Plant phenotypic plasticity- the Sede-Boker workshop

The roundtable discussions
Your contributions and comments are welcome.
Please send them to Ariel Novoplansky and/or to the coordinator of the relevant roundtable.

  Information processing and decision making by plants

  Within-plant phenotypic plasticity environmental heterogeneity

  Costs and limits of phenotypic plasticity

  Implications of phenotypic plasticity for populations and communities

  Classes and hierarchies of phenotypic plasticity

Information processing and decision making by plants

Carlos L. Ballare', University of Buenos Aires, Argentina.

Ariel has asked me to collaborate in the coordination of the roundtable discussions on "Information Processing and Decision making by Plants". He may be blamed for rushing me to do this; however I assume full responsibility for the content of this section of the Workshop Homepage. Nevertheless please keep in mind that the following paragraphs are not intended to conform a finished document. They should rather be viewed as an evolving set of ideas that, in my opinion at least, may lead to interesting discussions during our meetings.

Phenotypic plasticity is the expression of  variability among individuals of identical genotype.  Throughout the life of an individual plant, plastic responses are triggered by a variety of input signals and are constrained by the possible combinations of protein synthesis and action specified in the plantís genotype.

Input Signals
Plants of course do not make decisions in the way we do, as they do not have neural information-processing systems. Yet, they are certainly capable of actively changing their metabolic rates and developmental programs in response to a variety of input signals and, therefore, they are able to make "decisions", at the very least in the way computers do. The input signals that trigger  plastic responses in plants can be internal or external, and include, among other things:

(Signal Type 1) "Pure?" signals, i.e., internal or external variables that are correlated with the availability of resources or the presence of biotic challenges, such as neighboring plants, pathogens or insect consumers, but that are not, by themselves,  energy resources or stress factors (e.g., far-red radiation, temperature fluctuations, fungal and insect elicitors, etc.)

(Signal Type 2) Resource levels, both inside (e.g., the amount of hexose activating specific sugar sensors) and outside the plant (e.g., the irradiance level reaching the leaf surface).

(Signal Type 3) Products of cellular damage, such as DNA lesions, activated oxygen species, products of lipid peroxidation, etc.

An important point to highlight here is that although it is clear that what I have called "pure" signals induce plastic (presumably adaptive) responses in the plants, it is not equally appreciated that variations in"2" and "3" also convey information that is directly relevant to a variety of information circuits and reaction programs that control cellular and organismal functions. Water deprivation, shading, tissue damage, and other insults do not only slow down biomass accumulation; they engage very specific response pathways whereby the plant actively acclimates, eventually becoming less sensitive to the influence of the original stress factor.

Functions of plasticity
Plasticity is expressed over a variety of time scales, from the rapid movements of antenna proteins and pigments between PSII and PSI during short-term acclimation to fluctuations in light intensity, to the changes in crown shape or root architecture that may take years to develop. Plasticity is essential for plant survival, and indeed for the survival of any organism; dramatic examples that support this assertion come from studies with mutants. Therefore it does not seem to be very productive to ask questions about the adaptive value of plasticity in general, or in broad terms.

In order to ask fruitful questions about the ecological and evolutionary significance of plasticity it is convenient to consider different functional classes of plasticity. Although all classifications are arbitrary and context-dependent, one that may be suitable for the discussion of the mechanisms and adaptive significance of plasticity distinguishes at least three functions of plasticity: Maintenance of metabolic homeostasis, foraging for resources, and defense.

Maintenance of metabolic homeostasis. Metabolic plasticity is built in most metabolic routes and cellular transport processes in animals and plants and involves changes in the activation state of enzymes and function of other molecules in response to changes in their chemical and redox environment. Examples include the regulation of photosynthetic components by the electron pressure generated at the PSII reaction center, (which in turn result from variations in the amount of light that is harvested by the PSII antenna), the controlled activation of specific membrane carriers, etc. In general, this type of plasticity  plays the role of adjusting the capacity of a given metabolic or transport pathway in response to the input load, or to regulate the input load in response to the working capacity or the demand of the downstream components. At least upon superficial examination, metabolic plasticity does not seem to be fundamentally different between plants and animals.

