Based on the information presented which of the following best explains the difference in phenotype

Phenotypic Plasticity

Phenotypic plasticity is the ability of an organism to change in response to stimuli or inputs from the environment. Synonyms are phenotypic responsiveness, flexibility, and condition sensitivity. The response may or may not be adaptive, and it may involve a change in morphology, physiological state, or behavior, or some combination of these, at any level of organization, the phenotype being all of the characteristics of an organism other than its genes.

There is a great potential for confusion regarding definitions of phenotypic plasticity, including this one. Even though the phenotype is defined here to exclude the genome, in fact phenotypic plasticity always involves a change in gene expression or gene-product use (morphological, physiological, and behavioral traits always being products, in part, of gene expression). Some definitions of phenotypic plasticity refer to the environmental sensitivity of a genotype, a potentially confusing terminology because it uses the word ‘genotype’ to mean ‘organism bearing a particular gene or set of genes’ and may be mistakenly understood to imply that the organism’s genome, rather than its phenotype (whose nature has been influenced by both environment and genome), responds to the environment. Such definitions attempt to convey the correct idea that phenotypic plasticity involves a change in some aspect of the phenotype without a change in the individual’s genes, or the genetic underpinnings of a particular trait. Thus, one could examine the phenotypes of genetically identical individuals and find that they differ phenotypically in different environments, indicating phenotypic plasticity for particular traits. Or, conversely, one could begin with individuals from phenotypically different populations found in different environments, and subject them to the same environment in a ‘common garden’ experiment designed to control environmental variables, and see to what degree the phenotypic differences are maintained, indicating the degree to which genetic differences between the populations, rather than plasticity, account for the phenotypic differences between them.

Phenotypic plasticity can be a source of ‘noise’, or confounding variation, in genetic experiments. Such experiments are therefore often designed to control environmental variation and reduce the effects of plasticity. But research in behavioral ecology, rather than eliminating plasticity, often focuses on it. Behavioral phenotypes are eminently plastic, often in adaptively appropriate ways. Plasticity of behavioral responses – the occurrence of complex, condition-sensitive behavioral repertoires – can increase the diversity of phenotypes within populations. But behavioral plasticity can also reduce phenotypic variation, as when behavioral responses are stability increasing or homeostatic in their effects. For example, individuals may adopt postures or move to locations that help reduce extremes of variation in body temperature. Homeostatic behavior can be quite elaborate: some social insects engage in behaviors (water transport and application to nest surfaces, followed by fanning wing movements that promote evaporative cooling) and effectively lower the temperature of nest and brood.

Abstract

Phenotypic plasticity enables organisms to survive in the face of unpredictable environmental stress. Intimately related to the notion of phenotypic plasticity is the concept of the reaction norm that places phenotypic plasticity in the context of a genotype-specific response to environmental gradients. Whether reaction norms themselves evolve and which factors might affect their shape has been the object of intense debates among evolutionary biologists along the years. Since their discovery, viruses have been considered as pathogens. However, new viromic techniques and a shift in conceptual paradigms are showing that viruses are mostly non-pathogenic ubiquitous entities. Recent studies have shown how viral infections can even be beneficial for their hosts. This may happen especially in the context of stressed hosts, where the virus infection can induce beneficial changes in the host's physiological homeostasis, hence changing the shape of the reaction norm. Despite the fact that underlying physiological mechanisms and evolutionary dynamics are still not well understood, such beneficial interactions are being discovered in a growing number of plant-virus systems. Here, we aim to review these disperse studies and place them into the context of phenotypic plasticity and the evolution of reaction norms. This is an emerging field that is posing many questions that still need to be properly answered. The answers would clearly interest virologists, plant pathologists and evolutionary biologists and likely they will suggest possible future biotechnological applications, including the development of crops with higher survival rates and yield under adverse environmental situations.

Phenotypic Plasticity and Ecology

Phenotypic plasticity also has important implications for ecology, which, in turn, have additional evolutionary consequences. Recall from above that an organism’s phenotype is shaped by its ecology. Yet, the reciprocal is also true: an organism’s ecological interactions – and thus the selective regimes that it experiences – can be influenced by its developmental responses.

