Inhibition Of Bud Outgrowth Research Articles

CAMP inhibits bud growth in a yeast strain compromised for Ca2+ influx into the Golgi.

Biochemical and physiological studies have implicated cAMP and cAMP-dependent protein kinase (PKA) in a plethora of essential cellular processes. Here we show that yeast cells partially depleted of PKA activity (due to a tpkw mutation) and bearing a lesion in a Golgi-localized Ca2+ pump (Pmr1), arrest division with a small bud. The bud morphology of the arrested tpk1w pmr1 mutant cells is characteristic of cells in S phase; however, the terminal phenotype of processes such as DNA replication and nuclear division suggests arrest at the G2/M boundary. This small bud, G2-arrest phenotype is similar to that of strains with a defect in cell wall biosynthesis (pkc1) or membrane biogenesis (och1); however, the biochemical defect may be different since the tpk1w pmr1 double mutants retain viability. The growth defect of the tpk1w pmr1 mutant can be alleviated by preventing the increase in cellular cAMP levels that is known to be associated with a decrease in PKA activity, or by supplementing the medium with millimolar amounts of Ca2+. Although the biochemical consequences of this increase in cAMP concentration are not known, the small-bud phenotype of the double mutant and the known protein processing defect of the pmr1 lesion suggest that the localization or function of some membrane component might be compromised and susceptible to perturbations in cellular cAMP levels. One candidate for such a protein is the cAMP-binding membrane ectoprotein recently described in yeast.

CAMP Inhibits bud growth in a yeast strain compromised for Ca

cAMP Inhibits bud growth in a yeast strain compromised for Ca

Apical dominance in rhizomes of quackgrass, Elytrigia repens: the effect of auxin, cytokinins, and abscisic acid

Experiments were designed to determine the impact of abscisic acid, indole-3-acetic acid, and cytokinins on dormancy of quackgrass (Elytrigia repens (L.) Nevski) rhizome axillary buds using exogenous hormone treatments and analysis of endogenous hormones. Exogenous hormone treatments were applied in solution or in lanolin paste to 5-node segments of rhizome with an apical tip intact or removed. Abscisic acid inhibited bud growth except at concentrations of 0.5 – 1 μg ∙ mL−1 when it stimulated growth: this appeared to be based on an inhibition of apical dominance rather than a stimulation of bud growth per se. Both indole-3-acetic acid and cytokinins stimulated bud growth, indole-3-acetic acid at concentrations of 0.5 – 5 μg ∙ mL−1 and cytokinins at higher concentrations (i.e., 10 – 100 μg ∙ mL−1). Indole-3-acetic acid also increased elongation of the buds, whereas abscisic acid and cytokinins did not. Levels of endogenous hormones were measured in bud samples: indole-3-acetic acid was quantified as its methyl ester by combined gas chromatography – mass spectrometry – selected ion monitoring; abscisic acid was quantified as its methyl ester by gas chromatography – electron capture; and cytokinins were quantified using a soybean callus bioassay. Hormone levels were generally higher in the most active buds of a 5-node section. Abscisic acid was also measured in buds 24 h after sheath leaf removal, a practice known to promote bud sprouting. Sheath leaf removal had no significant effect on abscisic acid levels. Key words: quackgrass, Elytrigia repens, auxins, abscisic acid, cytokinins, apical dominance.

Expression of the Connexin43 Gap Junctional Protein in Tissues at the Tip of the Chick Limb Bud Is Related to the EpitheliaI-Mesenchymal Interactions That Mediate Morphogenesis

The pattern of connexin43 expression in developing chick limb buds was examined using a site-specific polyclonal antibody and confocal microscopy. Connexin43 is expressed at stages of limb development when epithelial-mesenchymal interactions are occurring that mediate morphogenesis. Extensive labeling was observed in the apical ectodermal ridge and labeling was also found in underlying mesenchyme cells at the tip of the bud. In mouse limb buds, the same gap junction protein is expressed only in the apical ridge. Manipulations of developing chick wing buds show that mesenchymal expression of connexin43 appears to be controlled by the apical ectodermal ridge. When the apical ridge is surgically removed and limb truncations result, mesenchymal labeling is markedly reduced and conversely the grafting of an additional ridge induces connexin43 expression between underlying mesenchymal cells which do not normally show expression at this stage of development. In addition, a treatment with retinoic acid that flattens the apical ridge and inhibits bud outgrowth reduces expression in both mesenchymal and epithelial tissues. The abolition of connexin43 expression in mesenchymal and epithelial domains when bud outgrowth is halted suggests that synthesis of this gap junction protein is related to the epithelial-mesenchymal interactions that mediate morphogenesis of the bud.

