Showing papers on "Developmental plasticity published in 2005"

The plastic human brain cortex.

Abstract: Plasticity is an intrinsic property of the human brain and represents evolution’s invention to enable the nervous system to escape the restrictions of its own genome and thus adapt to environmental pressures, physiologic changes, and experiences. Dynamic shifts in the strength of preexisting connections across distributed neural networks, changes in task-related cortico-cortical and corticosubcortical coherence and modifications of the mapping between behavior and neural activity take place in response to changes in afferent input or efferent demand. Such rapid, ongoing changes may be followed by the establishment of new connections through dendritic growth and arborization. However, they harbor the danger that the evolving pattern of neural activation may in itself lead to abnormal behavior. Plasticity is the mechanism for development and learning, as much as a cause of pathology. The challenge we face is to learn enough about the mechanisms of plasticity to modulate them to achieve the best behavioral outcome for a given subject.

Developmental plasticity and the origin of species differences

Abstract: Speciation is the origin of reproductive isolation and divergence between populations, according to the “biological species concept” of Mayr. Studies of reproductive isolation have dominated research on speciation, leaving the origin of species differences relatively poorly understood. Here, I argue that the origin of species differences, and of novel phenotypes in general, involves the reorganization of ancestral phenotypes (developmental recombination) followed by the genetic accommodation of change. Because selection acts on phenotypes, not directly on genotypes or genes, novel traits can originate by environmental induction as well as mutation, then undergo selection and genetic accommodation fueled by standing genetic variation or by subsequent mutation and genetic recombination. Insofar as phenotypic novelties arise from adaptive developmental plasticity, they are not “random” variants, because their initial form reflects adaptive responses with an evolutionary history, even though they are initiated by mutations or novel environmental factors that are random with respect to (future) adaptation. Change in trait frequency involves genetic accommodation of the threshold or liability for expression of a novel trait, a process that follows rather than directs phenotypic change. Contrary to common belief, environmentally initiated novelties may have greater evolutionary potential than mutationally induced ones. Thus, genes are probably more often followers than leaders in evolutionary change. Species differences can originate before reproductive isolation and contribute to the process of speciation itself. Therefore, the genetics of speciation can profit from studies of changes in gene expression as well as changes in gene frequency and genetic isolation.

Map plasticity in somatosensory cortex.

Abstract: Sensory maps in neocortex are adaptively altered to reflect recent experience and learning In somatosensory cortex, distinct patterns of sensory use or disuse elicit multiple, functionally distinct forms of map plasticity Diverse approaches-genetics, synaptic and in vivo physiology, optical imaging, and ultrastructural analysis-suggest a distributed model in which plasticity occurs at multiple sites in the cortical circuit with multiple cellular/synaptic mechanisms and multiple likely learning rules for plasticity This view contrasts with the classical model in which the map plasticity reflects a single Hebbian process acting at a small set of cortical synapses

Experimental models of developmental programming: consequences of exposure to an energy rich diet during development.

Abstract: Studies in both humans and experimental animals addressing the ‘Fetal Origins of Adult Disease’ hypothesis have established a relationship between an adverse intrauterine environment and offspring disease in adult life. This phenomenon, termed ‘fetal programming’ describes a process whereby a stimulus in utero establishes a permanent response in the fetus leading to enhanced susceptibility to later disease. However, the environment, during periods of developmental plasticity in postnatal life, can also ‘programme’ function. Thus, the terms ‘developmental programming’ and the ‘Developmental Origins of Adult Health and Disease’ are preferentially utilized. The ‘Thrifty Phenotype’ hypothesis explained the association between insufficient in utero nutrition and the later development of Type 2 diabetes. Most recently the ‘Predictive Adaptive Response’ hypothesis proposes that the degree of mismatch between the pre- and postnatal environments is an important determinant of subsequent disease. Epidemiological studies have indicated that fetal growth restriction correlates with later disease, implying that fetal nutritional deprivation is a strong programming stimulus. This prompted the development of experimental animal models using controlled maternal calorie, protein or macronutrient deficiency during key periods of gestation. However, in many societies, maternal and postnatal nutrition are either sufficient or excessive. Here, we examine findings from a range of nutritional studies examining maternal and/or postnatal nutritional excess. There is supportive evidence from a limited number of studies to test the ‘Predictive Adaptive Response’ hypothesis. These suggest that maternal over-nutrition is deleterious to the health of offspring and can result in a phenotype of the offspring that is characteristic of metabolic syndrome.