For instance, the individuals of many species respond adaptively to interspecific competition by facultatively modifying their resource-use traits through phenotypic plasticity (Pfennig and Pfennig, 2012). Species that can alter their phenotype in this way may persist in the face of novel competitive interactions because they can immediately (i.e., within a single generation) switch to a selectively favored phenotype. In the absence of such plasticity, species may be driven locally extinct through competitive exclusion (Pfennig and Pfennig, 2012). Thus, environmentally responsive development can reduce extinction risk, thereby influencing the composition of ecological communities (similar arguments can be made regarding the ability to respond rapidly to any sort of change in an organism’s biotic or abiotic environment). Of course, populations that do not go extinct should ultimately be more likely to diversify. This may explain, at least in part, why clades in which conspicuous phenotypic plasticity (e.g., Figure 1(c)) has evolved are more species rich than sister clades lacking such plasticity (Pfennig and McGee, 2010).

An Adaptive Strategy in Heterogeneous Environments

Phenotypic plasticity refers to the observation that a given genotype expresses different phenotypes in different ecological settings. At its most basic level, the concept applies to any differences in trait means between environments. For example, plants may show stunted growth in habitats other than the one to which they are adapted. However, when trait expression in different habitats has been shaped by natural selection, phenotypic plasticity represents an ecological strategy that adapts organisms to heterogeneous environments and forms an integral part of species interactions (Agrawal, 2000). Such adaptive plasticity can range from repeated ontogenetic adjustments in behavior, physiology, or life history to the expression of distinct, irreversible morphologies (polyphenism) such as fully winged and flightless forms in insects (Harrison, 1980; Roff, 1986), the shade avoidance growth form of plants (Schmitt et al., 2003) carnivorous and omnivorous tadpole morphs of spadefood toads (Pfennig et al., 2007) inducible defensive morphs of Daphnia water fleas (Tollrian and Dodson, 1999) and the seasonally alternating morphs of Bicyclus anynana butterflies (Lyytinen et al., 2004).

Abstract

Phenotypic plasticity is the ability of a species to adopt different forms depending on the environment. One of the most extreme forms of phenotypic plasticity known are the female castes of social insects. Despite have the same genome, the size, shape, and behavior of queens and workers are often radically different. The mechanisms underlying caste differentiation are incompletely understood, but in the honey bee the diet is central to whether a larva will develop as a queen or a worker. A queen-destined larva is fed a super-abundance of ‘royal jelly’ a glandular secretion of the nurse workers. A worker-destined larva is fed ‘worker jelly’ progressively, and the food contains less sugar than royal jelly. A key component of royal jelly is ‘royalactin’ an unstable protein that may be involved in caste differentiation. However whether it’s the amount or contents of the worker and royal jelly that cause the phenotypic change is unclear. Our best guess is that its both. DNA methylation plays a key role in cast differentiation, because knockdown of the DNA methylation system causes most larva to develop as queens. However the link between diet and DNA methylation is incompletely understood.

b Phenotypic Plasticity

Phenotypic plasticity is a phenomenon in which a given genotype may develop different states of a character or group of characters in different environments (King et al. 2006). This can include all types of environment-induced changes. Even though phenotype plasticity is expressed in all organisms, it is more widely expressed in plants. This is ascribed to the sedentism of plants (animals can move away from an adverse environment) and their presence in an open ontogeny in which functionally equivalent organs are produced sequentially through the growing season (e.g., variations observed in the size, shape and frequency of appearance of leaves depending on the environment, especially the availability of nutrients and moisture, population density, etc.) (Bradshaw 1965, Niklas 1997).

Character variation within an individual species is typically more determined by environmental factors than by genotype differences. The ability of a species to adaptively alter morphological and physiological functional traits to environmental variations is well expressed (Niklas 1997, Agrawal 2001). This attribute can then easily explain the tremendous variations in morphological and physiological characters that we notice, both in wild and cultivated rices, including in their life history traits. However, this phenomenon does not appear to have been studied in rice.

