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Changes in an environmental variable (e.g. temperature) cause different genes to be expressed in organisms

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.

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.[2] Nevertheless, some mobile organisms also have significant phenotypic plasticity; for example Acyrthosiphon pisum of the Aphid family exhibits the ability to interchange between asexual and sexual reproduction, as well as growing wings between generations when plants become too populated.[3]

Examples of Phenotypic Plasticity

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Plants

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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.[4] The transport proteins present in roots are also changed depending on the concentration of the nutrient and the salinity of the soil.[5] Some plants, Mesembryanthemum crystallinum for example, are able to alter their photosynthetic pathways to use less water when they become water- or salt-stressed.[6]

Animals

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Temperature

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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.[7]

Diet

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Phenotypic plasticity of the digestive system allows some animals to respond to changes in dietary nutrient composition[8][9], diet quality[10][11], and energy requirements.[12][13][14]

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.[8] Acclimatiing animals to high protein diets can increase the activity of aminopeptidase-N, which digests proteins.[9][15]

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[14], Mongolian gerbils[11], Japanese quail[10], wood ducks[16], mallards[17]). 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.[11]

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%.[12] 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.[12] Intermittent feeding also represents a temporal increase in food intake and can induce dramatic changes in the size of the gut; the Burmese python can triple the size of its small intestine just a few days after feeding.[18]


Parasitism

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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. [19] A reduction in fecundity may also occur, as a means of re-directing nutrients to an immune response [20] or to increase longevity of the host[21]. 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. [22]

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 [23].

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.[24] 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 [25] [1]. 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. [24]

Evolution of Phenotypic Plasticity

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Plasticity is thought to be an evolutionary adaptation to environmental variation, as it allows individuals to ‘fit’ their phenotype to different environments. If the optimal phenotype in a given environment changes with environmental conditions, the ability of individuals to express different traits should be advantageous and thus selected for. Hence, phenotypic plasticity can evolve if fitness is increased by changing phenotype.[26] 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.[27][28]

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.[29] 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.[30][31] 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.[32] Some researchers propose that direct measures of environmental variability, using factors such as precipitation, are better predictors of phenotypic plasticity than latitude alone.[33]

Plasticity in a Changing World

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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.[34] 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.[35]


