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Journal articles on the topic 'Phenotypic plasticity'
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1
Nicotra, Adrienne B., and Amy Davidson. "Adaptive phenotypic plasticity and plant water use." Functional Plant Biology 37, no. 2 (2010): 117. http://dx.doi.org/10.1071/fp09139.
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The emergence of new techniques in plant science, including molecular and phenomic tools, presents a novel opportunity to re-evaluate the way we examine the phenotype. Our increasing capacity for phenotyping means that not only can we consider increasing numbers of species or varieties, but also that we can effectively quantify the phenotypes of these different genotypes under a range of environmental conditions. The phenotypic plasticity of a given genotype, or the range of phenotypes, that can be expressed dependent upon environment becomes something we can feasibly assess. Of particular importance is phenotypic variation that increases fitness or survival – adaptive phenotypic plasticity. Here, we examine the case of adaptive phenotypic plasticity in plant water use traits and consider how taking an ecological and evolutionary perspective on plasticity in these traits might have relevance for agriculture, horticulture and the management of native and invasive plant species in an era of rapid climate change.
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Bibi, Zubaira, Muhammad Junaid Maqsood, Ayesha Idrees, Hafisa Rafique, Aliza Amjad Butt, Rameesha Ali, Zunaira Arif, and Mutie Un Nabi. "Exploring the Role of Phenotypic Plasticity in Plant Adaptation to Changing Climate: A Review." Asian Journal of Research in Crop Science 9, no. 1 (January 2, 2024): 1–9. http://dx.doi.org/10.9734/ajrcs/2024/v9i1241.
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Global ecosystems are threatened by climate change, thus understanding plant response is vital. Phenotypic plasticity allows genotypes to produce different phenotypes in response to different environmental conditions, helping plants adapt to changing climates. The reviewsynthesizes molecular, physiological, and morphological data on plant phenotypic plasticity as a dynamic and responsive survival strategy in unpredictable environments. Review analyses how phenotypic plasticity influences plant resilience and persistence under climate change using empirical data from diverse plant species and settings. The study also analyses how phenotypic plasticity influences plant community dynamics, biodiversity, and ecosystem functioning. Phenotypic plasticity's potential to attenuate climate change and facilitate range alterations is also explored, showing its importance in plant ranges. Study reviewsgenetic, genomic, ecological, and climatological research on plant phenotypic plasticity in climate adaptation. Findings stressplant species' resilience in reducing climate change's impact on global ecosystems and influencing conservation and management.
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Nishiura, Naoto, and Kunihiko Kaneko. "Evolution of phenotypic fluctuation under host-parasite interactions." PLOS Computational Biology 17, no. 11 (November 9, 2021): e1008694. http://dx.doi.org/10.1371/journal.pcbi.1008694.
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Robustness and plasticity are essential features that allow biological systems to cope with complex and variable environments. In a constant environment, robustness, i.e., insensitivity of phenotypes, is expected to increase, whereas plasticity, i.e., the changeability of phenotypes, tends to diminish. Under a variable environment, existence of plasticity will be relevant. The robustness and plasticity, on the other hand, are related to phenotypic variances. As phenotypic variances decrease with the increase in robustness to perturbations, they are expected to decrease through the evolution. However, in nature, phenotypic fluctuation is preserved to a certain degree. One possible cause for this is environmental variation, where one of the most important “environmental” factors will be inter-species interactions. As a first step toward investigating phenotypic fluctuation in response to an inter-species interaction, we present the study of a simple two-species system that comprises hosts and parasites. Hosts are expected to evolve to achieve a phenotype that optimizes fitness. Then, the robustness of the corresponding phenotype will be increased by reducing phenotypic fluctuations. Conversely, plasticity tends to evolve to avoid certain phenotypes that are attacked by parasites. By using a dynamic model of gene expression for the host, we investigate the evolution of the genotype-phenotype map and of phenotypic variances. If the host–parasite interaction is weak, the fittest phenotype of the host evolves to reduce phenotypic variances. In contrast, if there exists a sufficient degree of interaction, the phenotypic variances of hosts increase to escape parasite attacks. For the latter case, we found two strategies: if the noise in the stochastic gene expression is below a certain threshold, the phenotypic variance increases via genetic diversification, whereas above this threshold, it is increased mediated by noise-induced phenotypic fluctuation. We examine how the increase in the phenotypic variances caused by parasite interactions influences the growth rate of a single host, and observed a trade-off between the two. Our results help elucidate the roles played by noise and genetic mutations in the evolution of phenotypic fluctuation and robustness in response to host–parasite interactions.
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Karagic, Nidal, Axel Meyer, and C. Darrin Hulsey. "Phenotypic Plasticity in Vertebrate Dentitions." Integrative and Comparative Biology 60, no. 3 (June 16, 2020): 608–18. http://dx.doi.org/10.1093/icb/icaa077.
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Synopsis Vertebrates interact directly with food items through their dentition, and these interactions with trophic resources could often feedback to influence tooth structure. Although dentitions are often considered to be a fixed phenotype, there is the potential for environmentally induced phenotypic plasticity in teeth to extensively influence their diversity. Here, we review the literature concerning phenotypic plasticity of vertebrate teeth. Even though only a few taxonomically disparate studies have focused on phenotypic plasticity in teeth, there are a number of ways teeth can change their size, shape, or patterns of replacement as a response to the environment. Elucidating the underlying physiological, developmental, and genetic mechanisms that generate phenotypic plasticity can clarify its potential role in the evolution of dental phenotypes.
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Kishida, Osamu, Yuuki Mizuta, and Kinya Nishimura. "PHENOTYPIC PLASTICITY." Bulletin of the Ecological Society of America 87, no. 2 (April 2006): 106–7. http://dx.doi.org/10.1890/0012-9623(2006)87[106:pp]2.0.co;2.
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Phillips, K. "PHENOTYPIC PLASTICITY." Journal of Experimental Biology 209, no. 12 (June 15, 2006): i—iii. http://dx.doi.org/10.1242/jeb.02324.
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Callahan, Hilary S., Heather Maughan, and Ulrich K. Steiner. "Phenotypic Plasticity, Costs of Phenotypes, and Costs of Plasticity." Annals of the New York Academy of Sciences 1133, no. 1 (June 2008): 44–66. http://dx.doi.org/10.1196/annals.1438.008.
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Fusco, Giuseppe, and Alessandro Minelli. "Phenotypic plasticity in development and evolution: facts and concepts." Philosophical Transactions of the Royal Society B: Biological Sciences 365, no. 1540 (February 27, 2010): 547–56. http://dx.doi.org/10.1098/rstb.2009.0267.
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This theme issue pursues an exploration of the potential of taking into account the environmental sensitivity of development to explaining the evolution of metazoan life cycles, with special focus on complex life cycles and the role of developmental plasticity. The evolution of switches between alternative phenotypes as a response to different environmental cues and the evolution of the control of the temporal expression of alternative phenotypes within an organism's life cycle are here treated together as different dimensions of the complex relationships between genotype and phenotype, fostering the emergence of a more general and comprehensive picture of phenotypic evolution through a quite diverse sample of case studies. This introductory article reviews fundamental facts and concepts about phenotypic plasticity, adopting the most authoritative terminology in use in the current literature. The main topics are types and components of phenotypic variation, the evolution of organismal traits through plasticity, the origin and evolution of phenotypic plasticity and its adaptive value.
