Phenotypic plasticity

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 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. 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]


As compared with plants, animals clearly show less plasticity in gross morphology. Nonetheless, developmental effects of nutrition and temperature have been demonstrated.[8] Other generalities include the following: behavior is very plastic; in vertebrates, skeletal muscle is more plastic than the lung; skeletal muscle is more plastic in mammals than in lizards; snake guts are very plastic; carp are very plastic as a species. For example, in 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.[9] In amphibians, as of 2015, Pristimantis mutabilis is known to show a remarkable phenotypic plasticity.[10]


Plastic responses to 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.[11]


Phenotypic plasticity of the digestive system allows some animals to respond to changes in dietary nutrient composition,[12][13] diet quality,[14][15] and energy requirements.[16][17][18]

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.[12] Acclimatizing animals to high protein diets can increase the activity of aminopeptidase-N, which digests proteins.[13][19]

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,[18] Mongolian gerbils,[15] Japanese quail,[14] wood ducks,[20] mallards[21]). 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.[15]

Animals often consume more food during periods of high energy demand (e.g. lactation or cold exposure in degus (Octodon degus) increase the mass of their liver, small intestine, large intestine and cecum by 15-35%.[16] 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.[16] 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.[22]


Infection with [26] 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.[27]

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.[28]

Phenotypic plasticity can also be observed as changes in behaviour. In response to infection, both vertebrates and invertebrates practice [31] 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.[31]

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.[29]

Evolution of phenotypic plasticity

Plasticity is usually thought to be an selected for. Hence, phenotypic plasticity can evolve if Darwinian fitness is increased by changing phenotype.[32] 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.[33][34]

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.[35] 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.[36][37] 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.[38] Some researchers propose that direct measures of environmental variability, using factors such as precipitation, are better predictors of phenotypic plasticity than latitude alone.[39]

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.[40]

Plasticity in a changing world

Unprecedented rates of [41] 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.[42]

See also


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Further reading

  • See also:

External links

  • Special issue of the Journal of Experimental Biology concerning phenotypic plasticity
  • Developmental Plasticity and Evolution - review of the book from American Scientist
  • Isidro A. T. Savillo's Impermanence of Sexual Phenotypes from Biologybrowser (Thomson Reuters)
  • Phenotypic Plasticity lecture from the Institute for the Development of Educational Applications]