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.     

Concepts and terminology of apical dominance

Apical dominance is the control exerted by the shoot apex over lateral bud outgrowth. The concepts and terminology associated with apical dominance as used by various plant scientists sometimes differ, which may lead to significant misconceptions. Apical dominance and its release may be divided into four developmental stages: (I) lateral bud formation, (II) imposition of inhibition on lateral bud growth, (III) release of apical dominance following decapitation, and (IV) branch shoot development. Particular emphasis is given to discriminating between Stage III, which is accompanied by initial bud outgrowth during the first few hours of release and may be promoted by cytokinin and inhibited by auxin, and Stage IV, which is accompanied by subsequent bud outgrowth occurring days or weeks after decapitation and which may be promoted by auxin and gibberellin. The importance of not interpreting data measured in Stage IV on the basis of conditions and processes occurring in Stage III is discussed as well as the correlation between degree of branching and endogenous auxin content, branching mutants, the quantification of apical dominance in various species (including Arabidopsis ), and apical control in trees.     

Auxin-gibberellin interaction in apical dominance

Indoleacetic acid and gibberellic acid were added to decapitated light-grown `Alaska' pea seedlings as substitutes for the intact apex in the control of apical dominance. Of various concentrations and combinations tried, a combination of 1% indoleacetic acid + 1% gibberellic acid was the most inhibiting to side bud growth. The greatest degree of hormonally induced side bud inhibition was achieved when seedlings were deprived of soil nutrients.     

Polarity and apical dominance in Fucus vesiculosus

In Fucus vesiculosus L., culture experiments have illustrated that within 2 mm of the apical cell, the origin of new meristems is inhibited. Further behind the apex, the influence of apical dominance gradually diminishes and beyond about 2 cm its effect is negligible. Polarity, which is so marked in the young plant, is not obvious in older tissues. There is no morphological difference between the branches produced from both cut surfaces of a segment of thallus. But, particularly in young tissue, there is a greater potential for regeneration from what is morphologically the upper end of a segment.     

The fall and rise of apical dominance

The plant hormone auxin, synthesised in the shoot apex, moves down the stem and inhibits lateral branching. Auxin does not travel upward into the branches, so it must act indirectly; for example, through a second messenger. However, recent work on auxin transport suggests a possible additional mechanism whereby auxin transport in the stem prevents the establishment of auxin transport out of the branches, inhibiting their growth.     

Maintaining apical dominance in the fern gametophyte

A kinetic model is developed for cell differentiation in the fern gametophyte to test hypotheses on the role of spatially patterned plasmodesmata networks in development. Of particular interest is the establishment and maintenance of apical cell type in a single cell, with concurrent suppression of this character in all other cells (apical dominance). Steps towards understanding apical cell localization in geometrically simple gametophytes may shed light on the establishment and maintenance of apical meristems in higher plants. The model, based on the plasmodesmata maps of Tilney and colleagues and involving kinetics for a requisite minimum of two morphogens. successfully produces the apical/non-apical cell differentiation patterns of normal development, and redifferentiation due to cell isolation, in six stages from 0-30 d of development. Our results indicate that increasing apical cell plasmodesmata number, as development progresses, is not required for effective transport across apical cell walls in maintaining apical dominance.     

Nitrogen supply,apical dominance and branch growth inPinus radiata

Summary Branch development inP. radiata seedlings and young trees is affected by the level of nitrogen supply. A marginal nitrogen deficiency reduces branch and stem diameter growth much more than it does stem height growth. On soils of low N content mature trees have better than normal form. Fertilizing young trees may have undesirable side effects such as promoting branch growth and reducing leader dominance.     

Abscisic acid and apical dominance in Phaseolus coccineus L.

Abscisic acid (ABA) in lanolin, applied to the internode of decapitated runner bean plants enhances the outgrowth of lateral buds. The optimum concentration of the paste is 10^-5 M. The effect of ABA is counteracted by indoleacetic acid (IAA) but not by gibberellic acid (GA₃). There is no effect when ABA is applied to the apical bud or lateral buds of intact plants. However, 13.2 ng given to the lateral buds of decapitated plants stimulate their growth, whereas higher concentrations are inhibitory. Consequently, ABA enhances growth of lateral buds directly, but only when apical dominance is already weakened. The growth of the decapitated 2^nd internode was not affected by ABA. Radioactivity from [2-¹⁴C] ABA, applied to nonelongating 2^nd internode stumps of decapitated runner bean plants moves to the lateral buds, whereas [1-¹⁴C]IAA-and [³H]GA₁-translocation is much weaker. ABA transport is inhibited if IAA or [³H]GA₁ is applied simultaneously. In elongating internodes [¹⁴C]ABA is almost completely immobile. [¹⁴C]IAA-and [³H]GA₁-translocation is not affected by ABA. The amount of radioactivity from labelled ABA, translocated to the lateral buds, is highest during the early stages of bud outgrowth.Abbreviations ABA 2,4-cis, trans-(+)-abscisic acid - GA gibberellic acid - IAA indoleacetic acid - p.l. plain lanolin     

Steroid hormone effects on growth and apical dominance of sunflower

External application of estradiol-17β increased shoot growth but decreased root growth of sunflower seedlings. It completely inhibited cotyledonary axillary bud development in decapitated plants at the concentration of 1 μg/plant. Concentrations lower than this promoted cotyledonary axillary bud formation. Testosterone on the other hand inhibited both shoot and root growth and promoted cotyledonary axillary bud formation at all the concentrations used. Progesterone at high (0.25,μg/plant) concentration promoted shoot growth but inhibited root growth. A low concentration (0.1 μg/plant) of progesterone produced the opposite effect.     