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Zhang, Luna, Anqun Chen, Yanjiao Li, Duohui Li, Shiping Cheng, Liping Cheng, and Yinzhan Liu. "Differences in Phenotypic Plasticity between Invasive and Native Plants Responding to Three Environmental Factors." Life 12, no. 12 (November 25, 2022): 1970. http://dx.doi.org/10.3390/life12121970.
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The phenotypic plasticity hypothesis suggests that exotic plants may have greater phenotypic plasticity than native plants. However, whether phenotypic changes vary according to different environmental factors has not been well studied. We conducted a multi-species greenhouse experiment to study the responses of six different phenotypic traits, namely height, leaf number, specific leaf area, total biomass, root mass fraction, and leaf mass fraction, of native and invasive species to nutrients, water, and light. Each treatment was divided into two levels: high and low. In the nutrient addition experiment, only the leaf mass fraction and root mass fraction of the plants supported the phenotypic plasticity hypothesis. Then, none of the six traits supported the phenotypic plasticity hypothesis in the water or light treatment experiments. The results show that, for different environmental factors and phenotypes, the phenotypic plasticity hypothesis of plant invasion is inconsistent. When using the phenotypic plasticity hypothesis to explain plant invasion, variations in environmental factors and phenotypes should be considered.
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Wang, Ye, Huigan Xie, Tiechui Yang, Dan Gao, and Xiwen Li. "Primary Investigation of Phenotypic Plasticity in Fritillaria cirrhosa Based on Metabolome and Transcriptome Analyses." Cells 11, no. 23 (November 30, 2022): 3844. http://dx.doi.org/10.3390/cells11233844.
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Phenotypic plasticity refers to the adaptability of an organism to a heterogeneous environment. In this study, the differential gene expression and compositional changes in Fritillaria cirrhosa during phenotypic plasticity were evaluated using transcriptomic and metabolomic analyses. The annotation profiles of 1696 differentially expressed genes from the transcriptome between abnormal and normal phenotypes revealed that the main annotation pathways were related to the biosynthesis of amino acids, ABC transporters, and plant–pathogen interactions. According to the metabolome, the abnormal phenotype had 36 upregulated amino acids, including tryptophan, proline, and valine, which had a 3.77-fold higher relative content than the normal phenotype. However, saccharides and vitamins were found to be deficient in the abnormal phenotypes. The combination profiles demonstrated that phenotypic plasticity may be an effective strategy for overcoming potential stress via the accumulation of amino acids and regulation of the corresponding genes and transcription factors. In conclusion, a pathogen attack on F. cirrhosa may promote the synthesis of numerous amino acids and transport them into the bulbs through ABC transporters, which may further result in phenotypic variation. Our results provide new insights into the potential mechanism of phenotypic changes.
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Ramisetty, Sravani, Ayalur Raghu Subbalakshmi, Siddhika Pareek, Tamara Mirzapoiazova, Dana Do, Dhivya Prabhakar, Evan Pisick, et al. "Leveraging Cancer Phenotypic Plasticity for Novel Treatment Strategies." Journal of Clinical Medicine 13, no. 11 (June 5, 2024): 3337. http://dx.doi.org/10.3390/jcm13113337.
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Cancer cells, like all other organisms, are adept at switching their phenotype to adjust to the changes in their environment. Thus, phenotypic plasticity is a quantitative trait that confers a fitness advantage to the cancer cell by altering its phenotype to suit environmental circumstances. Until recently, new traits, especially in cancer, were thought to arise due to genetic factors; however, it is now amply evident that such traits could also emerge non-genetically due to phenotypic plasticity. Furthermore, phenotypic plasticity of cancer cells contributes to phenotypic heterogeneity in the population, which is a major impediment in treating the disease. Finally, plasticity also impacts the group behavior of cancer cells, since competition and cooperation among multiple clonal groups within the population and the interactions they have with the tumor microenvironment also contribute to the evolution of drug resistance. Thus, understanding the mechanisms that cancer cells exploit to tailor their phenotypes at a systems level can aid the development of novel cancer therapeutics and treatment strategies. Here, we present our perspective on a team medicine-based approach to gain a deeper understanding of the phenomenon to develop new therapeutic strategies.
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Tétard-Jones, C., M. A. Kertesz, and R. F. Preziosi. "Quantitative trait loci mapping of phenotypic plasticity and genotype–environment interactions in plant and insect performance." Philosophical Transactions of the Royal Society B: Biological Sciences 366, no. 1569 (May 12, 2011): 1368–79. http://dx.doi.org/10.1098/rstb.2010.0356.
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Community genetic studies generally ignore the plasticity of the functional traits through which the effect is passed from individuals to the associated community. However, the ability of organisms to be phenotypically plastic allows them to rapidly adapt to changing environments and plasticity is commonly observed across all taxa. Owing to the fitness benefits of phenotypic plasticity, evolutionary biologists are interested in its genetic basis, which could explain how phenotypic plasticity is involved in the evolution of species interactions. Two current ideas exist: (i) phenotypic plasticity is caused by environmentally sensitive loci associated with a phenotype; (ii) phenotypic plasticity is caused by regulatory genes that simply influence the plasticity of a phenotype. Here, we designed a quantitative trait loci (QTL) mapping experiment to locate QTL on the barley genome associated with barley performance when the environment varies in the presence of aphids, and the composition of the rhizosphere. We simultaneously mapped aphid performance across variable rhizosphere environments. We mapped main effects, QTL × environment interaction (QTL×E), and phenotypic plasticity (measured as the difference in mean trait values) for barley and aphid performance onto the barley genome using an interval mapping procedure. We found that QTL associated with phenotypic plasticity were co-located with main effect QTL and QTL×E. We also located phenotypic plasticity QTL that were located separately from main effect QTL. These results support both of the current ideas of how phenotypic plasticity is genetically based and provide an initial insight into the functional genetic basis of how phenotypically plastic traits may still be important sources of community genetic effects.
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Gabriel, Wilfried. "Selective advantage of irreversible and reversible phenotypic plasticity." Archiv für Hydrobiologie 167, no. 1-4 (October 5, 2006): 1–20. http://dx.doi.org/10.1127/0003-9136/2006/0167-0001.
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Schneider, Hannah M., Stephanie P. Klein, Meredith T. Hanlon, Eric A. Nord, Shawn Kaeppler, Kathleen M. Brown, Andrew Warry, Rahul Bhosale, and Jonathan P. Lynch. "Genetic control of root architectural plasticity in maize." Journal of Experimental Botany 71, no. 10 (February 21, 2020): 3185–97. http://dx.doi.org/10.1093/jxb/eraa084.
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Abstract Root phenotypes regulate soil resource acquisition; however, their genetic control and phenotypic plasticity are poorly understood. We hypothesized that the responses of root architectural phenes to water deficit (stress plasticity) and different environments (environmental plasticity) are under genetic control and that these loci are distinct. Root architectural phenes were phenotyped in the field using a large maize association panel with and without water deficit stress for three seasons in Arizona and without water deficit stress for four seasons in South Africa. All root phenes were plastic and varied in their plastic response. We identified candidate genes associated with stress and environmental plasticity and candidate genes associated with phenes in well-watered conditions in South Africa and in well-watered and water-stress conditions in Arizona. Few candidate genes for plasticity overlapped with those for phenes expressed under each condition. Our results suggest that phenotypic plasticity is highly quantitative, and plasticity loci are distinct from loci that control phene expression in stress and non-stress, which poses a challenge for breeding programs. To make these loci more accessible to the wider research community, we developed a public online resource that will allow for further experimental validation towards understanding the genetic control underlying phenotypic plasticity.
