scholarly journals The Evolution of Genomic Imprinting via Variance Minimization: An Evolutionary Genetic Model

Genetics ◽  
2003 ◽  
Vol 165 (1) ◽  
pp. 205-222
Author(s):  
Anton E Weisstein ◽  
Hamish G Spencer
Keyword(s):  
Genomic Imprinting ◽  
Genetic Model ◽  
Genetic System ◽  
Deleterious Mutations ◽  
Variance Minimization ◽  
Genetic Conflict ◽  
Evolutionary Genetic ◽  
The Face ◽  
Alternative Hypotheses ◽  
Selection For

Abstract A small number of mammalian loci exhibit genomic imprinting, in which only one copy of a gene is expressed while the other is silenced. At some such loci, the maternally inherited allele is inactivated; others show paternal inactivation. Several hypotheses have been put forward to explain how this genetic system could have evolved in the face of the selective advantages of diploidy. In this study, we examine the variance-minimization hypothesis, which proposes that imprinting arose through selection for reduced variation in levels of gene expression. We present an evolutionary genetic model incorporating both this selection pressure and deleterious mutations to elucidate the conditions under which imprinting could evolve. Our analysis implies that additional mechanisms such as genetic drift are required for imprinting to evolve from an initial nonimprinting state. Other predictions of this hypothesis do not appear to fit the available data as well as predictions for two alternative hypotheses, genetic conflict and the ovarian time bomb. On the basis of this evidence, we conclude that the variance-minimization hypothesis appears less adequate to explain the evolution of genomic imprinting.

scholarly journals Evolutionary Genetic Models of the Ovarian Time Bomb Hypothesis for the Evolution of Genomic Imprinting

Genetics ◽  
2002 ◽  
Vol 162 (1) ◽  
pp. 425-439 ◽  
Author(s):  
Anton E Weisstein ◽  
Marcus W Feldman ◽  
Hamish G Spencer
Keyword(s):  
Growth Factor ◽  
Genetic System ◽  
Early Embryogenesis ◽  
Genetic Models ◽  
Insulin Like Growth Factor ◽  
Deleterious Mutations ◽  
Trophoblastic Disease ◽  
Evolutionary Genetic ◽  
The Face ◽  
Selection For

Abstract At a small number of loci in eutherian mammals, only one of the two copies of a gene is expressed; the other is silenced. Such loci are said to be “imprinted,” with some having the maternally inherited allele inactivated and others showing paternal inactivation. Several hypotheses have been proposed to explain how such a genetic system could evolve in the face of the selective advantages of diploidy. In this study, we examine the “ovarian time bomb” hypothesis, which proposes that imprinting arose through selection for reduced risk of ovarian trophoblastic disease in females. We present three evolutionary genetic models that incorporate both this selection pressure and the effect of deleterious mutations to elucidate the conditions under which imprinting could evolve. Our findings suggest that the ovarian time bomb hypothesis can explain why some growth-enhancing genes active in early embryogenesis [e.g., mouse insulin-like growth factor 2 (Igf2)] have evolved to be maternally rather than paternally inactive and why the opposite imprinting status has evolved at some growth-inhibiting loci [e.g., mouse insulin-like growth factor 2 receptor (Igf2r)].

scholarly journals Understanding specialism when the jack of all trades can be the master of all

2012 ◽  
Vol 279 (1749) ◽  
pp. 4861-4869 ◽  
Author(s):  
Susanna Remold
Keyword(s):  
Habitat Use ◽  
Recent Work ◽  
Habitat Change ◽  
Directional Selection ◽  
Antagonistic Pleiotropy ◽  
Disease Emergence ◽  
Evolutionary Genetic ◽  
The Face ◽  
Genetic Mechanisms ◽  
Selection For