See also

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References

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  1. ^ Price TD, Qvarnström A, Irwin DE (July 2003). "The role of phenotypic plasticity in driving genetic evolution". Proc. Biol. Sci. 270 (1523): 1433–40. doi:10.1098/rspb.2003.2372. PMC 1691402. PMID 12965006.{{cite journal}}: CS1 maint: date and year (link) CS1 maint: multiple names: authors list (link)
  2. ^ http://arjournals.annualreviews.org/doi/abs/10.1146/annurev.es.17.110186.003315 Annual Review of Ecology and Systematics Vol. 17:667-693 (Volume publication date November 1986) doi:10.1146/annurev.es.17.110186.003315
  3. ^ http://www.plosbiology.org/article/info%3Adoi%2F10.1371%2Fjournal.pbio.1000313 PLoS Biology, Jan 19 2010, "Genome Sequence of the Pea Aphid Acyrthosiphon pisum". The International Aphid Genomics Consortium
  4. ^ Sultan SE (December 2000). "Phenotypic plasticity for plant development, function and life history". Trends Plant Sci. 5 (12): 537–542. doi:10.1016/S1360-1385(00)01797-0. PMID 11120476.{{cite journal}}: CS1 maint: date and year (link)
  5. ^ Differential regulation of the HAK5 genes encoding the high-affinity K+ transporters of Thellungiella halophila and Arabidopsis thaliana Environmental and Experimental Botany Volume 65, Issues 2-3, March 2009, Pages 263-269 Fernando Alemána, Manuel Nieves-Cordonesa, Vicente Martínez et al doi:10.1016/j.envexpbot.2008.09.011
  6. ^ http://pcp.oxfordjournals.org/cgi/content/abstract/38/3/236 Plant and Cell Physiology, 1997, Vol. 38, No. 3 236-242 Induction of CAM in Mesembryanthemum crystallinum Abolishes the Stomatal Response to Blue Light and Light-Dependent Zeaxanthin Formation in Guard Cell Chloroplasts. Gary Tallman, Jianxin Zhu, Bruce T. Mawson et al
  7. ^ Hazel JR (1995). "Thermal adaptation in biological membranes: is homeoviscous adapation the explanation?" (PDF). Annu. Rev. Physiol. 57: 19–42. doi:10.1146/annurev.ph.57.030195.000315. PMID 7778864.
  8. ^ a b Brzek P, Kohl K, Caviedes-Vidal E, Karasov WH (2009). "Developmental adjustments of house sparrow (Passer domesticus) nestlings to diet composition". J Exp Biol. 212 (9): 1284–1293. doi:10.1242/jeb.023911. PMID 19376949.{{cite journal}}: CS1 maint: multiple names: authors list (link)
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  12. ^ a b c Naya DE, Ebensperger LA, Sabat P, Bozinovic F. (2008). "Digestive and metabolic flexibility allows female degus to cope with lactation costs" (PDF). Physiol Biochem Zool. 81 (2): 186–194. doi:10.1086/527453. PMID 18190284.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  13. ^ Krockenberger AK, Hume ID (2007). "A flexible digestive strategy accommodates the nutritional demands of reproduction in a free-living folivore, the Koala (Phascolarctos cinereus)". Funct Ecol. 21 (4): 748–756. doi:10.1111/j.1365-2435.2007.01279.x.
  14. ^ a b Hammond KA, Wunder BA (1991). "The role of diet quality and energy need in the nutritional ecology of a small herbivore, Microtus ochrogaster". Physiol Zool. 64 (2): 541–567. doi:10.1086/physzool.64.2.30158190. JSTOR 30158190.
  15. ^ Sabat P, Riveros JM, López-Pinto C (2005). "Phenotypic flexibility in the intestinal enzymes of the Africanvclawed frog Xenopus laevis" (PDF). Comp Biochem Physiol a Mol Integr Physiol. 140 (1): 135–139. doi:10.1016/j.cbpb.2004.11.010. PMID 15664322.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  16. ^ Drobney RD (1984). "Effect of diet on visceral morphology of breeding wood ducks". Auk. 101 (1): 93–98. doi:10.1093/auk/101.1.93. JSTOR 4086226.
  17. ^ Kehoe FP, Ankney CD, Alisauskas RT (1988). "Effects of dietary fiber and diet diversity on digestive organs of captive Mallards (Anas platyrhynchos)". Can J Zool. 66 (7): 1597–1602. doi:10.1139/z88-233.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  18. ^ Starck JM, Beese K (2001). "Structural flexibility of the intestine of Burmese python in response to feeding" (PDF). J Exp Biol. 204 (Pt 2): 325–335. doi:10.1242/jeb.204.2.325. PMID 11136618.
  19. ^ Chadwick J, Little TJ (2005). "A parasite-mediated life-history shift in Daphnia magna". Proc. Roy. Soc. B. 272 (1562): 505–509. doi:10.1098/rspb.2004.2959. PMC 1578704. PMID 15799946.
  20. ^ Ahmed AM, Baggott SL, Maingon R, Hurd H (2002). "The costs of mounting an immune response are reflected in the reproductive fitness of the mosquito Anopheles gambiae". Oikos. 97 (3): 371–377. doi:10.1034/j.1600-0706.2002.970307.x.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  21. ^ Hurd H (2001). "Host fecundity reduction: a strategy for damage limitation?". Trends Parasitol. 17 (8): 363–369. doi:10.1016/S1471-4922(01)01927-4.x (inactive 2023-08-02).{{cite journal}}: CS1 maint: DOI inactive as of August 2023 (link)