Foraging for resources
Plants forage for resources by controlling the deployment of resource-capturing surfaces (both in space and time) and by regulating the resource-uptake capacity of these surfaces. Therefore, foraging for resources involves metabolic as well as morphological and developmental plasticity. Morphological and developmental plasticity is particularly striking in plants and is central to the processes that allow efficient capture of resources in the natural environment. Some of the evidence in this regard comes from studies on light regulated morphogenesis, which have clearly shown that specific informational photoreceptors play a key role in the control of the plastic morphological adjustments that allow plants to actively forage for light in patchy environments. The regulation of plant phenology in response to photoperiod and temperature signals also provides good examples of the critical role of developmental plasticity in regulating resource capture.

Plants exposed to abiotic and biotic insults usually respond with a series of  orchestrated changes in phenotype that include metabolic and developmental components. Because there are several classes of offending factors there are also many different types of defense-signaling agents or events; interestingly, however, evidence indicates that disparate stress factors may engage convergent transduction chains and elicit equivalent responses both at the cellular and organismal levels. As an example of defense to abiotic factors, plant acclimation to UV radiation involves an array of tissue-specific responses that tend to reduce UV penetration and to limit the extent of UV-induced cellular damage. Some responses appear to be specifically elicited by UV photoreceptors; others may be triggered by the very products of UV-induced damage, such as DNA lesions, activated oxygen species, products of lipid peroxidation, etc.  As an example of plant defense against biotic factors, plant responses to microbial attack are signaled by specific microbial elicitors that interact with the products of resistance genes of the host plant. The defense response consists of a localized, rapid hypersensitive response (HR) characterized by an oxidative burst and the activation of defense genes, followed by a systemic response that involves long-distance signaling. Plastic defense responses against alien organisms are very different between plants and animals. Plants do not have humoral (antibody-based) responses and they do not have specialized cells roaming through their fluids to mount defenses against invading organisms (such as the animal phagocytes and lymphocytes). However, some aspects of the defense responses at the cellular level are strikingly similar between plants and animals, including the important role that activated oxygen species play in plants and animals both as  defense weapons and as signaling molecules. Thus, the oxidative burst in a plant cell mounting a HR against an invading microorganism probably involves the same sort of cellular events and molecular partners that are called to fight an alien organism inside a white cell in our blood.

Appreciating the ubiquity and significance of plasticity
The realization that plasticity is present at all scales has important implications for our understanding of how plants work and for the design of experiments that seek to improve this understanding. In particular, it may be worth to emphasize the following points.

(1) All plants (actually all living organisms) are plastic, and at every point in time thousands of  "decisions" about gene expression and protein function are implemented in response internal and environmental signals.

(2) Plants (as well as animals) get information from many sources, including things that are frequently considered only in terms of their energetic value or deleterious effects. Thus sucrose is not only a key energy carrier within the plant; it is also a source of information for many developmental genes that are responsive to sucrose. Likewise, hydrogen peroxide is not only a dangerous molecule that builds up in response to several stresses and poses a risk to many cellular components; it is also a regular, critical signaling molecule in many defense pathways as well as in other transduction chains not necessarily linked to defense activities. At the organismal level, almost every manipulation of the plant and its environment involves much more than the proximate effect of the manipulation itself. For instance, putting holes in a leaf with a hole puncher does much more than just reducing the leaf area of the plant --it will also trigger changes in photosynthetic capacity in the remaining leaf area, turn on genes whose products play important roles in the defense against chewing insects, and elicit responses that may even have implications for the tolerance of the affected plant to a variety of stress agents.

(3) Although the coordination of activities at the organismal level is fundamentally different between plants and higher animals, the mechanisms of information transduction and the responses at the cellular level have striking parallels across kingdoms. Both plants and animals seem to use multigene families as one way to add versatility and plasticity to the genotype. Also some transduction chains described in animal models seem to apply, at least in broad terms, to plant cells. Therefore, critical steps in the evolution of response programs to stress are likely to have taken place very early in the evolution of living organisms.

(4) In plants different abiotic and biotic factors induce information transduction chains that have elements in common and lead to similar responses. For example, plastic responses to several stress factors (chilling, UV, water stress) may involve free radicals as messengers and result in the induction of antioxidant enzymes and enzymes of the phenylpropanoid pathway. Whether the experience of (and acclimation to) a particular stress factor leads to cross resistance to a different stress agent is an area of active research nowadays, and one of considerable theoretical and practical significance.

