Phenotypic plasticity

Phenotypic plasticity can be defined as the ability of one genotype to produce more than one phenotype when exposed to different environments.

Phenotypic plasticity is the ability of an organism to change its phenotype in response to changes in the environment.[1] Fundamental to the way in which organisms cope with environmental variation, phenotypic plasticity encompasses all types of environmentally induced changes (e.g. morphological, physiological, behavioural, phenological) that may or may not be permanent throughout an individual’s lifespan. The term was originally used to describe developmental effects on morphological characters, but is now more broadly used to describe all phenotypic responses to environmental change, such as acclimation or acclimatization, as well as learning.[2] The special case when differences in environment induce discrete phenotypes is termed polyphenism.

In many cases of phenotypic plasticity, changes in environmental conditions (e.g. temperature) cause different genes to be expressed in organisms.

Generally, phenotypic plasticity is more important for immobile organisms (e.g. plants) than mobile organisms (e.g. most animals), as mobile organisms can often move away from unfavourable environments.[3] Nevertheless, mobile organisms also have at least some degree of plasticity in at least some aspects of the phenotype. One mobile organism with substantial phenotypic plasticity is Acyrthosiphon pisum of the Aphid family, which exhibits the ability to interchange between asexual and sexual reproduction, as well as growing wings between generations when plants become too populated.[4]

Examples of phenotypic plasticity


Phenotypic plasticity in plants includes the allocation of more resources to the roots in soils that contain low concentrations of nutrients and the alteration of leaf size and thickness.[5] Dandelion are well known for exhibiting considerable plasticity in form when growing in sunny versus shaded environments. The transport proteins present in roots are also changed depending on the concentration of the nutrient and the salinity of the soil.[6] Some plants, Mesembryanthemum crystallinum for example, are able to alter their photosynthetic pathways to use less water when they become water- or salt-stressed.[7]


The developmental effects of nutrition and temperature have been demonstrated.[8] Within the Gray wolf (Canis lupus), the dog demonstrates wide phenotypic plasticity.[9][10] Additionally, the Speckled Wood butterfly, the males of this species have two morphs. One with three dots on its hind wing, and one with four dots on its hind wings. The development of the fourth dot is dependent on environmental conditions, more specifically location, and the time of year.[11] In amphibians, as of 2015, Pristimantis mutabilis is known to show a remarkable phenotypic plasticity.[12] Another example, is the Southern Rockhopper Penguin.[13] Rockhopper penguins are present at a variety of climates and locations; Amsterdam Island's subtropical waters,Kerguelen Archipelago's subarctic coastal waters, and Crozet Archipelago's subantarctic coastal waters.[13] Due to the species plasticity they are able to express different strategies and foraging behaviors depending on the climate and environment.[13] A main factor that has influenced the species' behavior is where food is located.[13]


Plastic responses to temperature are essential among ectothermic organisms, as all aspects of their physiology are directly dependent on their thermal environment. As such, thermal acclimation entails phenotypic adjustments that are found commonly across taxa, such as changes in the lipid composition of cell membranes. Temperature change influences the fluidity of cell membranes by affecting the motion of the fatty acyl chains of glycerophospholipids. Because maintaining membrane fluidity is critical for cell function, ectotherms adjust the phospholipid composition of their cell membranes such that the strength of van der Waals forces within the membrane is changed, thereby maintaining fluidity across temperatures.[14]


Phenotypic plasticity of the digestive system allows some animals to respond to changes in dietary nutrient composition,[15][16] diet quality,[17][18] and energy requirements.[19][20][21]

Changes in the nutrient composition of the diet (the proportion of lipids, proteins and carbohydrates) may occur during development (e.g. weaning) or with seasonal changes in the abundance of different food types. These diet changes can elicit plasticity in the activity of particular digestive enzymes on the brush border of the small intestine. For example, in the first few days after hatching, nestling house sparrows (Passer domesticus) transition from an insect diet, high in protein and lipids, to a seed based diet that contains mostly carbohydrates; this diet change is accompanied by two-fold increase in the activity of the enzyme maltase, which digests carbohydrates.[15] Acclimatizing animals to high protein diets can increase the activity of aminopeptidase-N, which digests proteins.[16][22]