Environmental influences during development and their later consequences for health and disease: implications for the interpretation of empirical studies.

Abstract: Early experience has a particularly great effect on most organisms. Normal development may be disrupted by early environmental influences; individuals that survive have to cope with the damaging consequences. Additionally, the responses required to cope with environmental challenges in early life may have long-term effects on the adult organism. A further set of processes, those of developmental plasticity, may induce a phenotype that is adapted to the adult environment predicted by the conditions of early life. A mismatch between prediction and subsequent reality can cause severe health problems in those human societies where economic circumstances and nutrition are rapidly improving. Understanding the underlying mechanisms of plasticity is, therefore, clinically important. However, to conduct research in this area, developmental plasticity must be disentangled from disruption and the adverse long-term effects of coping. The paper reviews these concepts and explores ways in which such distinctions may be made in practice.

The developmental origins of adult disease.

Abstract: Epidemiological and clinical observations have led to the hypothesis that the risk of developing some chronic diseases in adulthood is influenced not only by genetic and adult lifestyle factors, but also by environmental factors acting in early life. These factors act through the processes of developmental plasticity and possibly epigenetic modification, and can be distinguished from developmental disruption. The concept of predictive adaptation has been developed to explain the relationship between early life events and the risk of later disease. At its base, the model suggests that a mismatch between fetal expectation of its postnatal environment and actual postnatal environment contribute to later adult disease risk. This mismatch is exacerbated, in part, by the phenomenon of "maternal constraint" on fetal growth, which implicitly provides an upper limit of postnatal nutritional environment that humans have adapted for and is now frequently exceeded. These experimental, clinical and conceptual considerations have important implications for prevention and intervention in the current epidemic of childhood obesity and adult metabolic and cardiovascular disorders.

Phenotypic accommodation: adaptive innovation due to developmental plasticity

Abstract: Phenotypic accommodation is adaptive adjustment, without genetic change, of variable aspects of the phenotype following a novel input during development. Phenotypic accommodation can facilitate the evolution of novel morphology by alleviating the negative effects of change, and by giving a head start to adaptive evolution in a new direction. Whether induced by a mutation or a novel environmental factor, innovative morphological form comes from ancestral developmental responses, not from the novel inducing factor itself. Phenotypic accommodation is the result of adaptive developmental responses, so the novel morphologies that result are not "random" variants, but to some degree reflect past functionality. Phenotypic accommodation is the first step in a process of Darwinian adaptive evolution, or evolution by natural selection, where fitness differences among genetically variable developmental variants cause phenotype-frequency change due to gene-frequency change.

Fetal origins of developmental plasticity: are fetal cues reliable predictors of future nutritional environments?

Abstract: Evidence that fetal nutrition triggers permanent adjustments in a wide range of systems and health outcomes is stimulating interest in the evolutionary significance of these responses. This review evaluates the postnatal adaptive significance of fetal developmental plasticity from the perspective of life history theory and evolutionary models of energy partitioning. Birthweight is positively related to multiple metabolically costly postnatal functions, suggesting that the fetus has the capacity to distribute the burden of energy insufficiency when faced with a nutritionally challenging environment. Lowering total requirements may reduce the risk of negative energy balance, which disproportionately impacts functions that are not essential for survival but that are crucial for reproductive success. The long-term benefit of these metabolic adjustments is contingent upon the fetus having access to a cue that is predictive of its future nutritional environment, a problem complicated in a long-lived species by short-term ecologic fluctuations like seasonality. Evidence is reviewed suggesting that the flow of nutrients reaching the fetus provides an integrated signal of nutrition as experienced by recent matrilineal ancestors, which effectively limits the responsiveness to short-term ecologic fluctuations during any given pregnancy. This capacity for fetal nutrition to minimize the growth response to transient ecologic fluctuations is defined here as intergenerational “phenotypic inertia,” and is hypothesized to allow the fetus to cut through the “noise” of seasonal or other stochastic influences to read the “signal” of longer-term ecologic trends. As a mode of adaptation, phenotypic inertia may help the organism cope with ecologic trends too gradual to be tracked by conventional developmental plasticity, but too rapid to be tracked by natural selection. From an applied perspective, if a trait like fetal growth is designed to minimize the effects of short-term fluctuations by integrating information across generations, public health interventions may be most effective if focused not on the individual but on the matriline. Am. J. Hum. Biol. 17:5–21, 2005. © 2004 Wiley-Liss, Inc.

