scholarly journals Mechanism of evolution by genetic assimilation

2018 ◽  
Author(s):  
Ken Nishikawa ◽  
Akira R. Kinjo

AbstractConrad H. Waddington discovered the phenomenon of genetic assimilation through a series of experiments on fruit flies. In those experiments, artificially exerted environmental stress induced plastic phe-notypic changes in the fruit flies, but after some generations the same phenotypic variant started to appear without the environmental stress. Both the initial state (where the phenotypic changes were environmentally induced and plastic) and the final state (where the phenotypic changes were genetically fixed and constitutive) are experimental facts. However, it remains unclear how the environmentally induced phenotypic change in the first generation becomes genetically fixed in the central process of genetic assimilation itself. We have argued that the key to understanding the mechanism of genetic assimilation lies in epigenetics, and proposed the “cooperative model” in which the evolutionary process depends on both genetic and epigenetic factors. Evolutionary simulations based on the cooperative model reproduced the process of genetic assimilation. Detailed analysis of the trajectories has revealed genetic assimilation is a process in which epigenetically induced phe-notypic changes are incrementally and statistically replaced with multiple minor genetic mutations through natural selection. In this scenario, epigenetic and genetic changes may be considered as mutually independent but equivalent in terms of their effects on phenotypic changes. This finding rejects the common (and confused) hypothesis that epigenetically induced phe-notypic changes depend on genetic mutations. Furthermore, we argue that transgenerational epigenetic inheritance is not required for evolution by genetic assimilation.

2017 ◽  
Vol 114 (34) ◽  
pp. 8951-8956 ◽  
Author(s):  
Marina Alberti ◽  
Cristian Correa ◽  
John M. Marzluff ◽  
Andrew P. Hendry ◽  
Eric P. Palkovacs ◽  
...  

Humans challenge the phenotypic, genetic, and cultural makeup of species by affecting the fitness landscapes on which they evolve. Recent studies show that cities might play a major role in contemporary evolution by accelerating phenotypic changes in wildlife, including animals, plants, fungi, and other organisms. Many studies of ecoevolutionary change have focused on anthropogenic drivers, but none of these studies has specifically examined the role that urbanization plays in ecoevolution or explicitly examined its mechanisms. This paper presents evidence on the mechanisms linking urban development patterns to rapid evolutionary changes for species that play important functional roles in communities and ecosystems. Through a metaanalysis of experimental and observational studies reporting more than 1,600 phenotypic changes in species across multiple regions, we ask whether we can discriminate an urban signature of phenotypic change beyond the established natural baselines and other anthropogenic signals. We then assess the relative impact of five types of urban disturbances including habitat modifications, biotic interactions, habitat heterogeneity, novel disturbances, and social interactions. Our study shows a clear urban signal; rates of phenotypic change are greater in urbanizing systems compared with natural and nonurban anthropogenic systems. By explicitly linking urban development to traits that affect ecosystem function, we can map potential ecoevolutionary implications of emerging patterns of urban agglomerations and uncover insights for maintaining key ecosystem functions upon which the sustainability of human well-being depends.


1995 ◽  
Vol 78 (4) ◽  
pp. 1432-1441 ◽  
Author(s):  
M. Roelofs ◽  
A. J. Wein ◽  
F. C. Monson ◽  
G. Passerini-Glazel ◽  
V. E. Koteliansky ◽  
...  

Partial outlet obstruction of rabbit bladder induces serosal thickening and smooth muscle (SM) cell hypertrophy that are accompanied by phenotypic changes in the expression of cytoskeletal and cytocontractile proteins. In the present study, we compare the observed progressive phenotypic changes with the contractile responses of strips of the thickened serosa. At 15 days after partial outlet obstruction, although cells in thickened serosa demonstrate the presence of nonmuscle (NM) myosin of A-like type, vimentin, and SM alpha-actin, no contractile responses of this tissue were noted. At later times (30 days), this tissue expressed in addition SM myosin, and this pattern was paralleled by the development of KCl-stimulated contractility. It is only after 60 days that the serosa demonstrated the expression of desmin, phosphoglucomutase (PGM)-related protein, and was locally negative for NM myosin, indicating a maturation toward adult SM cells. Concomitant to this phenotypic change, the response to KCl increased, and a bethanechol-stimulated contractile response developed. At no time period did the serosal layer react with anti-synaptophysin or anti-neurofilament proteins nor did the strips respond to field stimulation (via release of neurotransmitters), showing that SM cell differentiation and development of contractile responses during serosal thickening are independent of innervation.


