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

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 Genetic conflict, genomic imprinting and establishment of the epigenotype in relation to growth

Reproduction ◽  
2001 ◽  
pp. 185-193 ◽  
Author(s):  
T Moore
Keyword(s):  
Genomic Imprinting ◽  
Parental Investment ◽  
Tandem Repeats ◽  
Cpg Islands ◽  
Subsequent Development ◽  
Imprinted Genes ◽  
Growth Disorders ◽  
Genetic Loci ◽  
Mammalian Embryo ◽  
Genetic Conflict

Genomic imprinting is the process that differentially modifies the parental alleles at certain genetic loci in the parental germlines. Such modifications of DNA and chromatin are somatically heritable and cause unequal expression of the parental alleles during subsequent development. In mammals, imprinted genes encode a relatively small number of functionally heterogeneous proteins. Nevertheless, imprinted genes exert important effects, primarily on fetal development, and their deregulation is implicated in a variety of pathologies including sporadic, inherited and induced growth disorders. Imprinted loci show several unusual structural and functional characteristics that may be related to mechanistic aspects of mono-allelic expression or to modes of evolution of imprinted genetic loci. Typically, imprinted genes are clustered in certain genomic regions and have relatively reduced intronic DNA content relative to non-imprinted genes. In addition, their regulatory regions frequently contain a combination of features including tandem repeats associated with differentially methylated CpG islands and overlapping transcription of coding or non-coding RNAs. The evolution of imprinting can be understood as the stable outcome of sexual selection acting differently on the parental alleles of genes that influence parental investment in offspring. Consistent with this explanation, imprinted genes are expressed predominantly during embryonic and postnatal development in mammals and in the developing endosperm of plants, and maternal or paternal expression at imprinted loci is associated with reduced or increased parental investment, respectively. Such selective forces have implications for understanding mechanistic aspects of genome reprogramming in the early mammalian embryo.

An earlier formulation of the genetic conflict hypothesis of genomic imprinting

2006 ◽  
Vol 38 (3) ◽  
pp. 271-271 ◽  
Author(s):  
David Haig ◽  
Mark Westoby
Keyword(s):  
Genomic Imprinting ◽  
Genetic Conflict

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 Males That Silence Their Father’s Genes: Genomic Imprinting of a Complete Haploid Genome

2021 ◽  
Author(s):  
Andrés G de la Filia ◽  
Andrew J Mongue ◽  
Jennifer Dorrens ◽  
Hannah Lemon ◽  
Dominik R Laetsch ◽  
...  
Keyword(s):  
Genomic Imprinting ◽  
Reproductive Tract ◽  
Expression Patterns ◽  
Mendelian Inheritance ◽  
Specific Gene ◽  
Paternal Genome ◽  
Genetic Conflict ◽  
Maternal Genome ◽  
Allele Specific ◽  
Parent Of Origin

AbstractGenetic conflict is considered a key driver in the evolution of reproductive systems with non-Mendelian inheritance, where parents do not contribute equally to the genetic makeup of their offspring. One of the most extraordinary examples of non-Mendelian inheritance is paternal genome elimination (PGE), a form of haplodiploidy which has evolved repeatedly across arthropods. Under PGE, males are diploid but only transmit maternally inherited chromosomes, while the paternally inherited homologues are excluded from sperm. This asymmetric inheritance is thought to have evolved through an evolutionary arms race between the paternal and maternal genomes over transmission to future generations. In several PGE clades, such as the mealybugs (Hemiptera: Pseudococcidae), paternal chromosomes are not only eliminated from sperm, but also heterochromatinized early in development and thought to remain inactive, which could result from genetic conflict between parental genomes. Here, we present a parent-of-origin allele-specific transcriptome analysis in male mealybugs showing that expression is globally biased toward the maternal genome. However, up to 70% of somatically expressed genes are to some degree paternally expressed, while paternal genome expression is much more restricted in the male reproductive tract, with only 20% of genes showing paternal contribution. We also show that parent-of-origin-specific gene expression patterns are remarkably similar across genotypes, and that genes with completely biparental expression show elevated rates of molecular evolution. Our results provide the clearest example yet of genome-wide genomic imprinting in insects and enhance our understanding of PGE, which will aid future empirical tests of evolutionary theory regarding the origin of this unusual reproductive strategy.

scholarly journals Males that silence their father’s genes: genomic imprinting of a complete haploid genome