Rapid in vitro propagation of Aloe barbadensis Mill

Axillary bud development and adventitious bud formation was obtained with decapitated shoot explants of Aloe barbadensis Mill. Maximal bud growth and rooting of shoots was obtained on a modified medium of Murashige and Skoog supplemented with 5 μM IBA. More adventitious and axillary buds developed on nutrient media supplemented with IBA than with NAA. Axillary buds but not adventitious buds developed with IAA in the medium. Morphogenesis was inhibited by 2,4-D. Kinetin, benzyladenine and thidiazuron were toxic to the explants and did not stimulate the development of axillary of adventitious buds. The optimal temperature for bud growth and development was 25°C. Axillary bud growth and the formation of adventitious buds was slowed down at 10°C and totally inhibited by 30°C. The optimal sucrose concentration was 3% with the inhibition of bud growth and development by higher sucrose levels.

Apical Dominance in Rhizomes of Quackgrass (Elytrigia repens): Inhibitory Effect of Scale Leaves

Surgical experiments were conducted on cultured five-node apical rhizome segments of quackgrass. Removal of scale leaves promoted an initial burst of growth within the axillary buds but did not support the continued growth of buds as effectively as removal of the rhizome apex. Replacement of detached scale leaves over denuded buds temporarily repressed the promotive effect of scale leaf removal. Aqueous extracts of scale leaf material inhibited apical growth in rhizome segments but did not inhibit bud growth. Anatomical sections revealed that removal of scale leaves promoted development of buds: cells enlarged, vascular tissues differentiated, and new nodes began to form within 4 days of the removal of scale leaves. It is suggested that scale leaves contribute to apical dominance by inhibiting the initial development of axillary buds.

Patterns of protein synthesis in dormant and growing vegetative buds of pea

Lateral buds on intact pea plants (Pisum sativum L. cv. Alaska) remain dormant until they are stimulated to develop by decapitating the terminal bud. Using two-dimensional gel electrophoresis, we have examined the protein content of terminal and lateral buds from intact plants and from plants at various times after decapitation. Silver-staining and in-vivo-labeling demonstrated very different sets of proteins. The level of expression of 18 stained and 25 labeled proteins was altered when growth was stimulated; this represents 3.4% and 9.1% of the total proteins detected by each method, respectively. Within 24 h of being stimulated, lateral buds doubled in length and their protein content was qualitatively nearly the same as that of terminal buds. Six hours after decapitation, before the onset of detectable growth, the overall pattern of protein synthesis in lateral buds was more like that of growing lateral buds or of terminal buds than that of dormant lateral buds. Direct application of N(6)-furfurylaminopurine (kinetin) to buds on intact plants stimulated their growth and resulted in the same pattern of protein synthesis as did decapitation. Inhibition of bud growth by addition of indole-3-acetic acid to the stumps of decapitated plants resulted in the synthesis of dormancy-related proteins. Lateral buds at all stages of development incorporated labeled amino acids at similar rates, indicating that metabolic activity is not a component of dormancy in these buds.

Ethylene, indoleacetic acid and apical dominance in peas: A reappraisal

Decapitation of peas (Pisum sativum L. cv. Greenfeast) promoted sprouting of the lower buds with the most active growth in the first week occurring in the bud at the lowest fully expanded leaf node. Addition of 3‐indolyl acetic acid (IAA; a 0.03 M solution, applied al 10 and 25 μg/plant) inhibited bud outgrowth whether added to the cut stump or injected above or below the lowest leaf node. Ethylene evolution by the nodal region decreased following decapitation, but increased greatly if IAA was added to the cut stump. Ethylene gas (3, 15 and 1 500 ul/l) or the precursor ACC (l‐aminocyclopropane‐I‐carboxylic acid) reduced bud outgrowth while factors which scrub ethylene (mercuric perchlorate). inhibit ethylene synthesis (canaline), or prevent its action (silver nitrate), enhanced bud growth on decapitated plants, It was concluded that auxin‐induced inhibition of bud growth through an increase in ethylene synthesis is a more logical hypothesis than the direct inhibition by auxin per se since a) acropetal movement of the inhibitory principle occurred whereas [14C] IAA movement in stems was basipetal, b) a decline in the levels of ethylene evolution was correlated with bud outgrowth in decapitated plants and c) exogenous application of chemical agents which increase or decrease ethylene level or response lead to correlative decreases or increases in bud outgrowth, respectively.