1996 ◽  
Vol 4 (3) ◽  
pp. 213-234 ◽  
Author(s):  
Giles Mayley

The evolution of a population can be guided by phenotypic traits acquired by members of that population during their lifetime. This phenomenon, known as the Baldwin effect, can speed the evolutionary process as traits that are initially acquired become genetically specified in later generations. This paper presents conditions under which this genetic assimilation can take place. As well as the benefits that lifetime adaptation can give a population, there may be a cost to be paid for that adaptive ability. It is the evolutionary trade-off between these costs and benefits that provides the selection pressure for acquired traits to become genetically specified. It is also noted that genotypic space, in which evolution operates, and phenotypic space, in which adaptive processes (such as learning) operate, are, in general, of a different nature. To guarantee that an acquired characteristic can become genetically specified, these spaces must have the property of neighborhood correlation, which means that a small distance between two individuals in phenotypic space implies that there is a small distance between the same two individuals in genotypic space.


1998 ◽  
Vol 66 (3) ◽  
pp. 932-937 ◽  
Author(s):  
Sudha Agarwal ◽  
Charu S. Chandra ◽  
Nicholas P. Piesco ◽  
Herman H. Langkamp ◽  
Lathe Bowen ◽  
...  

ABSTRACT Periodontal ligament (PDL) cells maintain the attachment of the tooth to alveolar bone. These cells reside at a site in which they are challenged frequently by bacterial products and proinflammatory cytokines, such as interleukin-1β (IL-1β), during infections. In our initial studies we observed that IL-1β down-regulates the osteoblast-like characteristics of PDL cells in vitro. Therefore, we examined the functional significance of the loss of the PDL cell’s osteoblast-like characteristics during inflammation. In this report we show that, during inflammation, IL-1β can modulate the phenotypic characteristics of PDL cells to a more functionally significant lipopolysaccharide (LPS)-responsive phenotype. In a healthy periodontium PDL cells exhibit an osteoblast-like phenotype and are unresponsive to gram-negative bacterial LPS. Treatment of PDL cells with IL-1β inhibits the expression of their osteoblast-like characteristics, as assessed by the failure to express transforming growth factor β1 (TGF-β1) and proteins associated with mineralization, such as alkaline phosphatase and osteocalcin. As a consequence of this IL-1β-induced phenotypic change, PDL cells become responsive to LPS and synthesize proinflammatory cytokines. The IL-1β-induced phenotypic changes in PDL cells were transient, as removal of IL-1β from PDL cell cultures resulted in reacquisition of their osteoblast-like characteristics and lack of LPS responsiveness. The IL-1β-induced phenotypic changes occurred at concentrations that are frequently observed in tissue exudates during periodontal inflammation (0.05 to 5 ng/ml). The results suggest that, during inflammation in vivo, IL-1β may modulate PDL cell functions, allowing PDL cells to participate directly in the disease process by assuming LPS responsiveness at the expense of their normal structural properties and functions.


2021 ◽  
Vol 7 (6) ◽  
pp. eabd9941
Author(s):  
Paul Vigne ◽  
Clotilde Gimond ◽  
Céline Ferrari ◽  
Anne Vielle ◽  
Johan Hallin ◽  
...  

