following cytoskeletal alterations. Results indicate that uptake of RF, TF, FA and HRP are markedly reduced (~30–65%) in the presence OA and BDM, suggesting differential sensitivities to modification of kinesin-driven microtubules. However, actin depolymerization negatively affected HRP endocytosis alone, while RF, FA and TF internalization remained unchanged. Disturbances in protein phosphorylation cascades also influenced apical recycling while net ligand transport across monolayers remained unaffected. In conclusion, apical RF trafficking in placental cells is tightly regulated by microtubules and supported by accessory actin involvement.     

Aluminum ions induce DNA synthesis but not cell proliferation in human fibroblasts in vitro

The effect in vitro of aluminum (Al) ions on DNA synthesis and human dermal fibroblast proliferation using [Al] concentrations from 1.85 to 74 μM and incubation periods of 1, 2, 3, 4, and 5 d was assessed. The lowest concentration of Al that exerted a slight positive, although not significant, effect on DNA synthesis was 1.85 μM, after d 3 or 5 of incubation. The stimulating action of Al was more evident and statistically significant from concentrations of 3.7 μM and 2 d exposure onward. This Al-induced effect on [³H] thymidine incorporation into DNA increased in a time-dependent manner as [Al] in the culture medium rose, provoking increments of up to 322% above the control at [Al] 74 μM and 5 d incubation. In contrast, Al salts moderately increased fibroblast division in a continuous manner only from 7.4 to 74 μM after 3 d of incubation. Although significant overall, the minimal and inconstant mitogenic activity of Al differs greatly from and is not parallel to DNA synthesis, which is not clearly related to exposure times or Al concentrations. Abnormalities in Al-induced cellular metabolic processes described herein and their influence on the cell cycle may constitute a toxicity mechanism for human tissues, leading to disease development. Further studies are required to determine whether these findings can be extrapolated to in vivo situations.     

Decreased biosynthesis of actin and cellular fibronectin during adipose conversion of 3T3-F442A cells. Reorganization of the cytoarchitecture and extracellular matrix fibronectin

Differentiation of 3T3-F442A cells was accompanied by changes in cell morphology, decreased synthesis and assembly of actin and fibronectin. The network of microfilament stress fibers detected with NBD-phallacidin was altered during adipose conversion of 3T3-F442A cells. Parallel to this, the disappearance of fibrillar bundles of extracellular matrix fibronectin was observed by immunofluorescence staining. The pericellular fibronectin content, detected by immunoblotting, strongly diminished during the differentiation process. An altered rate of biosynthesis of both proteins was also measured by [35S]-methionine pulse-labeling and immunoprecipitation. A 4-5-fold decrease in cellular fibronectin synthesis was observed in adipocytes compared to control preadipocytes. Conversely, non-differentiating 3T3-C2 control cells did not reorganize either the cytoskeletal architecture or the extracellular matrix fibronectin in the resting state. These results suggest that the decreased rate of biosynthesis of cell-associated fibronectin is correlated with that of actin. Moreover, both events can essentially be ascribed to differentiation.     

有机酸在植物解铝毒中的作用及生理机制

酸性土壤上铝毒是限制作物产量的一个重要障碍因子。具有螯合能力的有机酸在植物铝的外部排斥机制和内部耐受机制均具有重要作用。在铝的外部排斥解毒过程中,植物通过根系分泌有机酸进入根际,如柠檬酸、草酸、苹果酸等与铝形成稳定的复合体,阻止铝进入共质体,从而达到植物体外解除铝毒害效应的目的,且分泌的有机酸对铝的胁迫诱导表现出高度的专一性,分泌的关键点位于根尖。不同的物种间分泌的有机酸种类、分泌的模式及生理机理存在差异。在铝积累型植物的内部解毒过程中,有机酸与铝形成稳定的化合物,降低植物体内铝离子的生理活性,从而降低细胞内铝离子的毒害效应,如绣球花中铝与柠檬酸形成1:1的复合体,荞麦内铝与草酸形成1:3的复合体。本文就有机酸在植物忍耐和积累铝中的作用及生理机制作一简要综述。     

Auxins and Cytokinins as Antipodal Modulators of Elasticity within the Actin Network of Plant Cells