Effect of gravity on apical dominance in Pharbitis nil.

When the upper part of main shoot of morning glory (Pharbitis nil) is gently bent down, lateral bud on the bending region is released from apical dominance and starts to elongate. But, clinorotating the bending shoots prevents the release of the lateral bud from apical dominance. These results suggest that gravity affects apical dominance in morning glory. Here we verified the gravity-regulated apical dominance by using a weeping morning glory defective in gravitropic response due to abnormal differentiation of endodermis. That is, bending main shoot of the weeping morning glory hardly caused the lateral bud to elongate. In addition, decapitation of apical bud released the lateral bud from apical dominance, and exogenous auxin applied to the cut surface of the decapitated stem was inhibitory to the outgrowth of the lateral bud in the wild type. However, the effect of auxin was much less in the weeping morning glory. Thus, apical dominance of the weeping morning glory was weaker and less influenced by gravity than that of the wild type, which could occur due to abnormal differentiation of endodermis required for graviperception.     

Vacuolar processing enzyme activates programmed cell death in the apical meristem inducing loss of apical dominance

The potato (Solanum tuberosum L.) tuber is a swollen underground stem that can sprout in an apical dominance (AD) pattern. Bromoethane (BE) induces loss of AD and the accumulation of vegetative vacuolar processing enzyme (S. tuberosum vacuolar processing enzyme [StVPE]) in the tuber apical meristem (TAM). Vacuolar processing enzyme activity, induced by BE, is followed by programmed cell death in the TAM. In this study, we found that the mature StVPE1 (mVPE) protein exhibits specific activity for caspase 1, but not caspase 3 substrates. Optimal activity of mVPE was achieved at acidic pH, consistent with localization of StVPE1 to the vacuole, at the edge of the TAM. Downregulation of StVPE1 by RNA interference resulted in reduced stem branching and retained AD in tubers treated with BE. Overexpression of StVPE1 fused to green fluorescent protein showed enhanced stem branching after BE treatment. Our data suggest that, following stress, induction of StVPE1 in the TAM induces AD loss and stem branching.     

On the use of morphactin and triiodobenzoic acid in apical dominance studies

Summary Application of either CFM or TIBA to bean plants caused four main effects: (i) inhibition of main shoot and leaf growth; (ii) abscission of young leaflets and internodes; (iii) limited outgrowth of lateral buds below the point of application of the substances followed by abscission of these buds; (iv) abscission of all other lateral buds. Although the chemical pruning effects of CFM and TIBA may be the result of their action in blocking auxin transport, the use of these substances for analysing auxin effects in apical dominance is questionable.     

Ubiquitin lysine 63 chain forming ligases regulate apical dominance in Arabidopsis

Lys-63-linked multiubiquitin chains play important roles in signal transduction in yeast and in mammals, but the functions for this type of chain in plants remain to be defined. The RING domain protein RGLG2 (for RING domain Ligase2) from Arabidopsis thaliana can be N-terminally myristoylated and localizes to the plasma membrane. It can form Lys-63-linked multiubiquitin chains in an in vitro reaction. RGLG2 has overlapping functions with its closest sequelog, RGLG1, and single mutants in either gene are inconspicuous. rglg1 rglg2 double mutant plants exhibit loss of apical dominance and altered phyllotaxy, two traits critically influenced by the plant hormone auxin. Auxin and cytokinin levels are changed, and the plants show a decreased response to exogenously added auxin. Changes in the abundance of PIN family auxin transport proteins and synthetic lethality with a mutation in the auxin transport regulator BIG suggest that the directional flow of auxin is modulated by RGLG activity. Modification of proteins by Lys-63-linked multiubiquitin chains is thus important for hormone-regulated, basic plant architecture.     

Auxin acts in xylem-associated or medullary cells to mediate apical dominance

A role for auxin in the regulation of shoot branching was described originally in the Thimann and Skoog model, which proposes that apically derived auxin is transported basipetally directly into the axillary buds, where it inhibits their growth. Subsequent observations in several species have shown that auxin does not enter axillary buds directly. We have found similar results in Arabidopsis. Grafting studies indicated that auxin acts in the aerial tissue; hence, the principal site of auxin action is the shoot. To delineate the site of auxin action, the wild-type AXR1 coding sequence, which is required for normal auxin sensitivity, was expressed under the control of several tissue-specific promoters in the auxin-resistant, highly branched axr1-12 mutant background. AXR1 expression in the xylem and interfascicular schlerenchyma was found to restore the mutant branching to wild-type levels in both intact plants and isolated nodes, whereas expression in the phloem did not. Therefore, apically derived auxin can suppress branching by acting in the xylem and interfascicular schlerenchyma, or in a subset of these cells.     