An appreciation of the ubiquity of plasticity and its ramifications for acclimation to "change"  both vertically (i.e., across levels of organization), and horizontally ( i.e., within a particular level but for different environmental factors), is essential to understand how plants grow and reproduce in a dynamic environment. Neglecting the sophisticated sensory machinery of plants in conceptual models of plant function, which is not uncommon among physiological ecologists, may have the apparent effect of making our work easier in the short term. However, oversimplified frameworks are bound to slow down our attempts to gain a fruitful understanding of plant  function.

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Within-plant phenotypic plasticity and exploitation of environmental heterogeneity

M. J. Hutchings, University of Sussex, UK.

Much of the variation in form between different plants belonging to the same species is caused by responses to environmental patchiness.  Many responses take place at spatial scales smaller than that of individual plants and on temporal scales shorter than the lives of the plants.  Environmental quality affects rates of module proliferation and causes differences in the morphology of plant substructures developing at different places and at different times.  Perhaps because plant species can be recognised (at least by some people!) despite great differences in the extent of module proliferation and in sub-structural morphology between individual plants, ecologists have shown little interest in the past in explaining how speciesí local or global perceptions of their environment are translated into their form, or in how local environmental effects impinge on larger plant structures.  Presumably, the benefits of  morphological plasticity include improvement of resource acquisition and avoidance of places where resource supply is poor.  This roundtable discussion could begin by considering the following questions which arise out of this simple analysis of the "plant thinking" which lurks behind the form developed in a spatially and temporally inconstant world.

 (i) How effective are the morphological and developmental solutions adopted by plants in solving the problems posed at local spatial scales (i.e. spatial scales smaller than the size of the whole plant) and at brief temporal scales (i.e. time scales shorter than the plantís life cycle) in heterogeneous environments?  Can plant structures respond fast enough to environmental fluctuation, or is the morphology we see merely bet-hedging which creates a compromise response to the likely range of environments which will be encountered?  Does translocation of resources and signals between parts of plants in habitat of different quality blur the perception of local habitat quality, resulting in a low level of adaptation to local habitat quality throughout the plant?  Environmental heterogeneity is unlikely to be perceived in a similar way by whole plants and by the modules or ramets of which they are composed.  Does this create conflicts between these different structural scales so that responses can not be optimised for both, or can physiological and behavioural integration alleviate any potential for conflict?  Is either rapid development of physiological independence between modules or, in more extreme cases, programmed "falling apart" an evolved response to such incompatibility?  Can we predict the conditions under which retention of physiological integration between modules/ramets is beneficial and the conditions under which independence should be favoured?  Would we also expect conditions which favour physiological independence between modules to favour physical independence (i.e. falling apart)?

 (ii) At what resolution do different plant species sense and respond to temporal and spatial environmental heterogeneity?  (e.g. to what extent do plant growth habit or predictability of resource availability in space and time matter?).  Can we make any predictions about the spatial and temporal scales to which plants can respond to environmental heterogeneity?   Can we make any generalisations about the structural scales at which we will see plastic responses within plants?  What evidence is there of branch autonomy or of within-branch responsive plasticity?

 (iii) What is the basis for plants allocating more resources to organs sited in resource-rich patches in heterogeneous environments?  Does this occur at the expense of organs sited in resource-poor patches, or do differences merely reflect differences in capacity to grow in patches of different quality?   Is there evidence of reallocation of resources following local patch experience - do plants withdraw resources, and support of structures in locally disadvantageous patches, and reallocate to structures in more promising patches?  Does this culminate in enhanced growth?  What does it do to morphology?  Is this a facility which can be expressed at any time, or are there temporal windows of opportunity during which such re-distribution of favours can be expressed within the plant?

 (iv) Given amounts of resource do not always have the same value to the plant, regardless of the time and place at which they are supplied.  What potential is there for changing growth or economic yield by applying given quantities of resource to plants at different times or in different spatial arrangements?  Do different resources confer maximum benefit to a plant if supplied at the same or different times? Can a plant be good at getting all essential resources at the same time and from the same place, or is it better to divide resource acquisition activities in time and space?  (i.e. division of labour between resource-acquiring structures - this concept may have both a temporal and a spatial aspect to it).  Can we make any generalisations about whether most habitats provide high levels of all essential resources at the same time and in the same places, and whether different essential resources vary inversely in abundance in either time and/or space?  Have plants in different environmental situations evolved different solutions for resource acquisition needs because of constraints on efficiency of uptake, or habitat-specific differences in resource availability?

