Dose responses of cytokinins

Nissen, P.

doi:10.1111/j.1399-3054.1988.tb02002.x

Cited by 22 publications

(11 citation statements)

References 70 publications

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“…Like auxin, cytokinin generally inhibits root elongation (Stenlid, 1982;Nissen, 1988), but the hormone has been inferred to stimulate (Guttman, 1956;MacLeod, 1968), as well as to inhibit cell production (Butcher and Street, 1960;Van't Hof, 1968). We found that cytokinin reduced maximal strain rate significantly and so diminished the magnitude of cellular elongation.…”

Section: Comparison Of Cytokinin and Auxin Effects On Root Growthmentioning

confidence: 55%

STUNTED PLANT 1 Mediates Effects of Cytokinin, But Not of Auxin, on Cell Division and Expansion in the Root of Arabidopsis

2000

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Plants control organ growth rate by adjusting the rate and duration of cell division and expansion. Surprisingly, there have been few studies where both parameters have been measured in the same material, and thus we have little understanding of how division and expansion are regulated interdependently. We have investigated this regulation in the root meristem of the stunted plant 1 (stp1) mutation of Arabidopsis, the roots of which elongate more slowly than those of the wild type and fail to accelerate. We used a kinematic method to quantify the spatial distribution of the rate and extent of cell division and expansion, and we compared stp1 with wild type and with wild type treated with exogenous cytokinin (1 m zeatin) or auxin (30 nm 2,4-dichlorophenoxyacetic acid). All treatments reduced average cell division rates, which reduced cell production by the meristem. Auxin lowered root elongation by narrowing the elongation zone and reducing the time spent by a cell in this zone, but did not decrease maximal strain rate. In addition, auxin increased the length of the meristem. In contrast, cytokinin reduced root elongation by lowering maximal strain rate, but did not change the time spent by a cell within the elongation zone; also, cytokinin blocked the increase in length and cell number of the meristem and elongation zone. The cytokinin-treated wild type phenocopied stp1 in nearly every detail, supporting the hypothesis that cytokinin affects root growth via STP1. The opposite effects of auxin and cytokinin suggest that the balance of these hormones may control the size of the meristem.How does a plant regulate the rate at which its organs grow? This question is important because as a plant develops and responds to the environment, organ growth rate is regulated carefully. The rate at which organs grow depends on the rates of cell division and expansion. However, this straightforward answer belies considerable complexity. Division and expansion are not alternative or sequential processes, but instead are interdependent processes whose coordinated regulation we scarcely understand.The regulation of organ growth rate involves the rate at which new cells are produced and how fast these cells expand. Strictly, cell division does not enlarge an organ, but builds partitions within component cells (Green, 1976). Nevertheless, meristematic cells typically expand and divide at comparable rates, maintaining an approximately constant average cell size. Through this expansion, dividing cells do contribute to organ growth, albeit to a much lesser extent than non-meristematic cells (Volenec and Nelson, 1981;Volenec and Nelson, 1983). Beyond the small direct contribution to growth, cell division supplies the cells whose subsequent expansion causes the majority of organ expansion. If the rate of cell supply changes, then it is reasonable to expect the rate of organ expansion will change in parallel (Beemster and Baskin, 1998). Therefore, there are three processes that can modify organ growth rate: cell division, expansion of mer...

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Section: Comparison Of Cytokinin and Auxin Effects On Root Growthmentioning

confidence: 55%

STUNTED PLANT 1 Mediates Effects of Cytokinin, But Not of Auxin, on Cell Division and Expansion in the Root of Arabidopsis

2000

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“…Previous models for plant hormone responses have used a single Michaelis-Menten equation to model dose-response relationships, with variable success (Weyers et al, 1987;Nissen, 1988aNissen, , 1988b. The basic refinement we have added is the coupling of two dose-response systems, a primary and a secondary system, in which the signal output from the primary system acts as the input signal for the secondary pathways.…”

Section: Discussionmentioning

confidence: 99%

“…In the absence of detailed biochemical information, much of the research on hormone signal transduction in plants has been restricted to phenomenological studies in which the relationship between the dose of applied hormone and the increment of a chosen response has been quantified (for examples, see Nissen, 1985Nissen, , 1988aNissen, , 1988b. Koshland et al (1982) provided a general framework for considering the kinetics of signal-response relationships in biological systems.…”

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confidence: 99%

Analysis of Ethylene Signal-Transduction Kinetics Associated with Seedling-Growth Response and Chitinase Induction in Wild-Type and Mutant Arabidopsis