Manipulation of Apical Dominance in Sorghum with Growth Regulators 1

The hormonal control of apical dominance (inhibition of lateral bud formation and development) in sorghum [Sorghum bicolor (L.) Moench] was studied by applying plant growth regulators to two cultivars—SM100 (weak apical dominance) and BT×378 (strong apical dominance). In the field, SM100 produced an average of 1 tiller per 2 plants before anthesis and BT×378 produced none. Following anthesis, apical dominance diminished in both cultivars. Spray applications of 0.2 mM gibberellic acid (GA3) during the initial 7 weeks of seedling growth completely inhibited bud outgrowth before anthesis in SM100. Bud outgrowth increased rapidly in both cultivars after termination of GA3 applications. This rapid increase in bud outgrowth was similar to the normal release from apical dominance ocurrlng in untreated plants following anthesis except that it was earlier, occurred at a more rapid rate, and a larger final number of buds was released. Thus, two aspects of the normal pattern of tiller bud development were mimicked by GA3 application: i) intensification of the inhibition of bud outgrowth before anthesis and ii) acceleration of bud outgrowth occurring after anthesis. In plants grown hydroponically in the greenhouse, GA3 again inhibited bud outgrowth in SM100 plants during the vegetative period. A role for gibberellin(s) in sorghum apical dominance is suggested because bud outgrowth was promoted in BT×378 plants by a gibberellin synthesis inhibitor, ancymidol. Evidence for the participation of auxins and cytokinins in sorghum apical dominance was also obtained. The auxin naphthaleneacetic acid inhibited bud outgrowth in SM100. In BT×378 the auxin transport inhibitor naphthylphthalamic acid and the cytokinin benzyladenine caused bud outgrowth which resembled that obtained by apical bud removal.

Apical dominance in the rhizome of Agropyron repens: the influence of humidity and light on the regenerative growth of isolated rhizomes

The influence of humidity and light on the regenerative growth of isolated five-node segments from rhizomes of Agropyron repens was investigated under controlled conditions. When the rhizomes were incubated in the dark at 20 ± 1 °C shoot growth at the apical node was significantly reduced by each 0.5% reduction in relative humidity between 100 and 98.5% and at 98.0% growth at all nodes was completely inhibited. The restriction of these effects to the apical end of the rhizome (nodes 1 and 2) was attributed to their interaction with the basipetal gradient of decreasing N concentration previously identified as one of the causal factors in the polarity of bud activity. Bud inhibition at a relative humidity of 98% was eliminated by supplying water through the basal end of the rhizome. This treatment also released the buds from the inhibition induced by the exposure of the rhizomes to light. Since the uptake of water by the rhizomes was also greater in the light than in the dark it was postulated that the light-induced inhibition of bud growth was due to a reduction in rhizome water potential mediated by an increase in the rate of transpiration.

Abscisic Acid and Apical Dominance in Phaseolus coccineus L. The Role of Tissue Age

Abscisic acid (ABA) applied to the decapitated second internode of runner bean plants enhanced outgrowth of lateral buds only when internode stumps were no longer elongating. Applied to elongating internodes of slightly younger plants, ABA causes inhibition of bud outgrowth. Together with 10(−4) M indol-3-yl acetic acid (IAA), ABA stimulated internode elongation and interacted additively in the inhibition of bud outgrowth. A mixture of 10(−5) M ABA and 10(−6) M gibberellic acid (GA3 ) caused similar effects on internode growth as IAA + ABA, but was mutually antagonistic in effect on growth of the lateral buds.

Studies on the mode of action of asulam in bracken (Pteridium aquilinum L. Kuhn) II. Biochemical activity in the rhizome buds