Eiguchi et al. (1993) observed that the phenomenon of rapid elongation of internodes that takes place in deep water rice varieties, when the flood waters may rise by a meter or more in 24 hr, is an instance of this phenomenon. They used a perennial O. rufipogon strain possessing deep water tolerance together with a non-deep water cultivated rice variety. The authors determined that the tolerance for deep water was controlled by a recessive gene with major effects, dw3.

Shimizu et al. (2010) investigated the extent of genetic control of phenotypic plasticity in a cultivated rice (a japonica landrace) and a wild rice (an annual O. rufipogon) by studying their responses to five environmental conditions consisting of nutrient and plant population changes. They detected QTL clusters producing large effects on the studied characters on chromosome 7. They felt that these QTLs might have contributed to bringing about changes to the plant’s architecture during domestication. They proposed that allele-specific environmental specificity could be controlling plasticity; further that both cultivated and wild rices showed distinct genetic differences for phenotypic plasticity, and these must have contributed to adaptation under contrasting environmental heterogeneity during domestication.

Zhang et al. (2012) indentified a gene rice plasticity 1 (RPL1), that is responsible for causing environment-dependent plant height variations. A BLAST analysis showed that the gene was located in a putative gene (LOC–Os 06g 13640) on chromosome 6 (BLAST: Basic Local Alignment Search Tool, finds regions of local similarity between sequences).

The few studies that have been carried out on phenotypic plasticity in rices have been one-off studies using only limited experimental conditions. Other than confirming the prevalence of phenotypic plasticity, these studies do not appear to have contributed to estimating the extent, direction, and manner of its effect on the domestication process in rice.

Abstract

Phenotypic plasticity is the ability of organisms with a given genotype to develop varied phenotypes under fluctuating environmental conditions. This chapter provides an overview of the conditions under which adaptive phenotypic plasticity is expected to evolve, and the challenge of conducting rigorous tests of hypotheses for such plasticity. It is argued that advances in the field may be facilitated by focusing on species in which some of the complexity of plastic responses is naturally simplified. Here, the focus is on assessing adaptive plasticity of male spiders in response to spatio-temporal heterogeneity in demographic variables that cause changes in the mode and intensity of sexual selection. For web-building spiders in the genera Argiope, Nephila, and Latrodectus, males rarely mate more than once due to sexual cannibalism, male genital mutilation, and arduous, risky mate searching, simplifying predictions about adaptive phenotypes. Population density, the proximity of mates and competitors, and the operational sex ratio may all be linked to variation in the importance of traits that confer advantages in the different episodes of selection that determine male fitness. These links are reviewed in the context of the biology of representative species in each genus. Experimental studies of adaptive plasticity demonstrate that there are robust associations between pheromone-mediated assessment of social context and male development and behavior. The utility of continued study of these spiders with an eye to comparative studies is emphasized.

4 Phenotypic Plasticity

Phenotypic plasticity refers to the potential for the modification of survival- and reproduction-related phenotypes in response to social and ecological (e.g., food) conditions, but within genetically based constraints (Roff, 1992). The potential to modify the expression of life history traits presumably evolved as an adaptation to variability across seasons and generations in the ecologies in which the species evolved. Phenotypic plasticity enables a more optimal expression of life history traits as these relate to survival and reproductive demands in the local ecology. The mechanisms associated with plasticity include hormonal and/or other endocrine responses as well as ecological conditions (e.g., water availability) that affect the physical and behavioral condition of the individual (McNamara & Houston, 1996; Sinervo & Svensson, 1998). Phenotypic plasticity has been empirically demonstrated in a wide range of plant species (Fenner, 1998; Sultan, 2000) as well as in a diversity of other species ranging from plankton to primates (Alberts & Altmann, 1995; McLaren, 1966; McNamara & Houston, 1996; Miaud, Guyétant, Elmberg, 1999; Roff, 1992). In all of these species, phenotypic plasticity is expressed within the constraints of norms of reaction (Stearns & Koella, 1986). Norms of reaction represent a genotype whose phenotypic expression varies with ecological conditions, but only within a genetically constrained range.