1995

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Kinetic aspects of ethylene-mediated signal transduction leading to seedlinggrowth inhibition and chitinase induction in Arabidopsis were investigated by the introduction of defined mutations in components of these pathways. Dose-response analysis of wild-type responses indicated that the rate-limiting steps for seedling responses and Arabidopsis basic-chitinase induction displayed Michaelis-Menten kinetics with apparent dissociation constants of the response (K,) of 0.1 and 1.4 pL 1-' ethylene, respectively. In the ethylene-insensitive efrl-l and ein2-32 mutant lines, both Arabidopsis basíc-chitinase induction and seedling-growth responses were completely disrupted, whereas the weaker efrl-2 allele eliminated the chitinase-induction response but only partially disrupted the seedling responses. A heterologous reporter gene containing the chitinase promoter from bean (bean basic-chitinase-/3-glucuronidase) displayed subsensitive kinetics (K, 120 pL L-' ethylene) compared to the response of the endogenous basic-chitinase response (K, 1.4 p L L-' ethylene). A model for ethylene signal transduction that accounts for the observed variations in ethylene dose-response relationships is presented. The relationship between the model and the biochemical mechanisms of well-characterized signal-transduction systems in animals is discussed.The plant hormones, like most chemical signals in biology, appear to act on tissues in a dose-dependent manner.In fact, it is this property of these compounds that led to their original identifications as endogenous chemical signals (Davies, 1987). In the absence of detailed biochemical information, much of the research on hormone signal transduction in plants has been restricted to phenomenological studies in which the relationship between the dose of applied hormone and the increment of a chosen response has been quantified (for examples, see Nissen, 1985Nissen, , 1988aNissen, , 1988b. Koshland et al. (1982) provided a general framework for considering the kinetics of signal-response relationships in biological systems. Responses that obey simple Michaelis-Menten kinetics (i.e. operate over 100-fold changes in signal concentration) were referred to as hyperbolic. Deviations from this simple behavior were referred This work was funded by grants from the National Science Foundation (NSF; No. to as supersensitive or subsensitive, depending on whether the response occurred over a smaller or a larger range of signal concentrations.Nonhyperbolic dose-response relationships can be modeled empirically using a modification of the MichaelisMenten equation known as the Hill equation (Weyers et al., 1987). This type of analysis has been applied to a number of plant hormone responses, and the observation has been made that plant hormone dose-response relationships often fall into the subsensitive category (Nissen, 1985(Nissen, , 1988a. It has been pointed out that some such studies may be invalid because the concentration of hormone at the site of perception was not known or because the initial rate...

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“…Cytokinins applied to roots are known to inhibit elongation (Stenlid, 1982;Nissen, 1988) and to stimulate radial expansion (Svensson, 1972;Kappler and Kristen, 1986), but the relationship between these responses is not understood. Our finding a bell-shaped dose-response curve for the stimulation of radial expansion but a sigmoidal curve for the inhibition of elongation suggests that the two responses are separate.…”

Section: Cytokinins and Cell Expansionmentioning

confidence: 99%

STUNTED PLANT 1, A Gene Required for Expansion in Rapidly Elongating but Not in Dividing Cells and Mediating Root Growth Responses to Applied Cytokinin

Baskin¹,

Cork²,

Williamson³

et al. 1995

Plant Physiol.

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To understand the control of spatial patterns of expansion, we have studied root growth in wild type and in the stunted planf 1 mutant, stpl, of Arabidopsis thaliana. We measured profiles of cell length and calculated the distribution of elongation rate. Slow growth of stpl results both from a failure of dividing cell number to increase and from low elongation rates in the zone of rapid expansion. However, elongation of dividing cells was not greatly affected, and stpl and wild-type callus grew at identical rates.*Thus, rapid cellular expansion differs in mechanism from expansion in dividing cells and is facilitated by the STPl gene. Additionally, there was no difference between stpl and wild-type roots for elongation in response to abscisic acid, auxin, ethylene, or gibberellic acid or for radial expansion in response to ethylene; however, stpl responded to cytokinin much less than wild type. In contrast, both genotypes responded comparably to hormones when explants were cultured; in particular, there was no difference between genotypes in shoot regeneration in response to cytokinin. Thus, effects on root expansion mediated by cytokinin, but not effects mediated by other hormones or effects on other cytokinin-mediated responses, require the STPl locus.How is the expansion of plant organs regulated? In the growing zones of most organs, expansion rate is not a constant quantity; rather, there is a well-defined spatial pattern of expansion rate. Although we have learned a considerable amount about how certain compounds, such as auxin, modify overall expansion rate, we have learned less about the control of spatial patterns of expansion rate. Spatial patterns of expansion rate might reflect underlying profiles of concentration of (or sensitivity to) one or more growth-regulating substances, but, in general, this simple explanation has not been validated. Furthermore, expansion in an organ includes dividing cells. Although "growth by cell expansion" is commonly contrasted with

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Dose responses of cytokinins

Cited by 22 publications

References 70 publications

STUNTED PLANT 1 Mediates Effects of Cytokinin, But Not of Auxin, on Cell Division and Expansion in the Root of Arabidopsis

STUNTED PLANT 1 Mediates Effects of Cytokinin, But Not of Auxin, on Cell Division and Expansion in the Root of Arabidopsis

Analysis of Ethylene Signal-Transduction Kinetics Associated with Seedling-Growth Response and Chitinase Induction in Wild-Type and Mutant Arabidopsis

STUNTED PLANT 1, A Gene Required for Expansion in Rapidly Elongating but Not in Dividing Cells and Mediating Root Growth Responses to Applied Cytokinin

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