 (iv) Evidence is accumulating which suggests that some modular plants may be able to make better use of resources when the resources are distributed in patches or pulses rather than homogeneously.  Have we been missing opportunities for using the ability of plants to exploit environmental heterogeneity?  Is environmental heterogeneity better for plants than homogeneity?  Could we get more out of economically valuable species if we tap into their possible capacity to exploit heterogeneity?  Would the input of energy needed to create and maintain heterogeneity from which plants could benefit, cost more than the gains which we could expect to harness?  Should a large-scale research effort be initiated to investigate this potentially rewarding phenomenon?  Would the benefits of environmental heterogeneity only be apparent for plants in monocultures?   Is there any evidence that, through within-plant phenotypic plasticity, non-clonal plants can perfom better in heterogeneous than homogeneous conditions?  Scaling up from organisms to communities, is there any potential for managers of natural areas to manipulate community composition through manipulation of habitat heterogeneity?

 (vi) Finally, this may be an appropriate time to re-consider the way in which we perform experiments both on individual plants and on communities of plants.  Heterogeneity is ubiquitous in the natural world, and it displays itself in a variety of forms.  Given its ubiquity, it would seem natural to expect selection to have taken place in plants, which are largely sessile organisms within environments with great temporal and spatial variability, for the ability to respond to heterogeneity via within-plant plasticity, and perhaps even to make their best growth under such conditions, so that heterogeneous conditions may be advantageous compared with homogeneity.  We are still astonishingly ignorant about the types of heterogeneity which characterise different habitats, but might assume that morphological and physiological attributes of different species of plant have evolved as best solutions, or at least as reasonable compromises to the conditions met in different habitats.  If plants show within-plant responses to environmental heterogeneity, and because of this can alter their productivity and relative contribution to local vegetation composition, the effects of growing them either individually or in combinations will be different when we set up experiments, or farm, or forest, in homogeneous and heterogeneous environments.  Instead of experimenting in homogeneous conditions, it might therefore be informative to investigate the effects on species and on community composition, of various forms of heterogeneity.

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Costs and limits of phenotypic plasticity: physiological, ecological and evolutionary aspects

Tsvi Sachs, The Hebrew University, Jerusalem, Israel.

Plasticity is common, and many of its expressions are clearly adaptive, and yet
its scope is limited. Why shouldn't the equivalents of genetic adaptations in
related plants occur in the very same plant? An example of large differences
known to be accommodated by the very same genetic system are juvenile and mature phases in the life of the same plant - and these difference can be larger than
any expressions of developmental plasticity. Further, plasticity known to be
possible, because it occurs in one species, is absent in other species living in
the same habitats. It follows that though plasticity confers remarkable
advantages it must be limited by its costs. Any knowledge of these costs could
be expected to important and interesting.

As a first stage, we might define categories of possible costs of plastic
development. Of course, these are not meant to be mutually exclusive. Will the
following suffice? Should they be changed, and what might be missing? Most
important, to what extent are they supported by available facts? Which
possibilities could be ruled out as costs because they are required for dealing
with changes that occur during normal development?

a) Structural costs
Developmental changes that had not been pre-determined in early stages are
likely to lead to structures that are not as physically strong, nor as
parsimonious in their requirements for substrates, as they could have been. For
example: a major vehicle of plant plasticity is the cambium, which means the
presence of a thin walled meristem, rather than supporting fibers, in a critical
region of plant axes. The activity of the cambium also leads to a continuous
loss of tissues from the surface of the plant.

b) Need for extra genetic information
Plasticity could require special mechanisms for sensing the environment. It
could also require physiological controls and developmental mechanisms that are
used only in special environmental conditions. Forming and maintaining these
mechanisms would entail extra genetic information, a cost that must be balanced
by the advantages of plastic development.

c) Increased chance of developmental malfunction
Plasticity precludes what might be the simplest possibility, strict
deterministic development. It is likely that complex systems, especially ones
with extra controls, have a greater chance of malfunctioning.

d) The cost of mistaken decisions
Plant developmental responses are more expensive, and less readily reversible,
than the behavioral responses of animals. Most important, developmental
plasticity requires relatively slow developmental processes, and are thus valid
for future rather than immediate conditions. The information available to plants
about these future conditions, however, is limited and not necessarily reliable.
Plasticity could thus lead to developmental changes that would cost more than
they are worth. For example, growing a branch towards a light spot would be a
useless expenditure of energy and substrates if the location is likely to be
shaded after a short time.