Graded bidirectional synaptic plasticity is composed of switch-like unitary events.

Abstract: Biological information storage events are often rapid transitions between discrete states. In neural systems, the initiation of bidirectional plasticity by all-or-none events may help confer robustness on memory storage. Here, we report that at CA3-CA1 hippocampal synapses, individual potentiation and depression plasticity events are discrete and heterogeneous in nature. Individual synapses began from extreme high and low strength states. Unitary plasticity events were all-or-none and drove synaptic strength between extremes in <1 min. Under naive conditions, approximately three-fourths of synapses began in a low-strength state. The timing of these unitary events can account for the time course of macroscopic synaptic plasticity.

Alternative life histories shape brain gene expression profiles in males of the same population.

Abstract: Atlantic salmon (Salmo salar) undergo spectacular marine migrations before homing to spawn in natal rivers. However, males that grow fastest early in life can adopt an alternative 'sneaker' tactic by maturing earlier at greatly reduced size without leaving freshwater. While the ultimate evolutionary causes have been well studied, virtually nothing is known about the molecular bases of this developmental plasticity. We investigate the nature and extent of coordinated molecular changes that accompany such a fundamental transformation by comparing the brain transcription profiles of wild mature sneaker males to age-matched immature males (future large anadromous males) and immature females. Of the ca. 3000 genes surveyed, 15% are differentially expressed in the brains of the two male types. These genes are involved in a wide range of processes, including growth, reproduction and neural plasticity. Interestingly, despite the potential for wide variation in gene expression profiles among individuals sampled in nature, consistent patterns of gene expression were found for individuals of the same reproductive tactic. Notably, gene expression patterns in immature males were different both from immature females and sneakers, indicating that delayed maturation and sea migration by immature males, the 'default' life cycle, may actually result from an active inhibition of development into a sneaker.

Ancient origins of human developmental plasticity.

Abstract: Animals have the ability to alter development, physiology, growth, and behavior in response to different environmental conditions. These responses represent critical assessments of both external and internal factors. For example, the timing of metamorphosis, hatching, or birth depends on the trade-offs between growth opportunity and mortality risk in the developmental habitat. Physiological sensors compute these trade-offs as a function of energy balance and environmental stress, and effectors initiate physiological, developmental, and behavioral responses to these determinations. The neuroendocrine stress axis provides a means for animals to integrate information from multiple sources and to respond accordingly. Considerable evidence now supports the view that the secretion of hormones critical to development (corticosteroid and thyroid hormones) is controlled by a common neuroendocrine stress pathway involving corticotropin-releasing factor (CRF) and related peptides. CRF produced in the hypothalamus stimulates the biosynthesis and secretion of both thyroid and corticosteroid hormones, leading to accelerated tadpole metamorphosis. Similarly, in mammals CRF of fetal and placental origin has been shown to influence the timing of birth. Studies in several experimental animal models and in humans show that early life experience can have long-term phenotypic consequences. Furthermore, there is evidence that phenotypic expression is strongly influenced by the actions of stress hormones produced during development. The integrated neuroendocrine response to stress, and its role in timing critical life history transitions and establishing long-term phenotypic expression, arose early in the evolution of vertebrates. Am. J. Hum. Biol. 17:44–54, 2005. © 2004 Wiley-Liss, Inc.

Aspects of the homeostaic plasticity of GABAA receptor‐mediated inhibition

Abstract: Plasticity of ligand-gated ion channels plays a critical role in nervous system development, circuit formation and refinement, and pathological processes. Recent advances have mainly focused on the plasticity of channels gated by excitatory amino acids, including their acclaimed role in learning and memory. These receptors, together with voltage-gated ion channels, have also been known to be subjected to a homeostatic form of plasticity that prevents destabilization of the neurone's function and that of the network during various physiological processes. To date, the plasticity of GABAA receptors has been examined mainly from a developmental and a pathological point of view. Little is known about homeostatic mechanisms governing their plasticity. This review summarizes some of the findings on the homeostatic plasticity of tonic and phasic inhibitory activity.