Participation of gibberellin in the control of apical dominance in soybean and redwood

Summary Loss of apical dominance in soybeans and redwood was increased when the plants were treated with the growth retardant AMO-1618. Simultaneous application of gibberellin reduced the number of elongating buds and promoted growth of the first or second uppermost axillary bud, thus restoring apical dominance. It is concluded that gibberellin participates in the expression of apical dominance.     

Release of apical dominance in potato tuber is accompanied by programmed cell death in the apical bud meristem

Potato (Solanum tuberosum) tuber, a swollen underground stem, is used as a model system for the study of dormancy release and sprouting. Natural dormancy release, at room temperature, is initiated by tuber apical bud meristem (TAB-meristem) sprouting characterized by apical dominance (AD). Dormancy is shortened by treatments such as bromoethane (BE), which mimics the phenotype of dormancy release in cold storage by inducing early sprouting of several buds simultaneously. We studied the mechanisms governing TAB-meristem dominance release. TAB-meristem decapitation resulted in the development of increasing numbers of axillary buds with time in storage, suggesting the need for autonomous dormancy release of each bud prior to control by the apical bud. Hallmarks of programmed cell death (PCD) were identified in the TAB-meristems during normal growth, and these were more extensive when AD was lost following either extended cold storage or BE treatment. Hallmarks included DNA fragmentation, induced gene expression of vacuolar processing enzyme1 (VPE1), and elevated VPE activity. VPE1 protein was semipurified from BE-treated apical buds, and its endogenous activity was fully inhibited by a cysteinyl aspartate-specific protease-1-specific inhibitor N-Acetyl-Tyr-Val-Ala-Asp-CHO (Ac-YVAD-CHO). Transmission electron microscopy further revealed PCD-related structural alterations in the TAB-meristem of BE-treated tubers: a knob-like body in the vacuole, development of cytoplasmic vesicles, and budding-like nuclear segmentations. Treatment of tubers with BE and then VPE inhibitor induced faster growth and recovered AD in detached and nondetached apical buds, respectively. We hypothesize that PCD occurrence is associated with the weakening of tuber AD, allowing early sprouting of mature lateral buds.     

Some aspects of daughter bulb growth and development and apical dominance in bulbous Iris

Apical dominance appears to have minimal direct involvementin daughter bulb formation in the bulbous Iris cultivar Ideal.Daughter bulb number and growth relate to the size and reproductivestate of the mother bulb and are not markedly influenced bymeristem destruction. In contrast, destruction or removal ofthe apical meristem promotes lateral bud sprouting in intactbulbs, and lateral bud elongation in Iris meristem explants.These results show that, in contrast to certain other bulbousplants, apical dominance does not direcdy limit daughter bulbnumber in bulbous Iris, but does prevent lateral bud sprouting. (Received September 6, 1978; )     

Regulation of apical dominance in Aspergillus nidulans hyphae by reactive oxygen species

In fungal hyphae, apical dominance refers to the suppression of secondary polarity axes in the general vicinity of a growing hyphal tip. The mechanisms underlying apical dominance remain largely undefined, although calcium signaling may play a role. Here, we describe the localized accumulation of reactive oxygen species (ROS) in the apical region of Aspergillus nidulans hyphae. Our analysis of atmA (ATM) and prpA (PARP) mutants reveals a correlation between localized production of ROS and enforcement of apical dominance. We also provide evidence that NADPH oxidase (Nox) or related flavoproteins are responsible for the generation of ROS at hyphal tips and characterize the roles of the potential Nox regulators NoxR, Rac1, and Cdc42 in this process. Notably, our genetic analyses suggest that Rac1 activates Nox, whereas NoxR and Cdc42 may function together in a parallel pathway that regulates Nox localization. Moreover, the latter pathway may also include Bem1, which we propose represents a p40phox analog in fungi. Collectively, our results support a model whereby localized Nox activity generates a pool of ROS that defines a dominant polarity axis at hyphal tips.     

Execution of the auxin replacement apical dominance experiment in temperate woody species

The classic Thimann-Skoog or auxin replacement apical dominance test of exogenous auxin repression of lateral bud outgrowth was successfully executed in both seedlings and older trees of white ash, green ash, and red oak under the following conditions: (1) decapitation of a twig apex and auxin replacement were carried out during spring flush, (2) the decapitation was in the previous season's overwintered wood, and (3) the point of decapitation was below the upper large irrepressible lateral buds but above the lower repressible lateral buds. Although it has been suggested that neither auxin, the terminal bud, nor apical dominance have control over the outgrowth of the irrepressible buds during spring flush, there is evidence in the present study that indicates that such control over the repressible buds exists. In seedlings, second-order branching, which resulted from decapitation of elongating current shoots, was also inhibited by exogenous auxin in the three species. Hence, the auxin replacement experiments did work on year-old proleptic buds (of branches of older trees) that would have entered the bud bank and also on current buds of seedlings. Cytokinin treatments were ineffectual in promoting bud growth.