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Brunet, Johanne, and Zachary Larson-Rabin. "The response of flowering time to global warming in a high-altitude plant: the impact of genetics and the environment." Botany 90, no. 4 (April 2012): 319–26. http://dx.doi.org/10.1139/b2012-001.
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In high-altitude habitats, an increase in temperature and greater precipitation in the form of rain represent climate changes typically associated with global warming. We determined whether phenotypic plasticity and genetic changes in the mean phenotype could affect the adaptation of flowering time to changes in the environment resulting from global warming in a montane plant species, Aquilegia coerulea James. We collected seeds from 17 plants from each of three natural populations. For each of these 51 families, we assigned 3–4 individuals to each of four water and temperature treatments. We observed phenotypic plasticity in flowering time in response to both temperature and water availability but no genetic variance or genetic differentiation in phenotypic plasticity. These results indicate that phenotypic plasticity could provide a quick response to environmental changes but provides little evolutionary potential. In contrast to phenotypic plasticity in flowering time, the mean flowering time did vary among families and among populations, suggesting a genetic basis to flowering time and adaptation in the different populations. The most likely scenario for the adaptation of this plant species to climate change is a rapid response via phenotypic plasticity followed by selection and micro-evolutionary changes in the mean phenotype.
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Lema, Sean C., and Jun Kitano. "Hormones and phenotypic plasticity: Implications for the evolution of integrated adaptive phenotypes." Current Zoology 59, no. 4 (August 1, 2013): 506–25. http://dx.doi.org/10.1093/czoolo/59.4.506.
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Abstract It is generally accepted that taxa exhibit genetic variation in phenotypic plasticity, but many questions remain unanswered about how divergent plastic responses evolve under dissimilar ecological conditions. Hormones are signaling molecules that act as proximate mediators of phenotype expression by regulating a variety of cellular, physiological, and behavioral responses. Hormones not only change cellular and physiological states but also influence gene expression directly or indirectly, thereby linking environmental conditions to phenotypic development. Studying how hormonal pathways respond to environmental variation and how those responses differ between individuals, populations, and species can expand our understanding of the evolution of phenotypic plasticity. Here, we explore the ways that the study of hormone signaling is providing new insights into the underlying proximate bases for individual, population or species variation in plasticity. Using several studies as exemplars, we examine how a ‘norm of reaction’ approach can be used in investigations of hormone-mediated plasticity to inform the following: 1) how environmental cues affect the component hormones, receptors and enzymes that comprise any endocrine signaling pathway, 2) how genetic and epigenetic variation in endocrine-associated genes can generate variation in plasticity among these diverse components, and 3) how phenotypes mediated by the same hormone can be coupled and decoupled via independent plastic responses of signaling components across target tissues. Future studies that apply approaches such as reaction norms and network modeling to questions concerning how hormones link environmental stimuli to ecologically-relevant phenotypic responses should help unravel how phenotypic plasticity evolves.
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Morris, Matthew R. J., and Sean M. Rogers. "Overcoming maladaptive plasticity through plastic compensation." Current Zoology 59, no. 4 (August 1, 2013): 526–36. http://dx.doi.org/10.1093/czoolo/59.4.526.
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Abstract Most species evolve within fluctuating environments, and have developed adaptations to meet the challenges posed by environmental heterogeneity. One such adaptation is phenotypic plasticity, or the ability of a single genotype to produce multiple environmentally-induced phenotypes. Yet, not all plasticity is adaptive. Despite the renewed interest in adaptive phenotypic plasticity and its consequences for evolution, much less is known about maladaptive plasticity. However, maladaptive plasticity is likely an important driver of phenotypic similarity among populations living in different environments. This paper traces four strategies for overcoming maladaptive plasticity that result in phenotypic similarity, two of which involve genetic changes (standing genetic variation, genetic compensation) and two of which do not (standing epigenetic variation, plastic compensation). Plastic compensation is defined as adaptive plasticity overcoming maladaptive plasticity. In particular, plastic compensation may increase the likelihood of genetic compensation by facilitating population persistence. We provide key terms to disentangle these aspects of phenotypic plasticity and introduce examples to reinforce the potential importance of plastic compensation for understanding evolutionary change.
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Purkayastha, Purboja, Kavya Pendyala, Ayush S. Saxena, Hesamedin Hakimjavadi, Srikar Chamala, Purushottam Dixit, Charles F. Baer, and Tanmay P. Lele. "Reverse Plasticity Underlies Rapid Evolution by Clonal Selection within Populations of Fibroblasts Propagated on a Novel Soft Substrate." Molecular Biology and Evolution 38, no. 8 (April 19, 2021): 3279–93. http://dx.doi.org/10.1093/molbev/msab102.
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Abstract Mechanical properties such as substrate stiffness are a ubiquitous feature of a cell’s environment. Many types of animal cells exhibit canonical phenotypic plasticity when grown on substrates of differing stiffness, in vitro and in vivo. Whether such plasticity is a multivariate optimum due to hundreds of millions of years of animal evolution, or instead is a compromise between conflicting selective demands, is unknown. We addressed these questions by means of experimental evolution of populations of mouse fibroblasts propagated for approximately 90 cell generations on soft or stiff substrates. The ancestral cells grow twice as fast on stiff substrate as on soft substrate and exhibit the canonical phenotypic plasticity. Soft-selected lines derived from a genetically diverse ancestral population increased growth rate on soft substrate to the ancestral level on stiff substrate and evolved the same multivariate phenotype. The pattern of plasticity in the soft-selected lines was opposite of the ancestral pattern, suggesting that reverse plasticity underlies the observed rapid evolution. Conversely, growth rate and phenotypes did not change in selected lines derived from clonal cells. Overall, our results suggest that the changes were the result of genetic evolution and not phenotypic plasticity per se. Whole-transcriptome analysis revealed consistent differentiation between ancestral and soft-selected populations, and that both emergent phenotypes and gene expression tended to revert in the soft-selected lines. However, the selected populations appear to have achieved the same phenotypic outcome by means of at least two distinct transcriptional architectures related to mechanotransduction and proliferation.
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Sommer, Ralf J., Mohannad Dardiry, Masa Lenuzzi, Suryesh Namdeo, Tess Renahan, Bogdan Sieriebriennikov, and Michael S. Werner. "The genetics of phenotypic plasticity in nematode feeding structures." Open Biology 7, no. 3 (March 2017): 160332. http://dx.doi.org/10.1098/rsob.160332.
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Phenotypic plasticity has been proposed as an ecological and evolutionary concept. Ecologically, it can help study how genes and the environment interact to produce robust phenotypes. Evolutionarily, as a facilitator it might contribute to phenotypic novelty and diversification. However, the discussion of phenotypic plasticity remains contentious in parts due to the absence of model systems and rigorous genetic studies. Here, we summarize recent work on the nematode Pristionchus pacificus, which exhibits a feeding plasticity allowing predatory or bacteriovorous feeding. We show feeding plasticity to be controlled by developmental switch genes that are themselves under epigenetic control. Phylogenetic and comparative studies support phenotypic plasticity and its role as a facilitator of morphological novelty and diversity.
