**6.1 Physiological plasticity**

*Plant Communities and Their Environment*

**5. Genetic regulation of plasticity**

and higher plant abundance in unfavorable environments [63]. Associations have not been observed with flowering phenology among native and non-native plant populations, but this may be because flowering time is dependent on the environment [62–64]. Flower development and invasiveness in Purple loosestrife (*Lythrum salicaria*) demonstrate that both anther and stigma respond to changes in soil moisture during either of vegetative and reproductive development [65]. Tufted knotweed (*Polygonum cespitosum*) has been enhanced through adaptive responses to drought and high temperature without any observable decrease in fitness when grown in the shade [66]. Narrow-leaf plantain (Plantago lanceolata) is very sensitive to changes in light quality and modulates seed germination and leaf size as a mechanism for shade avoidance [67]. It is also the case in this weed species that leaf size and germination patterns share common physiological mechanisms where the short leaf phenotype is more plastic than the long leaf phenotype in shady conditions [20]. This discovery illustrates that wild plasticity is a dynamic network of processes that work synergistically to enhance the likelihood of survival [20]. Both trees and weeds demonstrate how, through the process of natural selection, non-cultivated plants have adopted very different and dynamic strate-

gies that ensure reproduction and survival [1, 4, 12, 16–21, 24].

There is not enough data about the genes, promoters, and regulatory elements that control "invasive" or "weedy" phenotypes commonly observed in wild plant populations. However, the phenotypes provide key insights into potential gene families and signaling pathways. Adaptive phenotypes also provide evidence that plasticity responses are controlled genetically and by specific plasticity genes [6]. The accumulation of genetic modifications associated with adaptive responses can be tracked through time and are genetically controlled [6]. Two models have been proposed to explore how changes in adaptive response occur. The first model proposes that the expression of structural genes varies as the environment changes [68]. Genetic plasticity is not regulated by plasticity genes, rather by changes in gene expression of structural genes resulting in phenotypic changes or plasticity [68]. The second model proposes that specific regulatory genes, i.e., plasticity genes mediate responses for structural genes [69, 70]. The resulting change in expression of the regulatory genes in response to environmental changes is what ultimately controls the pattern of

There are four primary mechanisms in wild plant populations that regulate plasticity through adaptive responses [6]. The four plasticity mechanisms are physiological, developmental, cellular, and epigenetic responses [6]. Physiological plasticity describes all physiological responses associated with phenotypic traits and signaling networks [40, 71]. Developmental plasticity is associated with human or animal neural developmental, and plant embryonic development, in response to stress [6, 40]. Cellular plasticity describes adaptive responses within cells that are often associated with reducing reactive oxygen species accumulation through redox mechanisms [72]. Epigenetic plasticity describes changes to molecular mechanisms in response to abiotic stresses resulting in altered gene expression and function

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plasticity [69, 70].

**6. Plasticity mechanisms**

without changes in the DNA [71].

Physiological plasticity is the most dynamic of plasticity mechanisms and is often involved in all other mechanisms of plasticity [40, 71]. Novel and emerging environments trigger many physiological responses such as carbon dioxide (CO2) assimilation, changes in chlorophyll content, water use efficiency, sugar sensing and photosynthesis [73]. Physiological changes correlate directly to plant fitness, and changes in plasticity determine how a plant responds to environmental stresses [73, 74]. Studying the association between a physiological phenotype and changes in gene expression within wild populations will make it is possible to identify and target genes that are responsible for adaptive responses, i.e., plasticity genes [24, 73, 74]. In this way plasticity genes and gene variants become a selective tool for understanding plasticity heritability dynamics, as well as identifying positively adapted populations [24, 73–75].

Seed dormancy is an excellent example of physiological plasticity [73, 74] Seed dormancy prevents germination out of season, even under favorable conditions, and ensures species survival of natural catastrophes [16, 76]. Environmental cues such as light, temperature, and moisture impact the depth of seed dormancy and the length of time required for dormancy release [76]. In weeds, discontinuous or extensive seed dormancy ensures germination only in favorable conditions and confers environmental plasticity, or the ability to respond to changing biotic or abiotic environmental factors [16].