Consider field voles as one example (Microtus agrestis; Ergon, Lambin, & Stenseth, 2001). In this species, populations residing in different locales vary significantly in two life history traits, adult body mass and timing of yearly reproduction. On one hand, if the population differences reflect genetic variance then individuals transplanted from one population to the other will show the body mass and reproductive timing of their natal group. On the other hand, if the population differences reflect variation in local ecologies, such as quality and availability of food, then, in the season following transplantation, body mass and reproductive timing of transplanted individuals should be the same as that of the local community. In fact, the life history traits of transplanted individuals were indistinguishable from those of the local community and differed significantly from those of their natal community. Regardless of natal community, individuals living in richer ecologies developed a higher wintering body size and as a result were able to reproduce earlier. Individuals living in poorer ecologies needed to devote added time to foraging and growth—somatic effort—and thus experienced a delay in the onset of reproduction—reproductive effort.

Phenotypic plasticity in growth and reproductive timing has also been demonstrated for many other species, including humans (Steams & Koella, 1986), as well as for many other life history traits (Roff, 1992). For some species, cross-generational plasticity has been demonstrated, whereby the ecological conditions experienced by the mother influence life history trade-offs in offspring (Hofer, 1987). For example, offspring of nutrient-deprived plants allocate more growth-related resources to root production, whereas offspring of light-deprived plants allocate more resources to leaf production (Sultan, 2000; see also Alekseev and Lampert, 2001, for an analogous mechanism in the crustacean Daphnia). In mammals, maternal condition during pregnancy and during offspring suckling can have long-term reproductive consequences. Healthy mothers give birth to heavier offspring and they provide more milk, both of which promote early growth and this, in turn, is associated with larger adult size and higher breeding success (Clutton-Brock, 1991). As an example involving social dynamics, testicular maturation and achievement of social dominance are accelerated in male baboons (Papio cynocephalus) borne to high-ranking females, thereby enhancing the males’ reproductive prospects (Alberts & Altmann, 1995).

YET ANOTHER DIMENSION TO THE PROBLEM: THE INTERACTION OF DEVELOPMENT AND PLASTICITY

Phenotypic plasticity is not just an environmental phenomenon. It is the result of complex genotype-environment interactions. However, these interactions do not occur at one point in time. Rather, phenotypic plasticity is a developmental process, and the reaction norms that we usually measure in the adult stage, or at reproductive maturity, are in fact the result of a positive feedback between environments and genes throughout the ontogeny of an organism (Schmalhausen, 1949; Smith-Gill, 1983; Pigliucci et al., 1996; Schlichting and Pigliucci, 1998).

The literature on developmental plasticity is assuming an increasingly important role in shaping our thinking about plasticity in particular and development in general. Clear empirical examples of how ontogenetic trajectories are shaped by the interaction between development, genotype, and environment have been published especially, but not uniquely, in plant biology (Dong and Pierdominici, 1995; Martin-Mora and James, 1995; Pigliucci and Schlichting, 1995; Brakefield et al., 1996; Bruni et al, 1996; Gedroc et al., 1996; Pigliucci et al., 1997).

The emerging picture from all these studies is that adult characters are shaped gradually by the way genetic instructions are expressed in an ever-changing environmental milieu. This is far from being a vague statement. We can now track the differential expression of genes at different times during ontogeny, in different tissues, and in response to distinct environmental conditions (Parsons and Mattoo, 1991; Nelson and Langdale, 1992; Wei and Deng, 1992; Estevez et al., 1993; Neyfakh and Hartl, 1993; Crews et al., 1994; Prandl et al., 1995). This promises to open the way to the construction of a long-awaited bridge between organismal and molecular biology, with epigenetics providing the link between the two.