Summary:The effect of asulam (methyl (4‐aminobenzenesulphonyl) carbamate) on the synthesis of RNA and protein was investigated in bracken sporeling plants and excised rhizome bud tissue. Foliage application of asulam (4.4 kg/ha) reduced the RNA levels in frond buds and young fronds within 3 days, while protein levels were significantly reduced after 14 days. A significant reduction in respiratory activity of buds was observed after 2 weeks, the level of inhibition being 54% after 8 weeks. During a 3‐h incubation period, O2 uptake by excised bud issue was stimulated by 5 and 10 ppm asulam and inhibited by higher concentrations; 32P uptake was inhibited at all concentrations. Asulam (5 ppm and above) inhibited bud growth and reduced RNA and protein levels in incubated buds (20 h at 30°C), and the incorporation of [14C]orotic acid into RNA and [14C]leucine into protein. Reduction of RNA levels and inhibition of [14C]ladenine incorporation into RNA in buds occurred entirely in the ribosomal and supernatant fractions of the cellular extract. Inhibition of RNA synthesis by asulam (50 ppm) as measured by [14C] orotic acid incorporation into RNA was completely antagonized by CEPA (3‐chloroethylphosphonic acid) (50 ppm) and partially by 2,4‐D (2,4‐dichlorophenoxyacetic acid) (50 ppm) and GA (Gibberellic acid) (50 ppm). These results suggest that the interference of asulam with RNA and protein synthesis at the metabolically active sinks (rhizome buds) could be one of its major mechanisms of action in bracken.

Inhibitory Effect of a Rhizobitoxine Analog on Bud Growth after Release from Dormancy

Application of the ethoxy analog of rhizobitoxine (l-2-amino-4-[2'-aminoethoxy]-trans-3-butenoic acid), an inhibitor of ethylene biosynthesis, inhibited growth of apple, crabapple, and apricot buds released from dormancy by chilling or by treatment with benzyladenine. When tea crabapple (Malus hupehensis [Pamp.] Rehd.) buds were sprayed once with 8.8 x 10(-3)m benzyladenine, ethylene production by the buds increased significantly 24 to 48 hours after benzyladenine treatment. Application of the rhizobitoxine analog to the buds at the time of benzyladenine treatment reduced ethylene evolution to the level of the controls for up to 2 weeks after treatment. Increase in bud weight was inhibited also but to a lesser extent. These data suggest that growth of buds is accompanied by ethylene production and that the inhibition of ethylene biosynthesis also inhibits bud growth. Since additional metabolic effects result from the action of the rhizobitoxine analog, no firm conclusions on its role can be drawn at this time.

Effects of Far-red Light on the Hormonal Control of Side Shoot Growth in the Tomato

Side shoot growth in young tomato plants was almost completely suppressed by a 5 min period of far-red light immediately following a 16 h photoperiod from fluorescent tubes, whereas plants given an identical photoperiod but lacking the far-red treatment branched profusely. The influence of far-red light on the degree of side shoot suppression and the correlated changes in the levels of auxins, gibberellins, cytokinins and abscisic acid is presented and discussed in relation to current hypotheses of correlative inhibition. It is suggested that far-red light causes increased auxin synthesis in the apex and young leaves, which in turn induces the formation of abscisic acid in or near the axillary buds, and it is this hormone which inhibits bud outgrowth. The role of cytokinins and gibberellins remains uncertain but they probably act in a sequential manner, the gibberellins promoting bud growth following cytokinin-mediated release from apical dominance.

Lateral bud growth on excised stem segments: effect of the stem

Lateral buds at the cotyledonary nodes of soybean plants grown under the conditions used in this study usually remain inhibited. These buds grow when the apical part of the plant is removed. They will grow, but less strongly, when the roots as well as the apex of the plant are removed and the basal end of the cut stem is placed in a mineral salt solution. Bud growth is further diminished by decreasing the length of stem left attached to the bud. The cotyledon is essential for bud growth on plant segments maintained in nutrient solution, but it can be replaced by a 1% sucrose solution during the early days of bud growth. Buds which are completely detached from the stem and placed in 1% sucrose do not elongate, but a small number of cell divisions are detectable, indicating that the early events of the release from inhibition have occurred. Buds elongate when they are apically or centrally located on stem segments. Increasing the length of the attached stem segments increases the growth of the buds. Additions of the cytokinin benzyladenine to plants causes a dramatic increase in bud growth when buds are attached to stem segments but does not stimulate growth of buds without stem segments. It is concluded that benzyladenine alone will not substitute for a factor(s) present in the stem which is necessary for bud growth. Increasing stem lengths above buds located at the basal ends of segments inhibits bud growth. It is suggested that this may be due to an accumulation of endogenous auxin at the site of the buds.