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Varankar, Sagar S., Madhuri More, Ancy Abraham, Kshama Pansare, Brijesh Kumar, Nivedhitha J. Narayanan, Mohit Kumar Jolly, Avinash M. Mali, and Sharmila A. Bapat. "Functional balance between Tcf21–Slug defines cellular plasticity and migratory modalities in high grade serous ovarian cancer cell lines." Carcinogenesis 41, no. 4 (June 25, 2019): 515–26. http://dx.doi.org/10.1093/carcin/bgz119.
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Abstract Cellular plasticity and transitional phenotypes add to complexities of cancer metastasis that can be initiated by single cell epithelial to mesenchymal transition (EMT) or cooperative cell migration (CCM). Our study identifies novel regulatory cross-talks between Tcf21 and Slug in mediating phenotypic and migration plasticity in high-grade serous ovarian adenocarcinoma (HGSC). Differential expression and subcellular localization associate Tcf21, Slug with epithelial, mesenchymal phenotypes, respectively; however, gene manipulation approaches identify their association with additional intermediate phenotypic states, implying the existence of a multistep epithelial-mesenchymal transition program. Live imaging further associated distinct migratory modalities with the Tcf21/Slug status of cell systems and discerned proliferative/passive CCM, active CCM and EMT modes of migration. Tcf21–Slug balance identified across a phenotypic spectrum in HGSC cell lines, associated with microenvironment-induced transitions and the emergence of an epithelial phenotype following drug exposure. Phenotypic transitions and associated functionalities following drug exposure were affirmed to ensue from occupancy of Slug promoter E-box sequences by Tcf21. Our study effectively provides a framework for understanding the relevance of ovarian cancer plasticity as a function of two transcription factors.
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Reed, Thomas E., Robin S. Waples, Daniel E. Schindler, Jeffrey J. Hard, and Michael T. Kinnison. "Phenotypic plasticity and population viability: the importance of environmental predictability." Proceedings of the Royal Society B: Biological Sciences 277, no. 1699 (June 16, 2010): 3391–400. http://dx.doi.org/10.1098/rspb.2010.0771.
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Phenotypic plasticity plays a key role in modulating how environmental variation influences population dynamics, but we have only rudimentary understanding of how plasticity interacts with the magnitude and predictability of environmental variation to affect population dynamics and persistence. We developed a stochastic individual-based model, in which phenotypes could respond to a temporally fluctuating environmental cue and fitness depended on the match between the phenotype and a randomly fluctuating trait optimum, to assess the absolute fitness and population dynamic consequences of plasticity under different levels of environmental stochasticity and cue reliability. When cue and optimum were tightly correlated, plasticity buffered absolute fitness from environmental variability, and population size remained high and relatively invariant. In contrast, when this correlation weakened and environmental variability was high, strong plasticity reduced population size, and populations with excessively strong plasticity had substantially greater extinction probability. Given that environments might become more variable and unpredictable in the future owing to anthropogenic influences, reaction norms that evolved under historic selective regimes could imperil populations in novel or changing environmental contexts. We suggest that demographic models (e.g. population viability analyses) would benefit from a more explicit consideration of how phenotypic plasticity influences population responses to environmental change.
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Coz, Clementine Le, John R. Christin, Talal Syed, Zejian Wang, Caroline J. Laplaca, Andrew T. Lenis, and Michael M. Shen. "Abstract B025: Luminal-to-basal phenotypic plasticity promotes invasive phenotypes in a live-imaging assay using patient-derived bladder tumor organoids." Clinical Cancer Research 30, no. 10_Supplement (May 17, 2024): B025. http://dx.doi.org/10.1158/1557-3265.bladder24-b025.
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Abstract Lineage plasticity in cancer is characterized by changes in cell state that are often associated with tumor progression and treatment resistance. While nearly all non-muscle invasive bladder cancer (NMIBC) tumors have a luminal epithelial phenotype, many muscle invasive bladder cancers (MIBC) display a basal identity. NMIBC to MIBC progression may therefore be related to a phenotypic switch from luminal-to-basal subtypes, which in turn may be associated with poorer clinical outcomes. However, current understanding of the molecular processes linking cell plasticity and tumor invasion is limited, due in part to a lack of physiologically relevant in vitro models and assays. To address these questions, we are utilizing a living biobank of 82 patient-derived bladder tumor organoid lines that our group has established. These organoids represent a 3-dimensional, heterogeneous model system for studying bladder cancer, as they can be genetically manipulated and recapitulate the molecular and histopathological features of the parental tumor. Notably, in previous work, we described luminal-to-basal phenotypic plasticity in a subset of organoid lines derived from luminal tumors, which display a shift to basal/squamous identity in culture that is reversible by orthotopic xenografting. In current studies, we are investigating cell migration and invasiveness using a live-imaging assay that we have developed to examine bladder tumor organoid outgrowth in vitro. Importantly, this assay allows longitudinal visualization as well as quantitation of invasiveness over a four-day time span. Analysis of over 25 organoid lines with plastic, stable luminal, and stable basal properties has revealed a broad spectrum of organoid outgrowth phenotypes that do not correlate with cell proliferation or clinical parameters. Instead, the degree of outgrowth correlates precisely with luminal-to-basal phenotypic plasticity, as assessed by transcriptome analyses, immunofluorescence microscopy, and in vivo xenografting. Organoid lines with minimal outgrowth have stable luminal phenotypes, whereas lines that produce their own extracellular matrix to create a leading edge of migrating cells have plastic phenotypes. Furthermore, movies of the invading organoids reveal distinct cell migratory patterns, as several organoid lines display collective migration that generates an invasive front at the leading edge. This collective migration phenotype is distinct from phenotypic plasticity, is at least partially independent from organoid outgrowth, and is undergoing further analysis. Thus, our organoid outgrowth assay identifies two different parameters of invasive potential, one of which correlates with phenotypic plasticity. Our findings characterize bladder tumor invasion patterns for the first time and suggest that lineage plasticity in NMIBC represents a key mechanism that promotes tumor invasion in MIBC. Citation Format: Clementine Le Coz, John R. Christin, Talal Syed, Zejian Wang, Caroline J. Laplaca, Andrew T. Lenis, Michael M. Shen. Luminal-to-basal phenotypic plasticity promotes invasive phenotypes in a live-imaging assay using patient-derived bladder tumor organoids [abstract]. In: Proceedings of the AACR Special Conference on Bladder Cancer: Transforming the Field; 2024 May 17-20; Charlotte, NC. Philadelphia (PA): AACR; Clin Cancer Res 2024;30(10_Suppl):Abstract nr B025.
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Patalano, Solenn, Anna Vlasova, Chris Wyatt, Philip Ewels, Francisco Camara, Pedro G. Ferreira, Claire L. Asher, et al. "Molecular signatures of plastic phenotypes in two eusocial insect species with simple societies." Proceedings of the National Academy of Sciences 112, no. 45 (October 19, 2015): 13970–75. http://dx.doi.org/10.1073/pnas.1515937112.