e) Exposure to parasites
Both higher plant parasites and the varied gall-inducing organisms make their
living by taking over the developmental mechanisms of their hosts. The more
plastic a plant is the easier it could be for its development to be modified by
the parasites to their own advantage. For example, where there is no cambium the
role of lateral organs cannot be readily modified - and higher plant parasites
cannot simulate highly successful branches, by using the appropriate signals, so
as to divert vascular differentiation in their direction.

f) Contrasting effects on evolutionary rates
By providing alternatives to gene selection, plasticity could slow down
evolutionary adaptations. It could also have the opposite [but not mutually
exclusive!] effect: allowing plants to survive long enough in new or extreme
stress conditions for selection to take place. Further, developmental plasticity
could accommodate evolutionary changes in the role of organs. For example, it
could provide for the diversion of vascular supplies from an organ that is being
reduced to one whose role is increasing.

g) The deterioration of genetic information
Developmental plasticity could mean that some properties are subject to
selection only in relatively unusual conditions. Since chance negative mutations
always occur, the absence of selection could act against the persistence of
special programs needed only in special habitats.

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Implications of phenotypic plasticity for populations and communities

Deborah Goldberg, University of Michigan, USA.

Since there is very little concrete in the literature on the implications of phenotypic plasticity for population or community dynamics and organization, I took this  opportunity to speculate and raise questions that have very little theoretical or empirical basis at this point.  However, unlike Carlos, who politely took full responsibility for his section of the workshop site, I prefer to blame any lacks on Ariel, for giving me a subject that has been badly neglected and therefore leaves me little to go on from the literature.  My goal for the discussion is that we end up by suggesting directions for future research or better organization/compilation of existing data.   In that spirit, I offer the following thoughts and questions.

I. Definitions and prerequisites for discussion of population and community consequences

To talk about consequences of plasticity (for individual fitness as well as for population or community dynamics or patterns of community structure), we need to ask how any of these phenomena would differ if plants were not plastic, were less plastic, or were differently plastic.  Therefore, a prerequisite for discussion (or at least testing any of the ideas below) is some way of quantifying degree of plasticity and/or categorizing types of plasticity.  This is the subject of some of the other roundtable discussions and therefore I assume we will have some consensus on the subject before getting to discussing consequences.  In the meantime, for purposes of starting discussion, I have in mind the following incomplete definition of degree of plasticity: degree of plasticity is the amount of change in morphology or physiology (but not direct measure of performance) for a unit change in environment.  This definition is problematic for a number of reasons.  For example, it is not always simple to separate nonperformance traits from performance measures, it ignores type of environmental change and the actual environmental change (e.g. the same quantitative change will have different impacts at low vs. high values of the environmental variable if response is nonlinear), and it does not incorporate different types of plasticity.  Neverthless, it is intuitively appealing and gives a sense of what I mean by degree of plasticity in the sections below.

To make questions concerning consequences of plasticity interesting, it is also important that taxa differ in their degree or type of plasticity; if all organisms had equal plasticity, consequences are rather moot. Such complete equality obviously does not exist but the existence and nature of consistent patterns in the degree/type of plasticity among types of taxa (e.g. correlations with other traits) and among types of environments is less obvious.  Such patterns will form the basis for developing generalizations about the consequences of plasticity and therefore understanding patterns in plasticity is an important prerequisite for discussion of the consequences of plasticity.  The sections below raise some points for discussion about patterns in plasticity (which will probably come up in other roundtables as well), and then the consequences of plasticity for population and community dynamics.

II.  Patterns in plasticity

What hypotheses have been/could be developed and what is actually known about the patterns?  Possible sources of patterns come from understanding the costs and benefits of plasticity.  For example, the argument that highly plastic plants could be more susceptible to parasites that take over a plantís developmental mechanisms suggests that plants that are more susceptible to parasites should be less plastic. Or, the benefits of plasticity are often expected to be higher in more spatially heterogeneous environments, suggesting that plasticity should be more common or stronger in such environments.