Discontinuous or extensive seed dormancy impacts environmental plasticity through variable emergence timing throughout a growing season [76]. Discontinuous seed dormancy is likely a major "weedy" characteristic contributing to physiological plasticity in many wild plants and weed populations [76]. Downy brome (*Bromus tectorum L.*) is an invasive grass weed in both natural and agricultural environments which produces seeds with discontinuous seed dormancy [77–80]. New downy brome seedlings have the capacity to emerge in any season; early and late in the fall, before and after cool season crops or native grasses emerge, and even in the spring [80]. Differences in emergence timing in downy brome may be due to differences in dormancy status and may occur because of phenotypic and genotypic variation within a single population cluster, the presence of multiple population clusters within a single location, and the viability of seed in the seed bank [80]. The successful invasion of wild plant populations is measured by the number of individuals in a population, reproductive output, the range of habitats occupied, and the ability for survival and adapt in new environments through time [16]. Therefore, downy brome is an excellent example of a model colonizing species as it allocates most of the developmental time to seed production [16]. Downy brome increases the chances for survival of future generations, by maximizing contributions to seed banks [76]. Physiological plasticity mechanisms like prolific seed production, discontinuous seed dormancy, and variable germination in weeds increase the likelihood of outcompeting wild and cultivated plant species in native and non-native environments [76].

There is currently very little information about the specific genes or molecular mechanisms regulating dormancy or dormancy loss in many weeds or wild plant species [77]. Gaps in molecular information slow the progress for understanding the impact of wild plasticity on adaptability [1, 16]. However, detailed physiological observations and translational research are useful tools. These are powerful tools for studying the mechanisms that drive physiological plasticity in the seed and throughout all plant life stages, in natural and agricultural environments, and in both wild and cultivated plant populations [1, 16, 82–86].

Basic research has established that a seed's transition from dormancy to germination is controlled by the plant hormones, abscisic acid (ABA) and gibberellin (GA) [81, 82]. ABA establishes seed dormancy during embryo maturation and maintains dormancy in mature seeds, whereas GA stimulates seed germination [34, 36]. Dormancy studies in model systems including *Arabidopsis thaliana*, *Brachypodium distachyon*, *Hordeum vulgare*, and *Triticum aestivum* draw a clear connection between ABA, GA signaling mechanisms, seed dormancy and dormancy loss [81–84]. These studies also provide a framework for comparing the similarities, differences of mechanisms regulating physiological plasticity, and the degree of conservation within wild plant populations [50, 76, 83–100]. Carefully documenting development from seedling to seed in wild plant populations including weeds, provides a wealth of information about phenotypic plasticity in varied environments, and demonstrates the value in using wild species as models for understanding the full capacity of phenotypic plasticity in nature [85].

### **6.2 Developmental plasticity**

Developmental plasticity was first identified in, and is most often associated with, human and animal development [40]. Developmental plasticity refers to the impact of environmental stimuli on embryonic development [6]. Within the plant biology community, there remains some skepticism surrounding the existence of plant developmental plasticity mechanisms, and how to best identify and characterize them [5–7]. Despite these challenges, recent paradigm shifts in conventional thought have resulted in significant efforts toward studying the impact of developmental plasticity in cultivated plant species [5–7, 40, 72].

Developmental plasticity directly impacts phenotypic plasticity and is characterized using GXE experiments that investigate the interactions of genotype in a given environment [7, 101–104]. Developmental plasticity occurs commonly within plant populations when a given population inhabits moderate environments [2, 18]. Abiotic stresses, like drought, trigger physiological and developmental plasticity in plants [7]. The degree of developmental plasticity observed in plants resulting from abiotic stress is directly connected to a plant's development phase [7]. Some phases of development are more responsive to environmental changes and display a more plastic response than others [7]. It was found in spring wheat that the early developmental stages tillering and heading (after spike formation) show more morphological and physiological plasticity than other developmental phases [7]. Cold tolerance in quinoa is also based on developmental plasticity, and associated with grain formation [105, 106]. Flowering time is another trait associated with developmental plasticity across plant species [6]. A shift in flowering time in response to drought allows for accelerated seed set, thus ensuring species survival, even in non-ideal growing conditions [6].

### **6.3 Cellular plasticity**

Plant cellular plasticity allows cells to respond to the negative impacts of biotic and abiotic stresses. Cellular plasticity occurs through long-range signaling via hydraulic, electrical, and chemical signaling mechanisms [107]. One example of chemical signaling directly connected with plant cellular plasticity occurs when plants experience oxidative stress. Environmental stresses stimulate the production of toxic chemicals known as reactive oxygen species (ROS) [108]. The function of scavenging enzymes is to quench the flux of ROS [108–114]. When ROS levels are elevated due to environmental stress, the activity of scavenging enzymes, including ascorbate peroxidase, superoxide dismutase (SOD), and catalase (CAT) increases [108–114].