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Phenotypic plasticity is important in adaptation and shapes the evolution of organisms. However, we understand little about what aspects of the genome are important in facilitating plasticity. Eusocial insect societies produce plastic phenotypes from the same genome, as reproductives (queens) and nonreproductives (workers). The greatest plasticity is found in the simple eusocial insect societies in which individuals retain the ability to switch between reproductive and nonreproductive phenotypes as adults. We lack comprehensive data on the molecular basis of plastic phenotypes. Here, we sequenced genomes, microRNAs (miRNAs), and multiple transcriptomes and methylomes from individual brains in a wasp (Polistes canadensis) and an ant (Dinoponera quadriceps) that live in simple eusocial societies. In both species, we found few differences between phenotypes at the transcriptional level, with little functional specialization, and no evidence that phenotype-specific gene expression is driven by DNA methylation or miRNAs. Instead, phenotypic differentiation was defined more subtly by nonrandom transcriptional network organization, with roles in these networks for both conserved and taxon-restricted genes. The general lack of highly methylated regions or methylome patterning in both species may be an important mechanism for achieving plasticity among phenotypes during adulthood. These findings define previously unidentified hypotheses on the genomic processes that facilitate plasticity and suggest that the molecular hallmarks of social behavior are likely to differ with the level of social complexity.
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Viney, Mark, and Anaid Diaz. "Phenotypic plasticity in nematodes." Worm 1, no. 2 (April 2012): 98–106. http://dx.doi.org/10.4161/worm.21086.
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Relyea. "Costs of Phenotypic Plasticity." American Naturalist 159, no. 3 (2002): 272. http://dx.doi.org/10.2307/3079078.
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Sugden, A. M. "ECOLOGY/EVOLUTION: Phenotypic Plasticity." Science 306, no. 5694 (October 8, 2004): 199a. http://dx.doi.org/10.1126/science.306.5694.199a.
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Relyea, Rick A. "Costs of Phenotypic Plasticity." American Naturalist 159, no. 3 (March 2002): 272–82. http://dx.doi.org/10.1086/338540.
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Martini, Alexandre Góes, and A. H. Jan Danser. "Juxtaglomerular Cell Phenotypic Plasticity." High Blood Pressure & Cardiovascular Prevention 24, no. 3 (May 19, 2017): 231–42. http://dx.doi.org/10.1007/s40292-017-0212-5.
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Schlichting, Carl D. "Phenotypic plasticity in Phlox." Oecologia 78, no. 4 (1989): 496–501. http://dx.doi.org/10.1007/bf00378740.
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Nanjundiah, Vidyanand, and Stuart A. Newman. "Phenotypic and Developmental Plasticity." Journal of Biosciences 34, no. 4 (October 2009): 493–94. http://dx.doi.org/10.1007/s12038-009-0067-6.
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Kaplan, Zdenek. "Phenotypic plasticity inPotamogeton (Potamogetonaceae)." Folia Geobotanica 37, no. 2 (June 2002): 141–70. http://dx.doi.org/10.1007/bf02804229.
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Green, Delbert A., and Cassandra G. Extavour. "Insulin signalling underlies both plasticity and divergence of a reproductive trait in Drosophila." Proceedings of the Royal Society B: Biological Sciences 281, no. 1779 (March 22, 2014): 20132673. http://dx.doi.org/10.1098/rspb.2013.2673.
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Phenotypic plasticity is the ability of a single genotype to yield distinct phenotypes in different environments. The molecular mechanisms linking phenotypic plasticity to the evolution of heritable diversification, however, are largely unknown. Here, we show that insulin/insulin-like growth factor signalling (IIS) underlies both phenotypic plasticity and evolutionary diversification of ovariole number, a quantitative reproductive trait, in Drosophila . IIS activity levels and sensitivity have diverged between species, leading to both species-specific ovariole number and species-specific nutritional plasticity in ovariole number. Plastic range of ovariole number correlates with ecological niche, suggesting that the degree of nutritional plasticity may be an adaptive trait. This demonstrates that a plastic response conserved across animals can underlie the evolution of morphological diversity, underscoring the potential pervasiveness of plasticity as an evolutionary mechanism.
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Saifudin, Saifudin, and Andi Salamah Andi Salamah. "The Influence of Season on Phenotypic Plasticity Symptoms in Hibiscus rosa-sinensis Crested Peach Flowers." Sains Malaysiana 51, no. 9 (September 30, 2022): 2817–27. http://dx.doi.org/10.17576/jsm-2022-5109-07.
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The variation of Hibiscus rosa-sinensis flower in the form of a crested peach is thought to show phenotypic plasticity symptoms in nature. Phenotypic plasticity is a condition in which genotypes give rise to different phenotypes in different environments. The aim of this study was to determine the plasticity response of H. rosa-sinensis crested peach flowers to seasonal changes, both morphologically and anatomically. Flower samples were taken from the residential area of Bojong Gede, Bogor, in two different seasons: the dry season in 2018 and the rainy season in 2021. Morphological observations were made by calculating the number and size of each flower section using measuring instruments and a Dino-Lite microscope. Anatomical observations were made by observing the internal structure of the ovaries using a 4× magnification light microscope. Measurement of environmental parameters, such as temperature, humidity, and light intensity, was also carried out in this study to determine the symptoms of phenotypic plasticity. The phenotypic plasticity responses of H. rosa-sinensis crested peach flower are clearly observed in the number and composition of the stamen, staminodium petaloid, intermediate stamen-petal, and external-internal structure of the ovary. H. rosa-sinensis, in the form of crested flowers, showed a different phenotypic plasticity response in different seasons. The light intensity and temperature factors play an important role in phenotypic plasticity. Research with various observation times is still needed to determine the range of phenotypic plasticity responses of the H. rosa-sinensis flower form of crested peach in nature.
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Mathis, Robert Austin, Ethan S. Sokol, and Piyush B. Gupta. "Cancer cells exhibit clonal diversity in phenotypic plasticity." Open Biology 7, no. 2 (February 2017): 160283. http://dx.doi.org/10.1098/rsob.160283.
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Phenotypic heterogeneity in cancers is associated with invasive progression and drug resistance. This heterogeneity arises in part from the ability of cancer cells to switch between phenotypic states, but the dynamics of this cellular plasticity remain poorly understood. Here we apply DNA barcodes to quantify and track phenotypic plasticity across hundreds of clones in a population of cancer cells exhibiting epithelial or mesenchymal differentiation phenotypes. We find that the epithelial-to-mesenchymal cell ratio is highly variable across the different clones in cancer cell populations, but remains stable for many generations within the progeny of any single clone—with a heritability of 0.89. To estimate the effects of combination therapies on phenotypically heterogeneous tumours, we generated quantitative simulations incorporating empirical data from our barcoding experiments. These analyses indicated that combination therapies which alternate between epithelial- and mesenchymal-specific treatments eventually select for clones with increased phenotypic plasticity. However, this selection could be minimized by increasing the frequency of alternation between treatments, identifying designs that may minimize selection for increased phenotypic plasticity. These findings establish new insights into phenotypic plasticity in cancer, and suggest design principles for optimizing the effectiveness of combination therapies for phenotypically heterogeneous tumours.
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Mallard, Francois, Viola Nolte, and Christian Schlötterer. "The Evolution of Phenotypic Plasticity in Response to Temperature Stress." Genome Biology and Evolution 12, no. 12 (October 6, 2020): 2429–40. http://dx.doi.org/10.1093/gbe/evaa206.