Genetic assimilation—the evolutionary process by which an environmentally induced phenotype is made constitutive—represents a fundamental concept in evolutionary biology. Thought to reflect adaptive phenotypic plasticity, matricidal hatching in nematodes is triggered by maternal nutrient deprivation to allow for protection or resource provisioning of offspring. Here, we report natural Caenorhabditis elegans populations harboring genetic variants expressing a derived state of near-constitutive matricidal hatching. These variants exhibit a single amino acid change (V530L) in KCNL-1, a small-conductance calcium-activated potassium channel subunit. This gain-of-function mutation causes matricidal hatching by strongly reducing the sensitivity to environmental stimuli triggering egg-laying. We show that reestablishing the canonical KCNL-1 protein in matricidal isolates is sufficient to restore canonical egg-laying. While highly deleterious in constant food environments, KCNL-1 V530L is maintained under fluctuating resource availability. A single point mutation can therefore underlie the genetic assimilation—by either genetic drift or selection—of an ancestrally plastic trait.


2019 ◽  
Author(s):  
Li He ◽  
Shaojun Chen ◽  
Jingao Li ◽  
Xiaoxue Xie ◽  
Lihua Huang ◽  
...  

Abstract Purpose Genetic mutations and phenotypic changes of CYP2C9, CYP2C19 and CYP2D6 are vital for individual variations in clinical drug responses. Elucidating the mutating frequencies and phenotypic distributions of these genes shall facilitate the implementation of preemptive pharmacogenetic testing. We analyzed the gene polymorphisms and phenotypic frequencies of CYP2C9, CYP2C19 and CYP2D6 in Han Chinese population. Methods Tests of CYP2C9, CYP2C19 and CYP2D6 were performed in over 3200 (3276-3293) samples in Han Chinese population; furthermore, systematic review was employed for analyzing the mutation frequency and phenotypic distribution of CYP2C9 and CYP2C19 in Han Chinese population. Results Among 9062 samples, the mutation frequency of CYP2C9 was 11.49% and the frequency of phenotypic changes 7.1%; in 8222 samples, the mutation frequency of CYP2C19 was 66.07% and the frequency of phenotypic changes 63.75%; among 3931 samples, the mutation frequency of CYP2D6 was 88.04% and the frequency of phenotypic changes 3.87%. Among 2690 samples, gene mutations and phenotypic distributions of CYP2C9, CYP2C19 and CYP2D6 were simultaneously examined and it was found that 96.36% samples became mutated and the frequency of phenotypic changes was 66.51%. Conclusions In Han Chinese population, the gene mutations and phenotypic changes of CYP2C9, CYP2C19 and CYP2D6 are all relatively frequent. Prior to dosing, preemptive pharmacogenetic testing of CYP2C9, CYP2C19 and CYP2D6 is recommended.


2014 ◽  
Author(s):  
Takaaki Horinouchi ◽  
Shingo Suzuki ◽  
Takashi Hirasawa ◽  
Naoaki Ono ◽  
Tetsuya Yomo ◽  
...  

Bacterial cells have a remarkable ability to adapt and evolve to environmental changes, a phenomenon known as adaptive evolution. Adaptive evolution can be explained by phenotypic changes caused by genetic mutations, and by phenotypic plasticity that occur without genetic alteration, although far less is known about the contributions of the latter. In this study, we analyzed phenotypic and genotypic changes in Escherichia coli cells during adaptive evolution to ethanol stress. Phenotypic changes were quantified by transcriptome and metabolome analyses and found similar among independently evolved ethanol tolerant strains. The contribution of identified mutations in the tolerant strain was evaluated by using site-directed mutagenesis, which suggested that the fixation of these mutations cannot fully explain the observed ethanol tolerance. The phenotype of ethanol tolerance was stably maintained after an environmental change, suggesting that a mechanism of non-genetic memory contributed to at least part of the adaptation process.


2021 ◽  
Author(s):  
Sarah Sanderson ◽  
Marc-Olivier Beausoleil ◽  
Rose E. O'dea ◽  
Zachary T. Wood ◽  
Cristian Correa ◽  
...  