There is another sense in which plasticity is relevant to the formation of characters through development. Schlichting and Pigliucci (1998) have argued that the internal conditions of an organism are somewhat analogous to the external environment. To be more precise, one can see the epigenetic processes occurring throughout development as an interaction of genes with two kinds of environments: the classical external environment comprising biotic and abiotic factors, and the internal environment, including diffusing chemicals, cell-cell interactions, and so on. While this perspective may be pushing the concept of “environment” too far for some people, it is still useful to think about how genetic instructions give origin to epigenetic processes. Considering internal and external environments as comparable interactors with the genes may shed some light onto the evolution of epigenetic systems themselves.

This suggestion of treating internal and external environments as analogous entities raises the question of what exactly we consider an “environment” and how do we measure it. This is one of the most important and deceptively simple questions related to the problem of how phenotypic plasticity changes our way of looking at characters.

The Epigenetic Control of Migration in Rainbow Trout

Phenotypic plasticity describes the process that allows individuals to alter their phenotype in response to environmental change alter their phenotype due to new environments. Altering the regulation of gene expression is one mechanism that allows organisms to change the amount of mRNA produced in direct response to environmental variance. This change in gene expression allows for phenotypic plasticity, as changes in mRNA expression have a direct link to protein abundance. This ability to respond to environmental stimuli necessitates a molecular mechanism that permits RNA polymerase to change the amount of mRNA produced in the targets gene or genes. There are many different molecular mechanisms that can induce changes in gene expression, including histone modification, changes in DNA methylation, and changes in the production of noncoding RNAs. All of these changes can be grouped together as epigenetic modification, i.e., modifications that are passed on through successive generations but do not involve changes in the DNA sequence. Until recently, relatively little information was available regarding the effects of modifications on the epigenome and their potential influence on the development of different life history tactics. Baerwald et al. (2016) have investigated patterns of DNA methylation in both resident and migrant Rainbow Trout finding 57 regions of the genome with altered methylation patterns (so called differential methylated regions: DMRs) between the two phenotypes. The presence of these regions suggests that epigenetic changes in rainbow trout are associated with the development of different migratory phenotypes (Fig. 5).

However, it is important to note that not all individuals showed methylation patterns that were consistent with their migratory status. Three samples deviated from expected; two residents had methylation patterns characteristic of smolts, and one smolt possessed methylation patterns characteristics of residents. This suggests that there is epigenetic plasticity in the development of the migratory phenotype, which is not surprising given how variable patterns of gene expression are between migrants and residents (McKinney et al., 2015; Hale et al., 2016). More than 50% of the differentially methylated regions identified by Baerwald et al. were found within or next to CpG islands. CpG islands are regions of the genome rich in cytosine and guanine bases, are often found in or adjacent to promoter regions in the 5 prime untranslated region (UTR). These regions are extremely important in RNA polymerase binding and transcription initiation. Hypermethylation of cytosines in CpG islands is often associated with a decrease in the expression of downstream genes, as adding methyl groups to cytosine restricts access of the promoter region to RNA polymerase thereby decreasing transcription. Alternatively, hypomethylation of cytosine in CpG islands is more commonly associated with increased expression of down stream genes, as fewer cytosines are methylated. Baerwald et al. (2016) found evidence for hypermethylation of several genes in resident fish, including two genes connected to circadian rhythm signaling: aryl hydrocarbon receptor 2 alpha (AHR2A) and RAS1. Circadian rhythm pathways help organisms anticipate and prepare for changes in photoperiod, both with respect to daily changes in the light-dark cycle and to annual changes in photoperiod. Previous research has suggested that several circadian rhythm genes are connected to the smoltification process, including CLOCK, BMAL, and several Cryptochromes (McKinney et al., 2015). Several of these genes are more expressed in the brains of migrants than they are in residents; Baerwald et al. found evidence for increased methylation in the promoter regions of AHR2A and RAS1 in residents compared to migrants, providing a mechanism for increased circadian rhythm gene expression in migrants. The expression of circadian rhythm genes is important in the timing of outmigration, as many studies in salmonids have found that the window of time for leaving natal areas is narrow. As Baerwald et al. (2016) studied out migrating individuals, it is possible that these methylation changes provide a mechanism that allow migrants to be more sensitive to the time of year than residents.