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Abstract Phenotypic plasticity is the ability of a single genotype to produce different phenotypes in response to environmental variation. The importance of phenotypic plasticity in natural populations and its contribution to phenotypic evolution during rapid environmental change is widely debated. Here, we show that thermal plasticity of gene expression in natural populations is a key component of its adaptation: evolution to novel thermal environments increases ancestral plasticity rather than mean genetic expression. We determined the evolution of plasticity in gene expression by conducting laboratory natural selection on a Drosophila simulans population in hot and cold environments. After more than 60 generations in the hot environment, 325 genes evolved a change in plasticity relative to the natural ancestral population. Plasticity increased in 75% of these genes, which were strongly enriched for several well-defined functional categories (e.g., chitin metabolism, glycolysis, and oxidative phosphorylation). Furthermore, we show that plasticity in gene expression of populations exposed to different temperatures is rather similar across species. We conclude that most of the ancestral plasticity can evolve further in more extreme environments.
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van Snick Gray, Ellen, and Jay Stauffer. "Phenotypic plasticity: its role in trophic radiation and explosive speciation in cichlids (Teleostei: Cichlidae)." Animal Biology 54, no. 2 (2004): 137–58. http://dx.doi.org/10.1163/1570756041445191.
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AbstractPhenotypic plasticity is the capacity of an organism's phenotype to vary in different environments. Although diet-induced phenotypic plasticity has been documented in New World cichlids, it has been hypothesised that this type of plasticity would be limited in certain Old World cichlids, because of the morphological constraints on the jaw imposed by mouth-brooding. This hypothesis was experimentally tested by determining the effect of different diets on the head and jaw morphology of split broods of several species of haplochromine cichlids from Lake Malaŵi, Africa, and two substrate-spawning cichlids, one from the Old World, Tilapia mariae (Boulenger), and one from the New World, Herichthys cyanoguttatum (Baird and Girard). Different feeding regimes resulted in differences in head morphologies in both New and Old World cichlid species. Although Old World mouth-brooding haplochromine cichlids exhibited phenotypic plasticity, the magnitude of head-shape plasticity observed was greater in the New World substrate-spawning cichlid, H. cyanoguttatum . The Old World tilapiine cichlid, T. mariae , did not exhibit phenotypic plasticity of head morphology. Experiments with modified foods demonstrated that the observed changes were unrelated to dietary nutrition, but were a result of differing feeding modes. Phenotypic plasticity might have contributed to the extensive trophic radiation and subsequent explosive speciation observed in Old World haplochromine cichlids. The existence of phenotypic plasticity has implications for morphology-based species descriptions as well.
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Rubtsova, Svetlana N., Irina Y. Zhitnyak, and Natalya A. Gloushankova. "Phenotypic Plasticity of Cancer Cells Based on Remodeling of the Actin Cytoskeleton and Adhesive Structures." International Journal of Molecular Sciences 22, no. 4 (February 12, 2021): 1821. http://dx.doi.org/10.3390/ijms22041821.
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There is ample evidence that, instead of a binary switch, epithelial-mesenchymal transition (EMT) in cancer results in a flexible array of phenotypes, each one uniquely suited to a stage in the invasion-metastasis cascade. The phenotypic plasticity of epithelium-derived cancer cells gives them an edge in surviving and thriving in alien environments. This review describes in detail the actin cytoskeleton and E-cadherin-based adherens junction rearrangements that cancer cells need to implement in order to achieve the advantageous epithelial/mesenchymal phenotype and plasticity of migratory phenotypes that can arise from partial EMT.
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Poort, Vera M., Rico Hagelaar, Mark van Roosmalen, Laurianne Trabut, Jessica G. C. A. M. Buijs-Gladdines, Diego Montiel González, Bram van Wijk, Jules P. P. Meijerink, and Ruben Van Boxtel. "Transient Differentiation-State Plasticity during Initiation of Pediatric Acute Lymphoblastic Leukemia." Blood 142, Supplement 1 (November 28, 2023): 42. http://dx.doi.org/10.1182/blood-2023-188891.
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Introduction Leukemia is characterized by oncogenic lesions that result in a block of differentiation while at the same time intratumor phenotypic plasticity is retained. It is unclear how these two phenomena arise during leukemogenesis in humans. Here we characterized T-cell acute lymphoblastic leukemia (T-ALL), as a model disease to investigate the coherence between leukemia initiating cells (LICs), developmental arrest, and phenotypic plasticity. Methods We characterized 31 primary T-ALL samples for differentiation state heterogeneity using multi parameter flow cytometry. Subsequently, for 5 patients, phenotypic subpopulations were single cell sorted. As leukemic cells do not expand in vitro primary template-directed amplification (PTA) was used to amplify the genome of single blasts to obtain enough DNA for WGS analysis with nucleotide resolution. Shared and unique mutations were used to construct retrospective lineage trees and assess the hierarchy of phenotypically diverse blasts. Results To assess phenotypic differentiation state heterogeneity in T-ALL, we designed a 17-parameter flow cytometry panel to discriminate T-lymphoid developmental cell populations. We characterized 31 samples (median blast count 98% (IQR = 94 - 99)), and defined immunophenotypic subpopulations as populations with a size of >10% of the total CD7+ population. Differentiation state heterogeneity (> 2 subpopulations) was observed in 26 out of the 31 T-ALL patients (83.9%). Interestingly, the most immature CD4-CD8-CD3- “DN-like” differentiation state was found in all samples, suggesting that developmental hierarchy is maintained. We then questioned whether genetic determinants were driving the phenotypic diversity we observed. Therefore 5 T-ALL patients harboring translocations of oncogenes commonly seen in T-ALL were selected, namely, TLX1 (n=1) , LMO2 (n=2) , TAL1 (n=2) and TLX3 (n=1) . For each patient cells of each differentiation state were single cell and bulk sorted for single cell WGS and bulk WGS, respectively. Structural variant analysis confirmed presence of the oncogenic translocation in all single blasts, validating their (pre-)leukemic origin. Moreover, driver analysis showed that type B mutations in e.g., NOTCH1 and PHF6 were shared among all blasts. Interestingly, there were no potential genetic drivers found that were unique to a subpopulation. Neutral passenger mutations were therefore used to construct phylogenetic trees. Herein, blasts with similar phenotypic differentiation states were genetically closer related than blasts of different phenotypes, revealing the heritability of phenotypes (Fig. 1A). The biased distribution of immunophenotypes across the different branches of the phylogenetic tree was then confirmed in bulk WGS samples of sorted phenotypic populations. Suggesting that switching between phenotypes is not a frequent process. Next, the plasticity of T-ALL was assessed by identifying the phenotypic cell state of the LIC. We assessed V(D)J recombination per single blast and identified monoclonal V(D)J recombination for most of the blasts. Moreover, in TAL1 T-ALL we observed monoclonal TRG, TRB and TRA translocation. This suggested that the LIC had undergone complete V(D)J recombination and was a more mature T-cell progenitor. However, blasts with an immature CD4-CD8- (DN) phenotype had undergone the same V(D)J recombination suggesting phenotypic de-differentiation of the LIC. Additionally, in TLX1 T-ALL, the blasts with the more mature CD4+CD8+ double positive (DP) phenotype had monoclonal TRG and TRB gene recombination, but polyclonal TRA recombination, whereas cells with a more immature DN phenotype had no TRA recombination (Fig. 1B). This indicated an immature T-cell progenitor as the LIC and continued differentiation after leukemia initiation resulting in DP cells with unique TRA recombination. Conclusion In conclusion, we show immunophenotypic differentiation state heterogeneity in diagnostic primary T-ALL samples. By coupling phenotypic data with novel single cell whole genome sequencing techniques, we identified heritability of phenotypic cell states. Moreover, we reveal the ability of the LIC to differentiate and de-differentiate after leukemia initiation. Taken together our results demonstrate a transient period of plasticity during leukemia initiation where phenotypic switches appear unidirectional.