Specialism is widespread in nature, generating and maintaining diversity, but recent work has demonstrated that generalists can be equally fit as specialists in some shared environments. This no-cost generalism challenges the maxim that ‘the jack of all trades is the master of none’, and requires evolutionary genetic mechanisms explaining the existence of specialism and no-cost generalism, and the persistence of specialism in the face of selection for generalism. Examining three well-described mechanisms with respect to epistasis and pleiotropy indicates that sign (or antagonistic) pleiotropy without epistasis cannot explain no-cost generalism and that magnitude pleiotropy without epistasis (including directional selection and mutation accumulation) cannot explain the persistence of specialism. However, pleiotropy with epistasis can explain all. Furthermore, epistatic pleiotropy may allow past habitat use to influence future use of novel environments, thereby affecting disease emergence and populations' responses to habitat change.

scholarly journals The Evolution of X-Linked Genomic Imprinting

Genetics ◽  
2001 ◽  
Vol 158 (4) ◽  
pp. 1801-1809 ◽  
Author(s):  
Yoh Iwasa ◽  
Andrew Pomiankowski
Keyword(s):  
Gene Expression ◽  
Gene Silencing ◽  
Experimental Evidence ◽  
Genomic Imprinting ◽  
Genetic Model ◽  
Deleterious Mutations ◽  
Genomic Conflict ◽  
Quantitative Genetic ◽  
Genetic Activity ◽  
Quantitative Genetic Model

Abstract We develop a quantitative genetic model to investigate the evolution of X-imprinting. The model compares two forces that select for X-imprinting: genomic conflict caused by polygamy and sex-specific selection. Genomic conflict can only explain small reductions in maternal X gene expression and cannot explain silencing of the maternal X. In contrast, sex-specific selection can cause extreme differences in gene expression, in either direction (lowered maternal or paternal gene expression), even to the point of gene silencing of either the maternal or paternal copy. These conclusions assume that the Y chromosome lacks genetic activity. The presence of an active Y homologue makes imprinting resemble the autosomal pattern, with active paternal alleles (X- and Y-linked) and silenced maternal alleles. This outcome is likely to be restricted as Y-linked alleles are subject to the accumulation of deleterious mutations. Experimental evidence concerning X-imprinting in mouse and human is interpreted in the light of these predictions and is shown to be far more easily explained by sex-specific selection.

scholarly journals The Evolution of Genomic Imprinting

Genetics ◽  
1996 ◽  
Vol 144 (3) ◽  
pp. 1283-1295 ◽  
Author(s):  
Atsushi Mochizuki ◽  
Yasuhiko Takeda ◽  
Yoh Iwasa
Keyword(s):  
Growth Factor ◽  
Genomic Imprinting ◽  
Parental Origin ◽  
Coding Region ◽  
Placental Development ◽  
Genetic Conflict ◽  
Multiple Partners ◽  
Zygotic Gene ◽  
Mammalian Genes ◽  
Maternal Resources

Abstract In some mammalian genes, the paternally and maternally derived alleles are expressed differently: this phenomenon is called genomic imprinting. Here we study the evolution of imprinting using multivariate quantitative genetic models to examine the feasibility of the genetic conflict hypothesis. This hypothesis explains the observed imprinting patterns as an evolutionary outcome of the conflict between the paternal and maternal alleles. We consider the expression of a zygotic gene, which codes for an embryonic growth factor affecting the amount of maternal resources obtained through the placenta. We assume that the gene produces the growth factor in two different amounts depending on its parental origin. We show that genomic imprinting evolves easily if females have some probability of multiple partners. This is in conflict with the observation that not all genes controlling placental development are imprinted and that imprinting in some genes is not conserved between mice and humans. We show however that deleterious mutations in the coding region of the gene create selection against imprinting.

scholarly journals Simulating Pattern-Process Relationships to Validate Landscape Genetic Models

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
A. J. Shirk ◽  
S. A. Cushman ◽  
E. L. Landguth
Keyword(s):  
Gene Flow ◽  
Genetic Model ◽  
Strong Relationship ◽  
Genetic Isolation ◽  
Landscape Resistance ◽  
Oreamnos Americanus ◽  
Landscape Models ◽  
Genetic Pattern ◽  
Alternative Hypotheses ◽  
Landscape Genetic