Altering cannabinoid signaling during development disrupts neuronal activity

Abstract: In adult cortical tissue, recruitment of GABAergic inhibition prevents the progression of synchronous population discharges to epileptic activity. However, at early developmental stages, GABA is excitatory and thus unable to fulfill this role. Here, we report that retrograde signaling involving endocannabinoids is responsible for the homeostatic control of synaptic transmission and the resulting network patterns in the immature hippocampus. Blockade of cannabinoid type 1 (CB1) receptor led to epileptic discharges, whereas overactivation of CB1 reduced network activity in vivo. Endocannabinoid signaling thus is able to keep population discharge patterns within a narrow physiological time window, balancing between epilepsy on one side and sparse activity on the other, which may result in impaired developmental plasticity. Disturbing this delicate balance during pregnancy in either direction, e.g., with marijuana as a CB1 agonist or with an antagonist marketed as an antiobesity drug, can have profound consequences for brain maturation even in human embryos.

Life-long echoes--a critical analysis of the developmental origins of adult disease model.

Abstract: The hypothesis that there is a developmental component to subsequent adult disease initially arose from epidemiological findings relating birth size to either indices of disease risk or actual disease prevalence in later life. While components of the epidemiological analyses have been challenged, there is strong evidence that developmental factors contribute to the later risk of metabolic disease--including insulin resistance, obesity, and heart disease--as well as have a broader impact on osteoporosis, depression and schizophrenia. We suggest that disease risk is greater when there is a mismatch between the early developmental environment (i.e., the phase of developmental plasticity) versus that experienced in mature life (i.e., adulthood), and that nutritional influences are particularly important. It is also critical to distinguish between those factors acting during the developmental phase that disrupt development from those influences that are less extreme and act through regulated processes of epigenetic change. A model of the relationship between the developmental and mature environment is proposed and suggests interventional strategies that will vary in different population settings.

Neural plasticity after spinal cord injury.

Abstract: Spinal cord injury (SCI) has devastating physical and socioeconomical impact. However, some degree of functional recovery is frequently observed in patients after SCI. There is considerable evidence that functional plasticity occurs in cerebral cortical maps of the body, which may account for functional recovery after injury. Additionally, these plasticity changes also occur at multiple levels including the brainstem, spinal cord, and peripheral nervous system. Although the interaction of plasticity changes at each level has been less well studied, it is likely that changes in subcortical levels contribute to cortical reorganization. Since the permeability of the blood-brain barrier (BBB) is changed, SCI-induced factors, such as cytokines and growth factors, can be involved in the plasticity events, thus affecting the final functional recovery after SCI. The mechanism of plasticity probably differs depending on the time frame. The reorganization that is rapidly induced by acute injury is likely based on unmasking of latent synapses resulting from modulation of neurotransmitters, while the long-term changes after chronic injury involve changes of synaptic efficacy modulated by long-term potentiation and axonal regeneration and sprouting. The functional significance of neural plasticity after SCI remains unclear. It indicates that in some situations plasticity changes can result in functional improvement, while in other situations they may have harmful consequences. Thus, further understanding of the mechanisms of plasticity could lead to better ways of promoting useful reorganization and preventing undesirable consequences.

Evolution of Morphological Integration: Developmental Accommodation of Stress‐Induced Variation

Abstract: Extreme environmental change during growth often re- sults in an increase in developmental abnormalities in the mor- phology of an organism. The evolutionary significance of such stress- induced variation depends on the recurrence of a stressor and on the degree to which developmental errors can be accommodated by an organism's ontogeny without significant loss of function. We sub- jected populations of four species of soricid shrews to an extreme environment during growth and measured changes in the patterns of integration and accommodation of stress-induced developmental errors in a complex of mandibular traits. Adults that grew under an extreme environment had lower integration of morphological vari- ation among mandibular traits and highly elevated fluctuating asym- metry in these traits, compared to individuals that grew under the control conditions. However, traits differed strongly in the magnitude of response to a stressor—traits within attachments of the same muscle (functionally integrated traits) had lower response and changed their integration less than other traits. Cohesiveness in func- tionally integrated complexes of traits under stress was maintained by close covariation of their developmental variation. Such devel- opmental accommodation of stress-induced variation might enable the individual's functioning and persistence under extreme environ- mental conditions and thus provides a link between individual ad- aptation to stress and the evolution of stress resistance.