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Kingsolver, Joel G., and Lauren B. Buckley. "Evolution of plasticity and adaptive responses to climate change along climate gradients." Proceedings of the Royal Society B: Biological Sciences 284, no. 1860 (August 16, 2017): 20170386. http://dx.doi.org/10.1098/rspb.2017.0386.
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The relative contributions of phenotypic plasticity and adaptive evolution to the responses of species to recent and future climate change are poorly understood. We combine recent (1960–2010) climate and phenotypic data with microclimate, heat balance, demographic and evolutionary models to address this issue for a montane butterfly, Colias eriphyle , along an elevational gradient. Our focal phenotype, wing solar absorptivity, responds plastically to developmental (pupal) temperatures and plays a central role in thermoregulatory adaptation in adults. Here, we show that both the phenotypic and adaptive consequences of plasticity vary with elevation. Seasonal changes in weather generate seasonal variation in phenotypic selection on mean and plasticity of absorptivity, especially at lower elevations. In response to climate change in the past 60 years, our models predict evolutionary declines in mean absorptivity (but little change in plasticity) at high elevations, and evolutionary increases in plasticity (but little change in mean) at low elevation. The importance of plasticity depends on the magnitude of seasonal variation in climate relative to interannual variation. Our results suggest that selection and evolution of both trait means and plasticity can contribute to adaptive response to climate change in this system. They also illustrate how plasticity can facilitate rather than retard adaptive evolutionary responses to directional climate change in seasonal environments.
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Robinson, Beren W., and David W. Pfennig. "Inducible competitors and adaptive diversification." Current Zoology 59, no. 4 (August 1, 2013): 537–52. http://dx.doi.org/10.1093/czoolo/59.4.537.
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Abstract Identifying the causes of diversification is central to evolutionary biology. The ecological theory of adaptive diversification holds that the evolution of phenotypic differences between populations and species—and the formation of new species—stems from divergent natural selection, often arising from competitive interactions. Although increasing evidence suggests that phenotypic plasticity can facilitate this process, it is not generally appreciated that competitively mediated selection often also provides ideal conditions for phenotypic plasticity to evolve in the first place. Here, we discuss how competition plays at least two key roles in adaptive diversification depending on its pattern. First, heterogenous competition initially generates heterogeneity in resource use that favors adaptive plasticity in the form of “inducible competitors”. Second, once such competitively induced plasticity evolves, its capacity to rapidly generate phenotypic variation and expose phenotypes to alternate selective regimes allows populations to respond readily to selection favoring diversification, as may occur when competition generates steady diversifying selection that permanently drives the evolutionary divergence of populations that use different resources. Thus, competition plays two important roles in adaptive diversification—one well-known and the other only now emerging—mediated through its effect on the evolution of phenotypic plasticity.
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Gianoli, Ernesto, and Kattia Palacio-López. "Phenotypic integration may constrain phenotypic plasticity in plants." Oikos 118, no. 12 (December 2009): 1924–28. http://dx.doi.org/10.1111/j.1600-0706.2009.17884.x.
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Kaarijärvi, Roosa, Heidi Kaljunen, and Kirsi Ketola. "Molecular and Functional Links between Neurodevelopmental Processes and Treatment-Induced Neuroendocrine Plasticity in Prostate Cancer Progression." Cancers 13, no. 4 (February 9, 2021): 692. http://dx.doi.org/10.3390/cancers13040692.
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Neuroendocrine plasticity and treatment-induced neuroendocrine phenotypes have recently been proposed as important resistance mechanisms underlying prostate cancer progression. Treatment-induced neuroendocrine prostate cancer (t-NEPC) is highly aggressive subtype of castration-resistant prostate cancer which develops for one fifth of patients under prolonged androgen deprivation. In recent years, understanding of molecular features and phenotypic changes in neuroendocrine plasticity has been grown. However, there are still fundamental questions to be answered in this emerging research field, for example, why and how do the prostate cancer treatment-resistant cells acquire neuron-like phenotype. The advantages of the phenotypic change and the role of tumor microenvironment in controlling cellular plasticity and in the emergence of treatment-resistant aggressive forms of prostate cancer is mostly unknown. Here, we discuss the molecular and functional links between neurodevelopmental processes and treatment-induced neuroendocrine plasticity in prostate cancer progression and treatment resistance. We provide an overview of the emergence of neurite-like cells in neuroendocrine prostate cancer cells and whether the reported t-NEPC pathways and proteins relate to neurodevelopmental processes like neurogenesis and axonogenesis during the development of treatment resistance. We also discuss emerging novel therapeutic targets modulating neuroendocrine plasticity.
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Smith, Gilbert, and Michael G. Ritchie. "How might epigenetics contribute to ecological speciation?" Current Zoology 59, no. 5 (October 1, 2013): 686–96. http://dx.doi.org/10.1093/czoolo/59.5.686.
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Abstract Speciation research has seen a renewed interest in ecological speciation, which emphasises divergent ecological selection leading to the evolution of reproductive isolation. Selection from divergent ecologies means that phenotypic plasticity can play an important role in ecological speciation. Phenotypic plasticity involves the induction of phenotypes over the lifetime of an organism and emerging evidence suggests that epigenetic marks such as cytosine and protein (histone) modifications might regulate such environmental induction. Epigenetic marks play a wide role in a variety of processes including development, sex differentiation and allocation, sexual conflict, regulation of transposable elements and phenotypic plasticity. Here we describe recent studies that investigate epigenetic mechanisms in a variety of contexts. There is mounting evidence for environmentally induced epigenetic variation and for the stable inheritance of epigenetic marks between generations. Thus, epigenetically-based phenotypic plasticity may play a role in adaptation and ecological speciation. However, there is less evidence for the inheritance of induced epigenetic variation across multiple generations in animals. Currently few studies of ecological speciation incorporate the potential for the involvement of epigenetically-based induction of phenotypes, and we argue that this is an important omission.
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Dennis, S. R., Mauricio J. Carter, W. T. Hentley, and A. P. Beckerman. "Phenotypic convergence along a gradient of predation risk." Proceedings of the Royal Society B: Biological Sciences 278, no. 1712 (November 17, 2010): 1687–96. http://dx.doi.org/10.1098/rspb.2010.1989.
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A long-standing question in ecology is whether phenotypic plasticity, rather than selection per se , is responsible for phenotypic variation among populations. Plasticity can increase or decrease variation, but most previous studies have been limited to single populations, single traits and a small number of environments assessed using univariate reaction norms. Here, examining two genetically distinct populations of Daphnia pulex with different predation histories, we quantified predator-induced plasticity among 11 traits along a fine-scale gradient of predation risk by a predator ( Chaoborus ) common to both populations. We test the hypothesis that plasticity can be responsible for convergence in phenotypes among different populations by experimentally characterizing multivariate reaction norms with phenotypic trajectory analysis (PTA). Univariate analyses showed that all genotypes increased age and size at maturity, and invested in defensive spikes (neckteeth), but failed to quantitatively describe whole-organism response. In contrast, PTA quantified and qualified the phenotypic strategy the organism mobilized against the selection pressure. We demonstrate, at the whole-organism level, that the two populations occupy different areas of phenotypic space in the absence of predation but converge in phenotypic space as predation threat increases.