Landscapes may resist gene flow and thereby give rise to a pattern of genetic isolation within a population. The mechanism by which a landscape resists gene flow can be inferred by evaluating the relationship between landscape models and an observed pattern of genetic isolation. This approach risks false inferences because researchers can never feasibly test all plausible alternative hypotheses. In this paper, rather than infer the process of gene flow from an observed genetic pattern, we simulate gene flow and determine if the simulated genetic pattern is related to the observed empirical genetic pattern. This is a form of inverse modeling and can be used to independently validate a landscape genetic model. In this study, we used this approach to validate a model of landscape resistance based on elevation, landcover, and roads that was previously related to genetic isolation among mountain goats (Oreamnos americanus) inhabiting the Cascade Range, Washington (USA). The strong relationship between the empirical and simulated patterns of genetic isolation we observed provides independent validation of the resistance model and demonstrates the utility of this approach in supporting landscape genetic inferences.

Paracelsus’ 16 th Century Philosophy Applied to Current Evolutionary Genetics

2017 ◽  
Author(s):  
Jenna Kewin
Keyword(s):  
Sixteenth Century ◽  
Intimate Relationships ◽  
Genetic Disease ◽  
Genetic Research ◽  
Evolutionary Genetics ◽  
Immunodeficiency Virus ◽  
Evolutionary Genetic ◽  
Health And Disease ◽  
Potential Impact ◽  
Selection For

Paracelsus contributed greatly to medical philosophy in the early sixteenth century, yet his reputation was so tainted by his hypocrisy that he left few followers and is often forgotten. Many aspects of his teachings, however, can be applied to current theories governing evolutionary genetic research. His claim, “Where diseases arise, one can also find the roots of health” hints at the intimate relationships between health and  disease that are the foundations of fascinating research. In many devastating medical cases, it has been  found that expression of one genetic disease can confer resistance for another. Sickle­cell anemia sufferers have an increased resistance to malaria, cystic fibrosis is associated with decreased susceptibility to  influenza, tuberculosis and cholera, and even the human immunodeficiency virus (HIV­1) is theorized to  have stemmed from a selection for resistance to the Bubonic Plague. These examples demonstrate the ambiguities in distinguishing between health and disease. While scientists today would likely scoff at Paracelsus’ dated medical rants, when they discover a disease favoured by natural selection, one of the first questions is how it could have conferred a benefit ancestrally. Applying Paracelsus’ theories to a discipline as contrary to evolutionary genetics demonstrates both the robustness of his claims, and the potential impact philosophy can have on medical, scientific and sociological questions surrounding challenging  epidemics

scholarly journals Higher-fitness yeast genotypes are less robust to deleterious mutations

Science ◽  
2019 ◽  
Vol 366 (6464) ◽  
pp. 490-493 ◽  
Author(s):  
Milo S. Johnson ◽  
Alena Martsul ◽  
Sergey Kryazhimskiy ◽  
Michael M. Desai
Keyword(s):  
Second Order ◽  
Order Selection ◽  
Deleterious Mutations ◽  
Mutational Robustness ◽  
First Order ◽  
Fitness Effects ◽  
Yeast Strains ◽  
Selection For ◽  
Microbial Systems ◽  
Insertion Mutations

Natural selection drives populations toward higher fitness, but second-order selection for adaptability and mutational robustness can also influence evolution. In many microbial systems, diminishing-returns epistasis contributes to a tendency for more-fit genotypes to be less adaptable, but no analogous patterns for robustness are known. To understand how robustness varies across genotypes, we measure the fitness effects of hundreds of individual insertion mutations in a panel of yeast strains. We find that more-fit strains are less robust: They have distributions of fitness effects with lower mean and higher variance. These differences arise because many mutations have more strongly deleterious effects in faster-growing strains. This negative correlation between fitness and robustness implies that second-order selection for robustness will tend to conflict with first-order selection for fitness.

scholarly journals The Effect of Genetic Conflict on Genomic Imprinting and Modification of Expression at a Sex-Linked Locus