Fetal origins of developmental plasticity: Animal models of induced life history variation

Abstract: The interaction of the genetic program with the environment shapes the development of an individual. Accumulating data from animal models indicate that prenatal and early-postnatal events (collectively called "early-life events") can initiate long-term changes in the expression of the genetic program which persist, or may only become apparent, much later in the individual's life. Researchers working with humans or animal models of human diseases often view the effects of early-life events through the lens of pathology, with a focus on whether the events increase the risk for a particular disease. Alternatively, comparative biologists often view the effects of early-life events through the lens of evolution and adaptation by natural selection; they investigate the processes by which environmental conditions present early in life may prompt the adoption of different developmental pathways leading to alternative life histories. Examples of both approaches are presented in this article. This article reviews the concepts of phenotypic plasticity, natural selection, and evidence from animal models that early-life events can program the activity of the neuroendocrine system, at times altering life history patterns in an adaptive manner. Data from seasonally breeding rodents are used to illustrate the use of maternally derived information to alter the life history of young. In several species, the maternal system transfers photoperiodic information to the young in utero. This maternally derived information alters the response of young to photoperiods encountered later and life, producing seasonally distinct life histories.

Ontogeny of cardiovascular control in zebrafish (Danio rerio): Effects of developmental environment

Abstract: The goal of this symposium paper was to identify and quantify developmental plasticity in the onset of cardiovascular responses in the zebrafish. Developmental plasticity was induced by altering the developmental environment in one of three ways: (1) by developing zebrafish in a constant current of 5 body lengths per second, (2) by developing zebrafish at a colder temperature (20 °C), and (3) by developing zebrafish in severe hypoxia (DO = 0.8 mg/L). Early morphological development was significantly affected by each of the treatment environments with hypoxia slowing development the most and producing the highest variation in measurements. Development in constant water current did not significantly affect the timing onset of cardiovascular responses to the pharmacological agents applied. Development at 20 °C significantly delayed the onset of all cardiovascular responses measured by 2–3 days. Development in hypoxia, however, not only delayed onset of all cardiovascular responses, but also shifted the onset relative to the developmental program. Hypoxia clearly has a profound affect on the onset of cardiovascular regulation and it will take many more studies to elucidate the mechanisms by which hypoxia is having its effect. Furthermore, long term studies are also needed to assess whether the plasticity measured in this study is adaptive in the evolutionary sense.

Developmental Environment Alters Conditional Aggression in Zebrafish

Abstract: The developmental environment influences a wide variety of phenotypic traits in the adults of many vertebrates (i.e., developmental plasticity). In this study, we test to see if developmental environment (EDEV) interacts with the adult behavioral environment (EBEHAV) in determining behavioral phenotypes. We reared Zebrafish (Danio rerio) from eggs in either continuously hypoxic or normoxic conditions. We then tested aggression and avoidance (i.e., hiding) levels of fish from each developmental treatment in both environments. Developmental environment was a significant source of variation in avoidance behavior while the stimulus environment did not influence avoidance. Without a period of acclimation we found that EBEHAV and an EDEV 3 EBEHAV interaction were both significant sources of variation. However, when the fish were allowed to physiologically acclimate to the environment for 16 h, aggression level was highest for fish tested in the environment in which they developed. In that case the EDEV 3 EBEHAV interaction was the only significant source of variation. These results demonstrate that a more complete understanding of phenotypic response can be gained by incorporating environmental conditions across multiple time scales.

Reversible blockade of experience-dependent plasticity by calcineurin in mouse visual cortex.

Abstract: Numerous protein kinases have been implicated in visual cortex plasticity, but the role of serine/threonine protein phosphatases has not yet been established. Calcineurin, the only known Ca2+/calmodulin-activated protein phosphatase in the brain, has been identified as a molecular constraint on synaptic plasticity in the hippocampus and on memory. Using transgenic mice overexpressing calcineurin inducibly in forebrain neurons, we now provide evidence that calcineurin is also involved in ocular dominance plasticity. A transient increase in calcineurin activity is found to prevent the shift of responsiveness in the visual cortex following monocular deprivation, and this effect is reversible. These results imply that the balance between protein kinases and phosphatases is critical for visual cortex plasticity.

Differential expression of two NMDA receptor interacting proteins, PSD-95 and SynGAP during mouse development.