  22. ^ Schallig HDFH, Hordijk PL, Oosthoek PW, de Jong-Brink M (1991). "Schistosomin, a peptide present in the haemolymph of Lymnaea stagnalis infected with Trichobilharzia ocellata is produced only in the snail's central nervous system". Parasitol. Res. 77 (2): 152–156. doi:10.1007/BF00935429.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  23. ^ Kristan DM, Hammond KA (2003). "Physiological and morphological responses to simultaneous cold exposure and parasite infection by wild-derived house mice". Func. Ecol. 17 (4): 464–471. doi:10.1046/j.1365-2435.2003.00751.x. JSTOR 3598983.
  24. ^ a b Singer MS, Mace KC, Bernays EA (2009). "Self-medication as adaptive plasticity: Increased ingestion of plant toxins by parasitized caterpillars". PLOS ONE. 4 (3). doi:10.1371/journalpone.0004796 (inactive 2023-08-02).{{cite journal}}: CS1 maint: DOI inactive as of August 2023 (link) CS1 maint: multiple names: authors list (link) CS1 maint: unflagged free DOI (link)
  25. ^ Huffman MA (August 2001). "Self-medicative behaviour in the African great apes: An evolutionary perspective into the origins of human traditional medicine" (PDF). BioSci. 51 (8): 651. doi:10.1641/0006-3568(2001)051[0651:SMBITA]2.0.CO;2.{{cite journal}}: CS1 maint: date and year (link)
  26. ^ De Jong G (April 2005). "Evolution of phenotypic plasticity: patterns of plasticity and the emergence of ecotypes". New Phytol. 166 (1): 101–117. doi:10.1111/j.1469-8137.2005.01322.x. PMID 15760355.{{cite journal}}: CS1 maint: date and year (link)
  27. ^ Langerhans, R. B., & Dewitt, T. J. (2002). "Plasticity constrained : over-generalized induction cues cause maladaptive phenotypes" (PDF). Evolutionary Ecology (4): 857–870.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  28. ^ Dewitt, Thomas J.; Siha, Andrew; Wilson, David (1998). "Costs and limits of phenotypic plasticity". Trends in Ecology and Evolution. 13 (2): 77–81. doi:10.1016/S0169-5347(97)01274-3. PMID 21238209.{{cite journal}}: CS1 maint: multiple names: authors list (link)
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  30. ^ Naya DE, Bozinovic F, Karasov WH (2008). "Latitudinal trends in digestive flexibility: testing the climatic variability hypothesis with data on the intestinal length of rodents". Am Nat. 174 (4): E122-134. doi:10.1086/590957. JSTOR 10.1086/590957. PMID 18717635.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  31. ^ Molina-Montenegro MA, Naya DE (2012). "Latitudinal patterns in phenotypic plasticity and fitness-related traits: Assessing the climatic variability hypothesis (CVH) with an invasive plant species". PLOS ONE. 7 (10): e47620. doi:10.1371/journal.pone.0047620. PMC 3478289. PMID 23110083.
  32. ^ Overgaard J, Kristensen TN, Mitchell KA, Hoffmann AA (2011). "Thermal tolerance in widespread and tropical Drosophila species: Does phenotypic plasticity increase with latitude?" (PDF). Am Nat. 178: S80–S96. doi:10.1086/661780. PMID 21956094.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  33. ^ Maldonado K, Bozinovic F, Rojas JM, Sabat P (2011). "Within-species digestive tract flexibility in rufous-collared sparrows and the climatic variability hypothesis". Physiol Biochem Zool. 84 (4): 377–384. doi:10.1086/660970. JSTOR 10.1086/660970. PMID 21743251.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  34. ^ Williams SE, Shoo LP, Isaac JL, Hoffmann AA, Langham G (2008). "Towards an integrated framework for assessing the vulnerability of species to climate change". PLOS Biol. 6 (12): 2621–2626. doi:10.1371/journal.pbio.0060325. PMC 2605927. PMID 19108608.{{cite journal}}: CS1 maint: multiple names: authors list (link) CS1 maint: unflagged free DOI (link)
  35. ^ Reale, D.; et al. (2003). "Genetic and plastic responses of a northern mammal to climate change". The Royal Society. 270 (1515): 591–596. doi:10.1098/rspb.2002.2224. PMC 1691280. PMID 12769458. {{cite journal}}: Explicit use of et al. in: |author= (help)
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Further reading

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  • Theunis Piersma, Jan A. Van Gils (2011). The Flexible Phenotype: A Body-Centred Integration of Ecology, Physiology, and Behaviour. Oxford University Press. ISBN 0191640158, 9780191640155. {{cite book}}: Check |isbn= value: invalid character (help)


Category:Evolutionary biology Category:Genetics

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