One of the most discussed patterns in plasticity is greater morphological plasticity of taxa with lower maximum relative growth rate and therefore of taxa from less fertile habitats. The cause of the association between plasticity and RGR is argued to be that high growth rate enables more flexibility in deployment of new resource-acquiring tissues to take advantage of patches of high resource availability. This is also a particularly important pattern because it has a direct tie to community consequences--it is an important component of Grimeís hypothesis that taxa from highly productive habitats are better competitors because the greater flexibility in foraging should increase ability to preempt resources from other individuals.  The community consequences are discussed in more detail below but some important questions about the hypothesis and pattern belong here: it has been suggested that the connection between potential RGR and plasticity might disappear if taxa are compared after a constant amount of biomass accumulation rather than after a constant time period.  Is this correct empirically?  Does this fully account for the mechanisms by which maximimum potential RGR and plasticity should be associated?  Even if this argument is correct, does the lower rate of morphological modification in low RGR taxa still put them at a competitive disadvantage in resource acquisition?

III.  Population dynamic consequences of plasticity

At the individual level, plasticity in morphology or physiology is assumed to buffer fitness against declines under poor conditions.   This might have two consequences with potentially opposing effects on stability of population size over time.  Over time, highly plastic taxa should be less sensitive to environmental fluctuations in terms of fitness components and this should reduce fluctuations in population size, especially buffering declines in poor years (poor years could mean years with high competition or herbivory as well as poor abiotic conditions).  On the other hand, to the extent that variation among individuals within a population is due to different microsite conditions, highly plastic taxa might have less variation among individuals in components of fitness at a particular time.  At least in even-aged monocultures, a well-developed body of theory suggests that less variation in size among individuals in a population decreases stability so that more plastic taxa should have greater fluctuations in population size over time.

Are either/both of these hypotheses consistent with existing theory? Can these two hypotheses be tested and if so, how?  Is there any currently available empirical evidence supporting or refuting them?

IV.  Community consequences of plasticity

The big question that can be asked here is whether degree of phenotypic plasticity changes the outcome of interactions?  For competitive interactions, this essentially askes whether the degree of phenotypic plasticity is an important component of competitive ability (or lack thereof)?  The main hypothesis in the literature to date follows up on the pattern described earlier:  species with high maximum potential RGR should be more plastic in foraging behavior and therefore be more likely to preempt patches with high resource availability. This should lead to better competitive response when similar-sized individuals are competing for limiting resources.  However, is this also correct in environments in which successful seedling establishment in the presence of adult vegetation is required for population persistence and coexistence?  That is, how important is resource preemption as a component of competitive ability in such strongly size-asymmetric interactions?  If the seedling environment can be viewed as having low productivity (either because of sequestering of resources by adult vegetation or low supply from the abiotic enviornment), then resource preemption should be less important and tolerance of depleted resources more important for determining persistence (whether this is called part of competitive ability or not has been subject to debate for at least the last ten years but doesnít change the essential mechanisms).  This entire argument then makes the prediction that plasticity in morphology is an important component of competitive ability in productive environments (or, more precisely, those with spatial heterogeneity in resources) while it does not contribute to competitive ability in unproductive environments (or those with low heterogeneity spatially).

An important next step would be to formalize this conceptual model so that quantitative predictions could be made or the consequences discovered of modifying various plant traits or the environment.  For example, how does the degree of spatial heterogeneity affect the importance of phenotypic plasticity?  How does ability to store resources (e.g. comparing nutrients vs. water) affect the results? How does incorporating different kinds and magnitudes of costs of phenotypic plasticity affect the results?

While data have been accumulating on foraging behavior and plasticity for taxa from different environments and with different growth rates, there is much less on actual resource uptake by whole plants under different conditions and with different degrees of plasticity.  More importantly, almost no experiments have incorporated competition into this kind of experiment so direct tests of the role of plasticity in determining the outcome of competition and the mechanisms involved do not exist.  Is it possible to infer something about this aspect of the consequences of plasticity from experiments done only in the absence of interactions?  If not, what kind of experiments should be done?   It should also be kept in mind that the connection between competitive ability and community structure is not always obvious so that confirming this hypothesis still does not complete the steps to explaining patterns in community structure--most current models of coexistence in plants do not necessarily predict a correlation between competitive ability and relative abundance in a community.

The Grime hypothesis on the connection between plasticity and competitive ability is based on plasticity in foraging behavior and assumes that foraging behavior maximizes resource uptake.  Is this a comprehensive view (albeit many modifications and additions of details are certainly possible) or are there any other possible kinds of links between plasticity and competitive ability? What might these involve?