Wild populations must continuously adapt to environmental changes or they risk extinction. Such adaptations can be measured as phenotypic rates of change and can allow us to predict patterns of contemporary evolutionary change. About two decades ago, a dataset of phenotypic rates of change in wild populations was compiled. Since then, researchers have used (and expanded) this dataset to look at microevolutionary processes in relation to specific types of human disturbances. Here, we have updated the dataset adding 5257 estimates of phenotypic changes and used it to revisit established patterns of contemporary evolutionary change. Using this newer version, containing 6920 estimates of phenotypic changes, we revisit the conclusions of four published articles. We then synthesize the expanded dataset to compare rates of change across different types of human disturbance. Analyses of this expanded dataset suggests that: 1) a small absolute difference in rates of change exists between human disturbed and natural populations, 2) harvesting by humans results in larger rates of change than other types of disturbances, 3) introduced populations have increased rates of change, and 4) body size does not increase through time. Overall, findings from earlier analyses have largely held-up in analyses of our new dataset that encompass a much larger breadth of species, traits, and human disturbances. Lastly, we found that types of human disturbances affect rates of phenotypic change and we call for this database to serve as a stepping stone for further analyses to understand patterns of contemporary evolution.


2019 ◽  
Vol 16 (2) ◽  
pp. 227-234 ◽  
Author(s):  
N. V. Gora ◽  
S. V. Serga ◽  
O. M. Maistrenko ◽  
O. V. Protsenko ◽  
I. A. Kozeretska

Aim. The study was performed to investigate the relationship between Wolbachia infection and phenotypes that distinct from wild-type of Drosophila melanogaster from different localities in Ukraine including those from Chornobyl Exclusion Zone during 2013–2014. Methods. We have established isofemale lines from populations: Uman’, Inkerman, Odesa, Varva, Kyiv, Drogobych, Yaniv, Poliske, Chornobyl, and Chornobyl Nuclear Power Plant (NPP). The ambient radiation (µSv/h) was measured in the sample sites. The flies were reared in the laboratory through two generations. We carried out the observation of F2 flies for visibly detectable phenotypes. According to whether the trait was inherited, observations were separated into three categories: with deviations of posterior cross-vein (C2) (incomplete penetrance), visible phenotypic changes (non-inherited) and mutations (inherited). Polymerase chain reaction (PCR) with primers specific to the 16S rRNA and Wolbachia surface protein (wsp) genes were used to determine infection presence in isofemale lines of the flies established for each population. Results. Examination of different phenotypes indicates that the highest mutation rate (but not C2 and not inherited changes) is in populations from Chornobyl Exclusion Zone and, therefore, connection with ambient radiation was detected (p = 0.0241). Generalized mixed linear regression has shown evidence that the presence of phenotypes with defects of C2 vein varies with endosymbiont infection presence (p = 0.03473) in the populations from radioactively polluted areas. Conclusion. Wolbachia is not related to occurring phenotypes neither with phenotypic changes nor with mutations, at least in surveyed populations. However, C2 defected phenotypes relates to the bacterial presence in populations from the contaminated area. Nonetheless, the origin of this relationship is unknown and the mechanisms of such a connection require further research. Keywords: Drosophila melanogaster, Wolbachia, endosymbiont, ambient radiation, mutation, phenotypic change, posterior cross-vein.


2021 ◽  
Author(s):  
Sara Lopez-Gomollon ◽  
Sebastian Y Mueller ◽  
David C Baulcombe

Hybridization and environmental stress trigger genome shock that perturbs patterns of gene expression leading to phenotypic changes. In extreme examples it is associated to transposon mobilization and genome rearrangement. Here we discover a novel alternative mechanism in interspecific Solanum hybrids in which changes to gene expression were associated with DCL2-mediated small (s)RNAs derived from endogenous (para)retroviruses (EPRVs). Correspondingly, the altered patterns of gene expression overlapped with the effects of dcl2 mutation and the changes to sRNA profiles involved 22nt species produced in the DCL2 biogenesis pathway. These findings implicate hybridization-induced genome shock leading to EPRV activation and sRNA silencing as causing changes in gene expression. Such hybridization-induced variation in gene expression could increase the range of traits available for selection in natural evolution or in breeding for agriculture.


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