Differential Responses of Buds along the Shoot to Factors Involved in Apical Dominance

Intact and decapitated 6-node shoots of Hygrophila sp. were grown aseptically immersed in liquid half-strength Knop's solution with microelements and 2% (w/v) sucrose (control medium), and in medium with 0.1 mg l−1 benzyladenine (BA). In intact shoots grown in control medium apical dominance suppressed outgrowth of the lateral buds; in decapitated shoots buds grew out at several of the most apical nodes, increasing in size acropetally. There was a lag in outgrowth of the bud at the most apical node, attributable to its initially smaller size. Lateral shoots grew out first at basal nodes of intact shoots in BA medium, decreasing in size acropetally; in decapitated shoots in BA medium lateral shoots of approximately equal size grew out at all nodes. Differential effects of decapitation and cytokinin treatment on lateral shoot outgrowth along the shoot could be interpreted by postulating a basipetally decreasing gradient of endogenous auxin concentration in the intact shoot. Application of 20 mg l−1 indoleacetic acid (IAA) in agar to decapitated shoots completely prevented bud outgrowth for at least 7 d in control medium, inhibiting it thereafter, and inhibited bud outgrowth in BA medium, thus supporting the hypothesis. Comparison of lateral shoot outgrowth in whole decapitated shoots and severed decapitated shoots (isolated nodes) lent no support to the alternative hypothesis that there might be an acropetally decreasing concentration gradient of a bud-promoting substance in the intact shoot, and demonstrated much greater lateral shoot growth in isolated nodes. The results emphasize important correlative relationships between the parts of a shoot with several nodes.

Hormonal interaction in controlling apical dominance in soybeans

Growth of cotyledonary buds in soybean plants is controlled by an interaction between hormones and is dependent on age of the plant and meristematic activity of the buds. Indoleacetic acid (IAA) applied to the cut surface of decapitated 7-day-old plants does not inhibit the growth of buds which are actively undergoing mitosis. Growth is inhibited, however, when IAA is applied in combination with benzyl-adenine(BA) and this inhibitory effect is minimized by gibberellic acid (GA). In 16-day-old plants where mitosis in the buds has ceased IAA alone inhibits bud growth. In both 7- and 16-day-old decapitated plants, application of GA, alone or in combination with BA promotes growth of the buds. Inhibited buds have two peroxidase isoenzymes with pronounced activity. The activity of one of these decreases when the buds are released from dominance. Benzyladenine applied directly to inhibited buds initiates growth in 16-day-old intact plants and this growth is further enhanced when GA is applied 48 h after BA treatment. The enhanced growth by GA is prevented if 5-fluorouracil (5-FU) or 5-fluorodeoxyuridine (5-FDU) are applied before but not after the GA treatment. These results indicate that the hormones have a sequential role in releasing buds from apical dominance.

Effect of relative hormone concentration on auxin-gibberellin interaction in correlative inhibition of axillary buds

Indole-3-acetic acid (IAA) applied to the fully elongated second internode of decapitated Phaseolus multiflorus plants always inhibited axillary bud elongation at concentrations down to 100 μg/g lanolin, whereas gibberellic acid (GA3) enhanced bud elongation at concentrations down to 1000 μg/g lanolin. Lower concentrations than these of either IAA or GA3 were without significant effect. All possible combinations of IAA and GA3 within the concentration range 10(1) to 10(5) μg/g lanolin were antagonistic; IAA tending to inhibit, and GA3 promote, axillary bud elongation growth. Treatment of an elongating internode with the hormones resulted in an increase in inhibition of bud growth by IAA in the presence of GA3.

The hormonal regulation of bud outgrowth in Phaseolus vulgaris L.

Aqueous solutions of indole acetic acid, kinetin, gibberellic acid and abscisic acid were applied singly and in combination to the decapitated stem stump of Phaseolus seedlings. Application of indole acetic acid will not completely replace the intact stem apex with regard to the inhibition of lateral bud extension. The greatest inhibition of bud growth is obtained when indole acetic acid is applied in combination with both kinetin and abscisic acid. Treatment with gibberellic acid causes massive bud growth even in the presence of indole acetic acid, kinetin and abscisic acid. Although both abscisic acid and kinetin have only a slight promoting effect on bud outgrowth when applied singly, these hormones will modify the effects of indole acetic acid and gibberellic acid.

Ethylene Formation in Pea Seedlings; Its Relation to the Inhibition of Bud Growth Caused by Indole-3-Acetic Acid

Indole-3-acetic acid stimulates ethylene production in the nodal region of pea stems, and the gas inhibits bud growth. At all concentrations of IAA there is a close correlation between the intensity and duration of ethylene production and the bud inhibition which results. Kinetin reverses the inhibitory actions of ethylene and IAA on bud growth. It is concluded that auxins suppress bud development by stimulating ethylene formation. The possibility that auxin induced ethylene formation controls apical dominance is considered.