About: Coleoptile is a research topic. Over the lifetime, 2281 publications have been published within this topic receiving 62591 citations.
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TL;DR: The Acid Growth Theory, which states that when exposed to auxin, susceptible cells excrete protons into the wall (apoplast) at an enhanced rate, resulting in a decrease in apoplastic pH, activates wall-loosening processes, the precise nature of which is unknown.
Abstract: Plant cells elongate irreversibly only when load-bearing bonds in the walls are cleaved. Auxin causes the elongation of stem and coleoptile cells by promoting wall loosening via cleavage of these bonds. This process may be coupled with the intercalation of new cell wall polymers. Because the primary site of auxin action appears to be the plasma membrane or some intracellular site, and wall loosening is extracellular, there must be communication between the protoplast and the wall. Some "wall-loosening factor" must be exported from auxin-impacted cells, which sets into motion the wall loosening events. About 20 years ago, it was suggested that the wall-loosening factor is hydrogen ions. This idea and subsequent supporting data gave rise to the Acid Growth Theory, which states that when exposed to auxin, susceptible cells excrete protons into the wall (apoplast) at an enhanced rate, resulting in a decrease in apoplastic pH. The lowered wall pH then activates wall-loosening processes, the precise nature of which is unknown. Because exogenous acid causes a transient (1-4 h) increase in growth rate, auxin must also mediate events in addition to wall acidification for growth to continue for an extended period of time. These events may include osmoregulation, cell wall synthesis, and maintenance of the capacity of walls to undergo acid-induced wall loosening. At present, we do not know if these phenomena are tightly coupled to wall acidification or if they are the products of multiple independent signal transduction pathways.
TL;DR: The response of antioxidants to acclimation and chilling in various tissues of dark-grown maize seedlings was examined in relation to chilling tolerance and protection from chilling-induced oxidative stress, illustrating the potential ways in which chilling tolerance may be improved in preemergent maize Seedlings.
Abstract: The response of antioxidants to acclimation and chilling in various tissues of dark-grown maize (Zea mays L.) seedlings was examined in relation to chilling tolerance and protection from chilling-induced oxidative stress. Chilling caused an accumulation of H2O2 in both the coleoptile + leaf and the mesocotyl (but not roots), and acclimation prevented this accumulation. None of the antioxidant enzymes were significantly affected by acclimation or chilling in the coleoptile + leaf or root. However, elevated levels of glutathione in acclimated seedlings may contribute to an enhanced ability to scavenge H2O2 in the coleoptile + leaf. In the mesocotyl (visibly most susceptible to chilling), catalase3 was elevated in acclimated seedlings and may represent the first line of defense from mitochondria-generated H2O2. Nine of the most prominent peroxidase isozymes were induced by acclimation, two of which were located in the cell wall, suggesting a role in lignification. Lignin content was elevated in mesocotyls of acclimated seedlings, likely improving the mechanical strength of the mesocotyl. One cytosolic glutathione reductase isozyme was greatly decreased in acclimated seedlings, whereas two others were elevated, possibly resulting in improved effectiveness of the enzyme at low temperature. When taken together, these responses to acclimation illustrate the potential ways in which chilling tolerance may be improved in preemergent maize seedlings.
TL;DR: The findings suggest that auxin induces a proton accumulation in a cell wall compartment and, as a consequence, enzymatic cell wall softening, which may be the last step in the process of cell elongation.