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Kronholm, Ilkka, Hanna Johannesson, and Tarmo Ketola. "Epigenetic Control of Phenotypic Plasticity in the Filamentous Fungus Neurospora crassa." G3 Genes|Genomes|Genetics 6, no. 12 (December 1, 2016): 4009–22. http://dx.doi.org/10.1534/g3.116.033860.
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Abstract Phenotypic plasticity is the ability of a genotype to produce different phenotypes under different environmental or developmental conditions. Phenotypic plasticity is a ubiquitous feature of living organisms, and is typically based on variable patterns of gene expression. However, the mechanisms by which gene expression is influenced and regulated during plastic responses are poorly understood in most organisms. While modifications to DNA and histone proteins have been implicated as likely candidates for generating and regulating phenotypic plasticity, specific details of each modification and its mode of operation have remained largely unknown. In this study, we investigated how epigenetic mechanisms affect phenotypic plasticity in the filamentous fungus Neurospora crassa. By measuring reaction norms of strains that are deficient in one of several key physiological processes, we show that epigenetic mechanisms play a role in homeostasis and phenotypic plasticity of the fungus across a range of controlled environments. In general, effects on plasticity are specific to an environment and mechanism, indicating that epigenetic regulation is context dependent and is not governed by general plasticity genes. Specifically, we found that, in Neurospora, histone methylation at H3K36 affected plastic response to high temperatures, H3K4 methylation affected plastic response to pH, but H3K27 methylation had no effect. Similarly, DNA methylation had only a small effect in response to sucrose. Histone deacetylation mainly decreased reaction norm elevation, as did genes involved in histone demethylation and acetylation. In contrast, the RNA interference pathway was involved in plastic responses to multiple environments.
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Weiss, Linda C. "Neurobiology of phenotypic plasticity in the light of climate change." Neuroforum 28, no. 1 (December 20, 2021): 1–12. http://dx.doi.org/10.1515/nf-2021-0029.
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Abstract Phenotypic plasticity describes the ability of an organism with a given genotype to respond to changing environmental conditions through the adaptation of the phenotype. Phenotypic plasticity is a widespread means of adaptation, allowing organisms to optimize fitness levels in changing environments. A core prerequisite for adaptive predictive plasticity is the existence of reliable cues, i.e. accurate environmental information about future selection on the expressed plastic phenotype. Furthermore, organisms need the capacity to detect and interpret such cues, relying on specific sensory signalling and neuronal cascades. Subsequent neurohormonal changes lead to the transformation of phenotype A into phenotype B. Each of these activities is critical for survival. Consequently, anything that could impair an animal’s ability to perceive important chemical information could have significant ecological ramifications. Climate change and other human stressors can act on individual or all of the components of this signalling cascade. In consequence, organisms could lose their adaptive potential, or in the worst case, even become maladapted. Therefore, it is key to understand the sensory systems, the neurobiology and the physiological adaptations that mediate organisms’ interactions with their environment. It is, thus, pivotal to predict the ecosystem-wide effects of global human forcing. This review summarizes current insights on how climate change affects phenotypic plasticity, focussing on how associated stressors change the signalling agents, the sensory systems, receptor responses and neuronal signalling cascades, thereby, impairing phenotypic adaptations.
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Williamson, Naomi G., Callee M. Walsh, and Teiya Kijimoto. "Comparative metabolomic analysis of polyphenic horn development in the dung beetle Onthophagus taurus." PLOS ONE 17, no. 3 (March 17, 2022): e0265222. http://dx.doi.org/10.1371/journal.pone.0265222.
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Organisms alter their phenotypes in response to changing environmental conditions. The developmental basis of this phenomenon, phenotypic plasticity, is a topic of broad interest in many fields of biology. While insects provide a suitable model for studying the genetic basis of phenotypic plasticity, the physiological aspects of plasticity are not fully understood. Here, we report the physiological basis of polyphenism, an extreme form of phenotypic plasticity by utilizing a dung beetle species, Onthophagus taurus. We highlighted the metabolome between sexes as well as two distinct male morphs—large and small horns. Unlike results from previous transcriptomic studies, the comparative metabolomic study revealed that differences in metabolite level were more prominent between animals with different body sizes than different sexes. Our results also indicate that specific metabolites and biochemical pathways may be active during horn size determination.
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Fox, Rebecca J., Jennifer M. Donelson, Celia Schunter, Timothy Ravasi, and Juan D. Gaitán-Espitia. "Beyond buying time: the role of plasticity in phenotypic adaptation to rapid environmental change." Philosophical Transactions of the Royal Society B: Biological Sciences 374, no. 1768 (January 28, 2019): 20180174. http://dx.doi.org/10.1098/rstb.2018.0174.
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How populations and species respond to modified environmental conditions is critical to their persistence both now and into the future, particularly given the increasing pace of environmental change. The process of adaptation to novel environmental conditions can occur via two mechanisms: (1) the expression of phenotypic plasticity (the ability of one genotype to express varying phenotypes when exposed to different environmental conditions), and (2) evolution via selection for particular phenotypes, resulting in the modification of genetic variation in the population. Plasticity, because it acts at the level of the individual, is often hailed as a rapid-response mechanism that will enable organisms to adapt and survive in our rapidly changing world. But plasticity can also retard adaptation by shifting the distribution of phenotypes in the population, shielding it from natural selection. In addition to which, not all plastic responses are adaptive—now well-documented in cases of ecological traps. In this theme issue, we aim to present a considered view of plasticity and the role it could play in facilitating or hindering adaption to environmental change. This introduction provides a re-examination of our current understanding of the role of phenotypic plasticity in adaptation and sets the theme issue's contributions in their broader context. Four key themes emerge: the need to measure plasticity across both space and time; the importance of the past in predicting the future; the importance of the link between plasticity and sexual selection; and the need to understand more about the nature of selection on plasticity itself. We conclude by advocating the need for cross-disciplinary collaborations to settle the question of whether plasticity will promote or retard species' rates of adaptation to ever-more stressful environmental conditions. This article is part of the theme issue ‘The role of plasticity in phenotypic adaptation to rapid environmental change’.
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Hoyle, Rebecca B., and Thomas H. G. Ezard. "The benefits of maternal effects in novel and in stable environments." Journal of The Royal Society Interface 9, no. 75 (May 9, 2012): 2403–13. http://dx.doi.org/10.1098/rsif.2012.0183.
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Natural selection favours phenotypes that match prevailing ecological conditions. A rapid process of adaptation is therefore required in changing environments. Maternal effects can facilitate such responses, but it is currently poorly understood under which circumstances maternal effects may accelerate or slow down the rate of phenotypic evolution. Here, we use a quantitative genetic model, including phenotypic plasticity and maternal effects, to suggest that the relationship between fitness and phenotypic variance plays an important role. Intuitive expectations that positive maternal effects are beneficial are supported following an extreme environmental shift, but, if too strong, that shift can also generate oscillatory dynamics that overshoot the optimal phenotype. In a stable environment, negative maternal effects that slow phenotypic evolution actually minimize variance around the optimum phenotype and thus maximize population mean fitness.
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Bergwall, Christer, and Goran Bengtsson. "Phenotypic Plasticity in Groundwater Denitrifiers." Oikos 87, no. 1 (October 1999): 123. http://dx.doi.org/10.2307/3547003.
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