Abstract: Patterns of neural activity mediated by N-methyl-D-aspartate (NMDA) receptors are known to play important roles in development of the central nervous system. However, the signalling pathways downstream from NMDA receptors that are critical for normal neuronal development are not yet clearly understood. NMDA receptors interact with various signalling proteins via scaffolding proteins, which are important in adult neuronal and behavioural plasticity. For example, the NR2B subunits of the NMDA receptor interact with postsynaptic density 95 (PSD-95), which in turn binds to synaptic ras GTPase-activating protein (SynGAP). Interestingly, the developmental phenotype of mice carrying null mutations in these genes differ. NR2B and SynGAP homozygote mice die within the first week of birth whereas PSD-95 homozygote mice survive to adulthood. We therefore examined the expression patterns of PSD-95 and SynGAP genes from embryonic stages to adult using lacZ (beta-galactosidase) marker gene knock-in mice. Dramatic changes of expression were observed throughout development in brain and other tissues. Although SynGAP binds PSD-95, both genes had distinct, as well as overlapping expression. SynGAP expression peaked at times of synaptogenesis and developmental plasticity in contrast to PSD-95, which was expressed throughout the brain from early embryonic stages. Furthermore, SynGAP showed a more spatially restricted pattern as illustrated by its restriction to forebrain in contrast to PSD-95, which was also found in mid- and hindbrain. These data support the model that synaptic signalling complexes are heterogeneous and individual components show temporal and spatial specificity during development.

Regulation of cpg15 Expression during Single Whisker Experience in the Barrel Cortex of Adult Mice

Abstract: Regulation of gene transcription by neuronal activity is thought to be key to the translation of sensory experience into long-term changes in synaptic structure and function. Here we show that cpgI5, a gene encoding an extracellular signaling molecule that promotes dendritic and axonal growth and synaptic maturation, is regulated in the somatosensory cortex by sensory experience capable of inducing cortical plasticity. Using in situ hybridization, we monitored cpgI5 expression in 4-week-old mouse barrel cortex after trimming all whiskers except D1. We found that cpgI5 expression is depressed in the deprived barrels and enhanced in the barrel column corresponding to the spared D1 whisker. Changes in cpgI5 mRNA levels first appear in layer IV, peak 12 h after deprivation, and then decline rapidly. In layers II/III, changes in cpgI5 expression appear later, peak at 24 h, and persist for days. Induction of cpgI5 expression is significantly diminished in adolescent as well as adult CREB knockout mice. cpgI5's spatio-temporal expression pattern and its regulation by CREB are consistent with a role in experience-dependent plasticity of cortical circuits. Our results suggest that local structural and/or synaptic changes may be a mechanism by which the adult cortex can adapt to peripheral manipulations. (c) 2005 Wiley Periodicals, Inc.

Culture and Developmental Plasticity: Evolution of the Social Brain

Abstract: The relation between culture and biology emerged as one of anthropology’s first intellectual responsibilities. It remains one of our most frustrating enigmas. The dichotomy of “nature and nurture” has been a persistent obstacle to consilience between the biological and social sciences. Anthropology has traditionally recognized that culture is inextricably linked to the evolution of mind and that the converse is equally important. In this chapter, I review a scenario in which the mind evolved as a “social tool” in an increasingly cultural environment. I posit that the human psyche was designed primarily to contend with social relationships, whereas the physical environment was relatively less important. Most natural selection in regard to brain evolution was a consequence of interactions with conspecifics, not with food and climate. The primary mental chess game was with other intelligent hominid competitors and cooperators, not with fruits, tools, prey, or snow. An extended juvenile period was favored by natural selection because of the need for more time to develop mental competencies used in forming coalitions and other aspects of social competition. “Culture,” shorthand for the information acquired and used by minds in social ways, was a

Do plants and animals differ in phenotypic plasticity

Abstract: This paper compares the flexibility in the nexus between phenotype and genotype in plants and animals. These taxa although considered to be fundamentally different are found to be surprisingly similar in the mechanisms used to achieve plasticity. Although non-cognitive behaviour occurs in plants, its range is limited, while morphological and developmental plasticity also occur to a considerable extent in animals. Yet both plants and animals are subject to unique constraints and thus need to find unique solutions to functional problems. A true comparison between the plant and animal phenotype would be a comparison between plants and sessile photosynthesizing colonial invertebrates. Such comparisons are lacking. However, they would provide important insights into the adaptive significance of plasticity in these groups. It is also suggested that a comparison of inflexible traits in these groups would provide an understanding of the constraints, as well as the costs and benefits, of a plastic versus non-plastic phenotype in plants and animals.