Abstract: 1. Sections of auxin-starved hypocotyls of Helianthus annuus do not show any significant growth rate in water of buffers of pH\>-6. However, in buffers with pH-values of approximately 4, elongation growth is observed; its rate is similar to the rate of auxin-stimulated growth (after 6 h incubation). \3- This phenomenon of acid-induced growth occurs also under anaerobic conditions in contrast to auxin-induced growth (Hager 1962). 2. Intact cell wall aggregates of Helianthus hypocotyls were obtained by complete plasmolysis of hypocotyls in 50% glycerol; cell wall associated enzymes were still active after this treatment, at least in part. While cell walls in solutions of pH\>-6 show only a small plastic extension during the first minute in response to a 50 g stretching force, a constant rate of elongation over longer periods of time (measured up to 1 h) is observed in weakly acid buffers. The highest rate of elongation is observed at about pH 4. This acid-induced plastic extension is completely inhibited by Cu(2+)-ions (5mM); the elongation of cell walls is apparently the consequence of an enzyme-catalysed increase in plasticity having a pH optimum of about 4. The pH optimum of acid-induced cell wall extension observed during stretching of plasmolysed hypocotyls coincides with the pH optimum of acid-induced growth of intact hypocotyl sections (around pH 4). 3. Under anaerobic conditions the growth rate of intact coleoptiles stays unchanged (at a low value) if the sections are incubated in a buffer of pH 5.0. Higher proton concentrations, however, stimulate growth immediately, whereas low proton concentrations are inhibitory (Fig. 7 and 8). The strongest initial growth response is elicited by buffers or acids of pH 3.9 (Fig. 9). Acid-induced growth of coleoptiles with a similar pH optimum is also found under anaerobic conditions. The growth of coleoptile cylinders can be switched on or off by repeatedly changing to acid or basic medium, respectively (under conditions of anaerobiosis) (Fig. 10). IAA-induced growth (aerobic conditions, pH≥5) can also be inhibited immediately by basic buffers or NaOH-solutions, and resumes after the pH value is lowered (Fig. 11). This pH-dependency may be taken as an indication that auxin affects the same reaction which is stimulated by high proton concentrations and which may be the last step in the process of cell elongation. CCCP, known to make membranes permeable for protons, rapidly inhibits the auxin-induced elongation growth (pH 6,5) when applied at a concentration which does not influence respiration; removal of CCCP shows that the growth inhibition by CCCp is partly reversible (Fig. 12). In contrast, acid-induced elongation growth (pH 4) shows inhibition by CCCP not before 10 min after application.-These findings suggest that auxin induces a proton accumulation in a cell wall compartment and, as a consequence, enzymatic cell wall softening. Such an accumulation could be brought about by an auxin-activated, membrane-bound, anisotropic ATPase or ion pump. The notion that ATPases or pumps may be located in the outer layers of the cell membrane is supported by the observation that addition of ATP to coleoptile cylinders under anaerobic conditions results in an immediate stimulation of elongation (Fig. 14). This effect is further enhanced by Mg(2+)-and K(+)-ions (Figs. 15 and 16). Mg(2+) can be partly replaced by Ca(2+). The stimulatory effect of ATP is increased considerably if the coleoptiles are treated with IAA under aerobic conditions prior to ATP addition (Figs. 15 b and 14). ITP, GTP, UTP, and CTP induce elongation growth under anaerobiosis similarly to ATP. In the presence of ITP or GTP the increase in growth rate is maintained over a longer period of time than in the presence of the other nucleoside triphosphates (Fig. 17). IAA, which causes no elongation growth under anaerobiosis (Fig. 13) is also unable to further stimulate the elongation growth induced by ATP, UTP, or CTP under anaerobiosis (Fig. 18); however, if IAA is added after growth has been stimulated by GTP or ITP, a temporary inhibition and, 10 min later, a strong stimulation is noticed (Fig. 19). If the sequence of addition is reversed, -that is, if IAA (without growth effect) and, after 20 min, GTP or ITP are added to the coleoptiles-, the same initial inhibition and subsequent increase of the growth rate is found (Fig. 20). Thus, IAA can stimulate growth of coleoptiles even under anaerobic conditions if GTP or ITP is present at the same time. 4. The results support the following hypothesis (Fig. 21): auxin acts cooperatively with GTP (ITP) as an effector of a membrane-bound, anisotropic ATPase or proton pump. This pump, activated by auxin, utilizes respiration energy (ATP or other nucleoside triphosphates) to raise the proton concentration in a compartment at the cell wall. This event leads to an increase in the activity of enzymes softening cell walls and thus triggers cell elongation. The transport or secretion of protons into the cell wall compartment should be compensated by a flow of cations into the interior of the cytoplasm or by a flow of anions to the cell periphery, thus causing secondary auxin effects.
TL;DR: It is concluded that OH fulfils basic criteria for a wall-loosening factor acting in auxin-mediated elongation growth of plant species with widely differing cell-wall polysaccharide compositions.
Abstract: Hydroxyl radicals (OH) are capable of unspecifically cleaving cell-wall polysaccharides in a site-specific reaction. I investigated the hypothesis that cell-wall loosening underlying the elongation growth of plant organs is controlled by apoplastically produced OH attacking load-bearing cell-wall matrix polymers. Isolated cell walls (operationally, frozen/thawed, abraded segments from coleoptiles or hypocotyls, respectively) from maize, cucumber, soybean, sunflower or Scots pine seedlings were pre-loaded with catalytic Cu or Fe ions and then incubated in a mixture of ascorbate + H 2 O 2 for generating OH in the walls. This treatment induced irreversible wall extension (creep) in walls stretched in an extensiometer. The reaction could be promoted by acid pH and inhibited by several OH scavengers. Generation of OH by the same reaction in living coleoptile or hypocotyl segments caused elongation growth. Auxin-induced elongation growth of maize coleoptiles could be inhibited by OH scavengers. Auxin promoted the production of superoxide radicals (O 2 - ), an OH precursor, in the growth-controlling outer epidermis of maize coleoptiles. It is concluded that OH fulfils basic criteria for a wall-loosening factor acting in auxin-mediated elongation growth of plant species with widely differing cell-wall polysaccharide compositions.
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