2020 ◽  
Author(s):  
Andrés G. de la Filia ◽  
Andrew J. Mongue ◽  
Jennifer Dorrens ◽  
Hannah Lemon ◽  
Dominik R. Laetsch ◽  
...  
Keyword(s):  
Gene Expression ◽  
Genomic Imprinting ◽  
Mendelian Inheritance ◽  
Specific Gene ◽  
Paternal Genome ◽  
Genetic Conflict ◽  
Specific Gene Expression ◽  
Maternal Genome ◽  
Allele Specific ◽  
Parent Of Origin

AbstractGenetic conflict is considered a key driver in the evolution of new reproductive and sex determining systems. In particular, reproductive strategies with non-Mendelian inheritance, where parents do not contribute equally to the genetic makeup of their offspring. One of the most extraordinary examples of non-Mendelian inheritance is paternal genome elimination (PGE), a form of haplodiploidy which has evolved repeatedly across arthropods. Under PGE, males are diploid but only transmit maternally-inherited chromosomes to their offspring, while the paternal homologues are excluded from sperm. This asymmetric inheritance is thought to have evolved through an evolutionary arms race between paternal and maternal genomes over transmission to future generations. In several clades with PGE, such as the mealybugs (Hemiptera: Pseudococcidae), paternal chromosomes are not just eliminated from sperm, but also heterochromatinised early in development and thought to remain inactive. Such paternal genome silencing could alleviate genetic conflict between paternal alleles over transmission. However, it is unclear if paternal chromosomes are indeed genetically inert in both soma and germline. Here, we present a parent-of-origin allele-specific transcriptome analysis in male mealybugs. We show that expression is globally biased towards the maternal genome, but detect activity of paternal chromosomes in both somatic and reproductive tissues. Up to 70% of somatically-expressed genes are to some degree paternally-expressed. However, paternal genome expression is much more restricted in the testis, with only 20% of genes showing paternal contribution. Finally, we show that the patterns of parent-of-origin-specific gene expression are remarkably similar across genotypes and that those genes with biparental expression show elevated rates of molecular evolution. Our results provide the clearest example yet of genome-wide genomic imprinting (parent-of-origin specific gene expression) in insects. Furthermore, it enhances our understanding of PGE, which will aid future empirical tests of evolutionary theory regarding the origin of this unusual reproductive strategy.

scholarly journals Genetic conflict reflected in tissue-specific maps of genomic imprinting in human and mouse

2015 ◽  
Vol 47 (5) ◽  
pp. 544-549 ◽  
Author(s):  
Tomas Babak ◽  
Brian DeVeale ◽  
Emily K Tsang ◽  
Yiqi Zhou ◽  
Xin Li ◽  
...  
Keyword(s):  
Genomic Imprinting ◽  
Genetic Conflict ◽  
Tissue Specific ◽  
Human And Mouse

scholarly journals Genetic Conflicts, Multiple Paternity and the Evolution of Genomic Imprinting

Genetics ◽  
1998 ◽  
Vol 148 (2) ◽  
pp. 893-904
Author(s):  
Hamish G Spencer ◽  
Marcus W Feldman ◽  
Andrew G Clark
Keyword(s):  
Genomic Imprinting ◽  
Multiple Paternity ◽  
The Other ◽  
Growth Inhibitors ◽  
Genetic Conflict ◽  
Quantitative Genetic ◽  
Mean Fitness ◽  
Genetic Conflicts ◽  
Maternal Imprinting ◽  
Over Time

Abstract We present nine diallelic models of genetic conflict in which one allele is imprintable and the other is not to examine how genomic imprinting may have evolved. Imprinting is presumed to be either maternal (i.e., the maternally derived gene is inactivated) or paternal. Females are assumed to be either completely monogamous or always bigamous, so that we may see any effect of multiple paternity. In contrast to previous verbal and quantitative genetic models, we find that genetic conflicts need not lead to paternal imprinting of growth inhibitors and maternal imprinting of growth enhancers. Indeed, in some of our models—those with strict monogamy—the dynamics of maternal and paternal imprinting are identical. Multiple paternity is not necessary for the evolution of imprinting, and in our models of maternal imprinting, multiple paternity has no effect at all. Nevertheless, multiple paternity favors the evolution of paternal imprinting of growth inhibitors and hinders that of growth enhancers. Hence, any degree of multiple paternity means that growth inhibitors are more likely to be paternally imprinted, and growth enhancers maternally so. In all of our models, stable polymorphism of imprinting status is possible and mean fitness can decrease over time. Neither of these behaviors have been predicted by previous models.

Sign in / Sign up

Export Citation Format

Share Document