Poor quality diets (those that contain a large amount of non-digestible material) have lower concentrations of nutrients, so animals must process a greater total volume of poor-quality food to extract the same amount of energy as they would from a high-quality diet. Many species respond to poor quality diets by increasing their food intake, enlarging digestive organs, and increasing the capacity of the digestive tract (e.g. prairie voles,[21] Mongolian gerbils,[18] Japanese quail,[17] wood ducks,[23] mallards[24]). Poor quality diets also result in lower concentrations of nutrients in the lumen of the intestine, which can cause a decrease in the activity of several digestive enzymes.[18]

Animals often consume more food during periods of high energy demand (e.g. lactation or cold exposure in endotherms), this is facilitated by an increase in digestive organ size and capacity, which is similar to the phenotype produced by poor quality diets. During lactation, degus (Octodon degus) increase the mass of their liver, small intestine, large intestine and cecum by 15-35%.[19] Increases in food intake do not cause changes in the activity of digestive enzymes because nutrient concentrations in the intestinal lumen are determined by food quality and remain unaffected.[19] Intermittent feeding also represents a temporal increase in food intake and can induce dramatic changes in the size of the gut; the Burmese python (Python molurus bivittatus) can triple the size of its small intestine just a few days after feeding.[25]

AMY2B (Alpha-Amylase 2B) is a gene that codes a protein that assists with the first step in the digestion of dietary starch and glycogen. An expansion of this gene in dogs would enable early dogs to exploit a starch-rich diet as they fed on refuse from agriculture. Data indicated that the wolves and dingo had just two copies of the gene and the Siberian Husky that is associated with hunter-gatherers had just three or four copies, whereas the Saluki that is associated with the Fertile Crescent where agriculture originated had 29 copies. The results show that on average, modern dogs have a high copy number of the gene, whereas wolves and dingoes do not. The high copy number of AMY2B variants likely already existed as a standing variation in early domestic dogs, but expanded more recently with the development of large agriculturally based civilizations.[26]


Infection with parasites can induce phenotypic plasticity as a means to compensate for the detrimental effects caused by parasitism. Commonly, invertebrates respond to parasitic castration or increased parasite virulence with fecundity compensation in order to increase their reproductive output, or fitness. For example, water fleas (Daphnia magna), exposed to microsporidian parasites produce more offspring in the early stages of exposure to compensate for future loss of reproductive success.[27] A reduction in fecundity may also occur as a means of re-directing nutrients to an immune response,[28] or to increase longevity of the host.[29] This particular form of plasticity has been shown in certain cases to be mediated by host-derived molecules (e.g. schistosomin in snails Lymnaea stagnalis infected with trematodes Trichobilharzia ocellata) that interfere with the action of reproductive hormones on their target organs.[30] Changes in reproductive effort during infection is also thought to be a less costly alternative to mounting resistance or defence against invading parasites, although it can occur in concert with a defence response.[31]

Hosts can also respond to parasitism through plasticity in physiology aside from reproduction. House mice infected with intestinal nematodes experience decreased rates of glucose transport in the intestine. To compensate for this, mice increase the total mass of mucosal cells, cells responsible for glucose transport, in the intestine. This allows infected mice to maintain the same capacity for glucose uptake and body size as uninfected mice.[32]

Phenotypic plasticity can also be observed as changes in behaviour. In response to infection, both vertebrates and invertebrates practice self-medication, which can be considered a form of adaptive plasticity.[33] Various species of non-human primates infected with intestinal worms engage in leaf-swallowing, in which they ingest rough, whole leaves that physically dislodge parasites from the intestine. Additionally, the leaves irritate the gastric mucosa, which promotes the secretion of gastric acid and increases gut motility, effectively flushing parasites from the system.[34] The term "self-induced adaptive plasticity" has been used to describe situations in which a behavior under selection causes changes in subordinate traits that in turn enhance the ability of the organism to perform the behavior.[35] For example, birds that engage in altitudinal migration might make "trial runs" lasting a few hours that would induce physiological changes that would improve their ability to function at high altitude.[35]