Finally, the role of plasticity in the outcome of plant-herbivore (or pathogen) interactions has also been largely neglected, although it is well known herbivores can induce both chemical and morphological changes in plants.  But, similar to the situation for competition, taking these plastic responses to herbivores (as to competitors) and examining how the presence/magnitude/type of these responses changes individual fitness of both partners or their population dynamics has been little investigated both empirically and theoretically.

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Classes and hierarchies of phenotypic plasticity

Philip Grime, University of Sheffield, UK.

In this final roundtable discussion I hope that we can recognise and address three challenges.  First, using insights from plant physiology and molecular biology, can we produce a mechanistic classification of the ways in which plants sense their environment and adjust their development and functioning?  Second, can we recognise consistent patterns in the distribution of plasticity mechanisms within the plant kingdom and across biomes, ecosystems and habitats?  Third, can we distil from these broad perspectives a succinct understanding of the role of plasticity in large-scale ecological and evolutionary processes? Here are some more specific questions to stimulate discussion on each of the three topics:

Mechanisms of plastic response

1.  In the light of new molecular insights, is it still possible and useful to observe a distinction between physiological and morphological responses?

2.  How clear and consistent is the distinction between reversible and irreversible phenotypic responses?

3.  Are we leaving this conference with a clear understanding of the role of gene induction, gene amplification and nucleotypic effects (sensu M D Bennett, H J Price) in various types of plastic response?

4.  Is there a relationship between mechanisms of plastic response and the potential life-span of cells, tissues, organs, modules or individuals?

5.  Can we distinguish mechanistically between plasticity that occurs locally in response to the immediate environments of leaves and roots and that which operates through `general switches' at the level of the entire plant?

6.  Is it useful to try to classify plastic responses according to the extent to which their expression is strongly determined by other plant traits (morphology, resources
allocation, mutualistic associations etc).  Are these the `true' controllers of the rate, scale, precision and fitness benefit of plastic responses?

7.  How does plasticity mechanism vary with ontogeny?  Is it helpful to classify plasticity mechanisms according to tissues and life-stages (seeds maturing on the mother plant, dormant or germinating seeds, juveniles, vegetative shoots and roots,
flowering individuals)?

The distribution of plastic response

8.  How are the mechanisms of plastic response (classified above) distributed with respect to phylogeny?  Are there consistent differences between autotrophs and heterotrophs and between cryptograms and higher plants?  Does the rate, scale or precision of adjustment vary across plant families in accordance with Sporne's
Advancement Index? Are any broad patterns of variation in plasticity that are associated with phylogeny due to differences in plasticity itself or to associated traits (see 6 above)?

9.  Have the plastic `foraging' responses of roots and shoots co-evolved in each species? Is it correct to predict that root and shoot responses will be most closely linked in fast-growing plants of productive habitats?  Is uncoupling of root and shoot foraging most obvious in slow-growing plants with low rates of tissue turnover and high resource storage capacity?

10.  Can we safely predict correlations between long tissue life-span, low habitat productivity and reversible physiological adjustments to climate?

11.  How do the forms and rates of phenotypic adjustment to environmental cues vary in relation to plant life-history?  Do ephemerals sustain allocation to flowering under stressed circumstances where perennials abhort?  Do the form, rate and
extent of flowering  responses vary according to the nature and intensity of stress?

12.  Does the distinction between constitutive and inducible defences against herbivory and pathogens relate to taxonomy, habitat productivity, plant maturity or other factors?

Plasticity and large-scale ecological processes

13.  Are differences in the mechanism, scale, precision and rate of plastic responses consistently associated with distinctive sets of traits that show predictable patterns of occurrence across taxa or between ecosystems?  Do any such associations justify recognition of plant functional types?  Can any such functional types point to specific roles for plasticity in community and ecosystem dynamics?

14.  What is the changing relationship between plant life-histories, plastic responses of plants to resource supply, plant-plant interactions and plant-animal interactions during vegetation succession and the maturation of ecosystems?  Is there usually a shift from patch to pulse exploitation and from irreversible morphological responses to reversible physiological responses as succession proceeds?  Is inducible defence more characteristic of early-successional species?

15.  What are the consequences for herbivores, carnivores and decomposers when plant functional types with different types of plastic responses replace each other during succession?

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