Genetics ◽  
2004 ◽  
Vol 166 (1) ◽  
pp. 565-579 ◽  
Author(s):  
Hamish G. Spencer ◽  
Marcus W. Feldman ◽  
Andrew G. Clark ◽  
Anton E. Weisstein
Keyword(s):  
Genomic Imprinting ◽  
Genetic Conflict

Genetic variation in a line of mice selected to its limit for high body weight

1974 ◽  
Vol 19 (3) ◽  
pp. 273-289 ◽  
Author(s):  
W. K. Al-Murrani ◽  
R. C. Roberts
Keyword(s):  
Body Weight ◽  
Genetic Variance ◽  
Genetic Model ◽  
Random Mating ◽  
Inbred Lines ◽  
High Body Weight ◽  
High Body ◽  
Lower Body Weight ◽  
Recessive Genes ◽  
Selection For

SUMMARYA line of mice, at its limit to selection for high body weight did not decline in performance over 11 generations of random mating, neither did it respond when selection was renewed. The experiment tested a method of improving body weight by a scheme which had earlier increased litter size under similar circumstances. The scheme was to derive partially inbred lines from the plateaued line, to select during inbreeding and, finally, to cross the best inbreds. Body weight was not increased, but the study allowed further examination of the residual genetic variance in the line.During inbreeding, the inbred lines became clearly differentiated in body weight, proving that loci controlling body weight had not become fixed. There was also a significant response to selection for a lower body weight during inbreeding. The pattern of results suggested the segregation of recessive genes, detrimental to high body weight but which selection had become inefficient at removing. A genetic model compatible with the results accommodated several such recessives, perhaps as many as 10, each with an effect of about two-thirds of a standard deviation (or some equivalent combination of gene number and effect), and at frequencies of around 0·2. Nevertheless, the total improvement in body weight to be gained by their elimination was only half a gram, or less than 2 %. Thus, substantial genetic effects can occur at individual loci despite trivially low heritabilities and negligible potential gains.

scholarly journals Alternate-day feeding leads to improved glucose regulation on fasting days without significant weight loss in genetically obese mice

2019 ◽  
Vol 317 (3) ◽  
pp. R461-R469 ◽  
Author(s):  
Steven J. Swoap ◽  
Mark J. Bingaman ◽  
Elissa M. Hult ◽  
Noah J. Sandstrom
Keyword(s):  
Weight Loss ◽  
Insulin Sensitivity ◽  
Glucose Control ◽  
Genetic Model ◽  
Body Weight Loss ◽  
Littermate Control ◽  
The Face ◽  
Alternate Day Fasting ◽  
Ad Libitum ◽  
Ad Libitum Feeding

Alternate-day fasting (ADF) is effective for weight loss and increases insulin sensitivity in diet-induced obese rodents. However, the efficacy of ADF in genetic models of obesity has not been comprehensively studied. Mice that are deficient in leptin ( ob/ob mice) are obese, diabetic, and prone to deep bouts of torpor when fasted. We tested the hypotheses that an ADF protocol in ob/ob mice would result in 1) induction of torpor on fasted days, 2) minimal body weight loss if the mice experienced torpor, and 3) no improvement in glucose control in the absence of weight loss. Female ob/ob mice and littermate controls were assigned to 1) an ad libitum regimen or 2) an ADF regimen, consisting of fasting every other day with ad libitum feeding between fasts. Over a 19-day period, littermate control mice on the ADF regimen consumed the same amount of food as littermate control mice on the ad libitum regimen, whereas the ADF ob/ob mice consumed 37% less food than ad libitum ob/ob mice. Fasting days, but not fed days, led to torpor in both genotypes. Fasting days, but not fed days, led to weight loss in both genotypes relative to ad libitum controls. Fasting days, but not fed days, produced enhanced insulin sensitivity in both genotypes and normalized circulating glucose in ob/ob mice. These data demonstrate improved glucose control on fasting days with the use of ADF in a genetic model of obesity in the face of minimal weight loss.

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