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*Phenological Plasticity of Wild and Cultivated Plants DOI: http://dx.doi.org/10.5772/intechopen.85070*

ROS homeostasis [123, 124].

and changing climates [74, 75].

**6.4 Epigenetic plasticity**

Cellular plasticity is a very dynamic process whereby ROS scavengers are acting simultaneously in different cellular compartments including the cell wall membrane, cytoplasm, chloroplast, mitochondria, peroxisomes, and the apoplast [115–117]. The peroxisomes are the most important indicators of environmental stress, ROSscavenger activity, and cellular plasticity [115]. Peroxisomes proliferate in response to an array of environmental stresses including light, ozone, metal, and salt [119]. Peroxisome number may fluctuate depending on cultivar or genotype [118–122]. An emerging hypothesis about cellular plasticity is that relative peroxisome abundance may be a good predictor for cellular plasticity mechanisms [123, 124]. Peroxisomal proliferation occurs because of environmental stress, and, any change in a phenological trait occurring from a change in environment is defined as cellular plasticity [123, 124]. Investigations of peroxisome proliferation in response to drought tolerance demonstrate that peroxisome abundance is correlated with abiotic stress response and impacts GXE interactions [123, 124]. A negative correlation also exists between peroxisome abundance and several phenological traits including plant biomass, root dry weight, and grain yield [123, 124]. Therefore, peroxisome abundance is an emerging tool for measuring cellular plasticity mechanisms of adaptation, and

Plasticity responses exist as both the inherent genetic machinery (past regulatory events), and as part of regulation occurring outside of the genetic code (epigenetically) [71]. Epigenetic mechanisms include DNA methylation, non-coding RNA, chromatin remodeling, and histone modifications [71]. Changes in the environment trigger heritable changes in gene expression which result in stable phenotypes [71]. DNA methylation is the most common, and perhaps best understood mechanisms controlling epigenetic plasticity in plants [71]. Studies using Arabidopsis epigenetic recombinant inbred lines (epiRILS), i.e., lines with nearly identical genomes but contrasting DNA methylation patterns, demonstrated that plasticity to water availability and nutrient loss is controlled through changes in DNA methylation [80]. Epigenetic changes rather than genetic changes contribute to changes impacting phenotypic plasticity [71]. Other research has demonstrated that epigenetic regulation impacts heritability in specific phenological traits like plant height, plant biomass, seed/fruit production, the root-to-shoot ratio, and flowering time [71, 125–127]. Heritable traits are very important in breeding programs, and the role of epigenetics in regulating these traits is now only being characterized and understood [128].

**7. The path to domestication: learning from transitional models**

Decreased genetic diversity in plants populations is often associated with increased cultivation [7, 129]. Less cultivated plant populations tend to have more genetic diversity or "wildness" than plants that have been domesticated [129]. Wild characteristics broaden genetic responses and are valuable for maintaining phenotypic plasticity [129–131]. Leveraging broad genetic responses to enhance plasticity is especially important for the survival of plant species in unpredictable

Since the dawn of agriculture, farmers have used selective breeding techniques for cultivating and domesticating wild plants for food [132]. Seeds from wild plant populations are smaller, an adaptation thought to enhance dispersal [132]. From an agricultural perspective, increased domestication is useful for reliable germination, uniform emergence, uniform stand establishment, larger seed size, increased yield,

*Phenological Plasticity of Wild and Cultivated Plants DOI: http://dx.doi.org/10.5772/intechopen.85070*

*Plant Communities and Their Environment*

**6.2 Developmental plasticity**

Basic research has established that a seed's transition from dormancy to germination is controlled by the plant hormones, abscisic acid (ABA) and gibberellin (GA) [81, 82]. ABA establishes seed dormancy during embryo maturation and maintains dormancy in mature seeds, whereas GA stimulates seed germination [34, 36]. Dormancy studies in model systems including *Arabidopsis thaliana*, *Brachypodium distachyon*, *Hordeum vulgare*, and *Triticum aestivum* draw a clear connection between ABA, GA signaling mechanisms, seed dormancy and dormancy loss [81–84]. These studies also provide a framework for comparing the similarities, differences of mechanisms regulating physiological plasticity, and the degree of conservation within wild plant populations [50, 76, 83–100]. Carefully documenting development from seedling to seed in wild plant populations including weeds, provides a wealth of information about phenotypic plasticity in varied environments, and demonstrates the value in using wild species as models for understand-