Woolly bear caterpillars (Grammia incorrupta) infected with tachinid flies increase their survival by ingesting plants containing toxins known as pyrrolizidine alkaloids. The physiological basis for this change in behaviour is unknown; however, it is possible that, when activated, the immune system sends signals to the taste system that trigger plasticity in feeding responses during infection.[33]

Evolution of phenotypic plasticity

Plasticity is usually thought to be an evolutionary adaptation to environmental variation that is reasonably predictable and occurs within the lifespan of an individual organism, as it allows individuals to ‘fit’ their phenotype to different environments.[36][37] If the optimal phenotype in a given environment changes with environmental conditions, then the ability of individuals to express different traits should be advantageous and thus selected for. Hence, phenotypic plasticity can evolve if Darwinian fitness is increased by changing phenotype.[38] However, the fitness benefits of plasticity can be limited by the energetic costs of plastic responses (e.g. synthesizing new proteins, adjusting expression ratio of isozyme variants, maintaining sensory machinery to detect changes) as well as the predictability and reliability of environmental cues (see Beneficial acclimation hypothesis).

Freshwater snails (Physa virgata), provide an example of when phenotypic plasticity can be either adaptive or maladaptive. In the presence of a predator, bluegill sunfish, these snails make their shell shape more rotund and reduce growth. This makes them more crush-resistant and better protected from predation. However, these snails cannot tell the difference in chemical cues between the predatory and non-predatory sunfish. Thus, the snails respond inappropriately to non-predatory sunfish by producing an altered shell shape and reducing growth. These changes, in the absence of a predator, make the snails susceptible to other predators and limit fecundity. Therefore, these freshwater snails produce either an adaptive or maladaptive response to the environmental cue depending on whether the predatory sunfish is actually present.[39][40]

Given the profound ecological importance of temperature and its predictable variability over large spatial and temporal scales, adaptation to thermal variation has been hypothesized to be a key mechanism dictating the capacity of organisms for phenotypic plasticity.[41] The magnitude of thermal variation is thought to be directly proportional to plastic capacity, such that species that have evolved in the warm, constant climate of the tropics have a lower capacity for plasticity compared to those living in variable temperate habitats. Termed the “climatic variability hypothesis”, this idea has been supported by several studies of plastic capacity across latitude in both plants and animals.[42][43] However, recent studies of Drosophila species have failed to detect a clear pattern of plasticity over latitudinal gradients, suggesting this hypothesis may not hold true across all taxa or for all traits.[44] Some researchers propose that direct measures of environmental variability, using factors such as precipitation, are better predictors of phenotypic plasticity than latitude alone.[45]

Selection experiments and experimental evolution approaches have shown that plasticity is a trait that can evolve when under direct selection and also as a correlated response to selection on the average values of particular traits.[46]

Plasticity in a changing world

Unprecedented rates of climate change are predicted to occur over the next 100 years as a result of human activity. Phenotypic plasticity is a key mechanism with which organisms can cope with a changing climate, as it allows individuals to respond to change within their lifetime.[47] This is thought to be particularly important for species with long generation times, as evolutionary responses via natural selection may not produce change fast enough to mitigate the effects of a warmer climate.

The North American Red Squirrel (Tamiasciurus hudsonicus) has experienced an increase in average temperature over this last decade of almost 2 °C. This increase in temperature has caused an increase in abundance of white spruce cones, the main food source for winter and spring reproduction. In response, the mean lifetime parturition date of this species has advanced by 18 days. Food abundance showed a significant effect on the breeding date with individual females, indicating a high amount of phenotypic plasticity in this trait.[48]

See also


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