The cytoskeleton of plant and animal cells serves as a transmitter, transducer, and effector of cell signaling mechanisms. In plants, pathways for proliferation, differentiation, intracellular vesicular transport, cell-wall biosynthesis, symbiosis, secretion, and membrane recycling depend on the organization and dynamic properties of actin- and tubulin-based structures that are either associated with the plasma membrane or traverse the cytoplasm. Recently, a new in vivo cytoskeletal assay (cell optical displacement assay) was introduced to measure the tension within subdomains (cortical, transvacuolar, and perinuclear) of the actin network in living plant cells. Cell optical displacement assay measurements within soybean (Glycine max [L.]) root cells previously demonstrated that lipophilic signals, e.g. linoleic acid and arachidonic acid or changes in cytoplasmic pH gradients, could induce significant reductions in the tension within the actin network of transvacuolar strands. In contrast, enhancement of cytoplasmic free Ca2+ resulted in an increase in tension. In the present communication we have used these measurements to show that a similar antipodal pattern of activity exists for auxins and cytokinins (in their ability to modify the tension within the actin network of plant cells). It is suggested that these growth substances exert their effect on the cytoskeleton through the activation of signaling cascades, which result in the production of lipophilic and ionic second messengers, both of which have been demonstrated to directly effect the tension within the actin network of soybean root cells.     

Hypertonicity triggers RhoA-dependent assembly of myosin-containing striated polygonal actin networks in endothelial cells

Endothelial cells respond to mechanical stresses of the circulation with cytoskeletal rearrangements such as F-actin stress fiber alignment along the axis of fluid flow. Endothelial cells are exposed to hypertonic stress in the renal medulla or during mannitol treatment of cerebral edema. We report here that arterial endothelial cells exposed to hypertonic stress rearranged F-actin into novel actin-myosin II fibers with regular 0.5-µm striations, in which -actinin colocalizes with actin. These striated fibers assembled over hours into three-dimensional, irregular, polygonal actin networks most prominent at the cell base, and occasionally surrounding the nucleus in a geodesic-like structure. Hypertonicity-induced assembly of striated polygonal actin networks was inhibited by cytochalasin D, blebbistatin, cell ATP depletion, and intracellular Ca²⁺ chelation but did not require intact microtubules, regulatory volume increase, or de novo RNA or protein synthesis. Striated polygonal actin network assembly was insensitive to inhibitors of MAP kinases, tyrosine kinases, or phosphatidylinositol 3-kinase, but was prevented by C3 exotoxin, by the RhoA kinase inhibitor Y-27632, and by overexpressed dominant-negative RhoA. In contrast, overexpression of dominant-negative Rac or of dominant-negative cdc42 cDNAs did not prevent striated polygonal actin network assembly. The actin networks described here are novel in structure, as striated actin-myosin structures in nonmuscle cells, as a cellular response to hypertonicity, and as a cytoskeletal regulatory function of RhoA. Endothelial cells may use RhoA-dependent striated polygonal actin networks, possibly in concert with cytoskeletal load-bearing elements, as a contractile, tension-generating component of their defense against isotropic compressive forces. mannitol; Rho kinase; blebbistatin; bovine aortic endothelial cells     

Signals,Motors, Morphogenesis -the Cytoskeleton in Plant Development1

Abstract: Plant shape can adapt to a changing environment. This requires a structure that (1) must be highly dynamic, (2) can respond to a range of signals, and (3) can control cellular morphogenesis. The cytoskeleton, microtubules, actin microfi-laments, and cytoskeletal motors meets these requirements, and plants have evolved specific cytoskeletal arrays consisting of both microtubules and microfilaments that can link signal transduction to cellular morphogenesis: cortical microtubules, preprophase band, phragmoplast on the microtubular side, transvacuolar microfilament bundles, and phragmosome on the actin side. These cytoskeletal arrays are reviewed with special focus on the signal responses of higher plants. The signal-triggered dynamic response of the cytoskeleton must be based on spatial cues that organize assembly and disassembly of tu-bulin and actin. In this context the great morphogenetic potential of cytoskeletal motors is discussed. The review closes with an outlook on new methodological approaches to the problem of signal-triggered morphogenesis.