Developmental plasticity was first identified in, and is most often associated with, human and animal development [40]. Developmental plasticity refers to the impact of environmental stimuli on embryonic development [6]. Within the plant biology community, there remains some skepticism surrounding the existence of plant developmental plasticity mechanisms, and how to best identify and characterize them [5–7]. Despite these challenges, recent paradigm shifts in conventional thought have resulted in significant efforts toward studying the impact of develop-

Developmental plasticity directly impacts phenotypic plasticity and is characterized using GXE experiments that investigate the interactions of genotype in a given environment [7, 101–104]. Developmental plasticity occurs commonly within plant populations when a given population inhabits moderate environments [2, 18]. Abiotic stresses, like drought, trigger physiological and developmental plasticity in plants [7]. The degree of developmental plasticity observed in plants resulting from abiotic stress is directly connected to a plant's development phase [7]. Some phases of development are more responsive to environmental changes and display a more plastic response than others [7]. It was found in spring wheat that the early developmental stages tillering and heading (after spike formation) show more morphological and physiological plasticity than other developmental phases [7]. Cold tolerance in quinoa is also based on developmental plasticity, and associated with grain formation [105, 106]. Flowering time is another trait associated with developmental plasticity across plant species [6]. A shift in flowering time in response to drought allows for accelerated seed set, thus ensuring species survival, even in non-ideal growing conditions [6].

Plant cellular plasticity allows cells to respond to the negative impacts of biotic and abiotic stresses. Cellular plasticity occurs through long-range signaling via hydraulic, electrical, and chemical signaling mechanisms [107]. One example of chemical signaling directly connected with plant cellular plasticity occurs when plants experience oxidative stress. Environmental stresses stimulate the production of toxic chemicals known as reactive oxygen species (ROS) [108]. The function of scavenging enzymes is to quench the flux of ROS [108–114]. When ROS levels are elevated due to environmental stress, the activity of scavenging enzymes, including ascorbate peroxidase, superoxide dismutase (SOD), and catalase (CAT) increases

ing the full capacity of phenotypic plasticity in nature [85].

mental plasticity in cultivated plant species [5–7, 40, 72].

**46**

[108–114].

**6.3 Cellular plasticity**

Cellular plasticity is a very dynamic process whereby ROS scavengers are acting simultaneously in different cellular compartments including the cell wall membrane, cytoplasm, chloroplast, mitochondria, peroxisomes, and the apoplast [115–117]. The peroxisomes are the most important indicators of environmental stress, ROSscavenger activity, and cellular plasticity [115]. Peroxisomes proliferate in response to an array of environmental stresses including light, ozone, metal, and salt [119]. Peroxisome number may fluctuate depending on cultivar or genotype [118–122]. An emerging hypothesis about cellular plasticity is that relative peroxisome abundance may be a good predictor for cellular plasticity mechanisms [123, 124]. Peroxisomal proliferation occurs because of environmental stress, and, any change in a phenological trait occurring from a change in environment is defined as cellular plasticity [123, 124]. Investigations of peroxisome proliferation in response to drought tolerance demonstrate that peroxisome abundance is correlated with abiotic stress response and impacts GXE interactions [123, 124]. A negative correlation also exists between peroxisome abundance and several phenological traits including plant biomass, root dry weight, and grain yield [123, 124]. Therefore, peroxisome abundance is an emerging tool for measuring cellular plasticity mechanisms of adaptation, and ROS homeostasis [123, 124].

### **6.4 Epigenetic plasticity**

Plasticity responses exist as both the inherent genetic machinery (past regulatory events), and as part of regulation occurring outside of the genetic code (epigenetically) [71]. Epigenetic mechanisms include DNA methylation, non-coding RNA, chromatin remodeling, and histone modifications [71]. Changes in the environment trigger heritable changes in gene expression which result in stable phenotypes [71]. DNA methylation is the most common, and perhaps best understood mechanisms controlling epigenetic plasticity in plants [71]. Studies using Arabidopsis epigenetic recombinant inbred lines (epiRILS), i.e., lines with nearly identical genomes but contrasting DNA methylation patterns, demonstrated that plasticity to water availability and nutrient loss is controlled through changes in DNA methylation [80]. Epigenetic changes rather than genetic changes contribute to changes impacting phenotypic plasticity [71]. Other research has demonstrated that epigenetic regulation impacts heritability in specific phenological traits like plant height, plant biomass, seed/fruit production, the root-to-shoot ratio, and flowering time [71, 125–127]. Heritable traits are very important in breeding programs, and the role of epigenetics in regulating these traits is now only being characterized and understood [128].
