G-enomic imprinting is an epigenetic mechanism that produces functional differences between the paternal and mammal genomes and plays an essential role in mammalian development and growth. There are a number of genes ...G-enomic imprinting is an epigenetic mechanism that produces functional differences between the paternal and mammal genomes and plays an essential role in mammalian development and growth. There are a number of genes in our genomes that are subject to genomic imprinting where one parent＇s copy of the gene is expressed while the other is silent. Silencing of one allele predetermines that any function ascribed to that gene are now dependant on the single active copy. Possession of only a single active allele can lead to deleterious health consequences in humans. If imprinted genes are crucial in mammalian development, one would also expect mutations in these genes to cause diseases. Since imprinting is an epigenetic mechanism, mistakes in maintaining epigenetic mark also cause imprinting disorders. Here we in this review focus on the current understanding of this unique genetic mechanism more than two decades after the first description of the imprinting phenomenon was given by McGrath and Solter. Although the possible molecular mechanisms by which imprinting is imposed and maintained are being identified, we have a long way to go in understanding the molecular mechanisms that regulate the expression of these oddly behaving genes, the function of imprinting and the evolution. Post genomic technologies might ultimately lead to a better understanding of the ＇imprinting effects＇.展开更多
Polycomb group proteins （PcG） play important roles in epigenetic regulation of gene expression. Some core PeG proteins, such as Enhancer of Zeste （E（z））, Suppressor of Zeste （12） （Su（z）12）, and Extra Sex C...Polycomb group proteins （PcG） play important roles in epigenetic regulation of gene expression. Some core PeG proteins, such as Enhancer of Zeste （E（z））, Suppressor of Zeste （12） （Su（z）12）, and Extra Sex Combs （ESC）, are conserved in plants. The rice genome contains two E（z）-Iike genes, OsiEZ1 and OsCLF, two homologs of Su（z）12, OsEMF2a and OsEMF2b, and two ESC-like genes, OsFIE1 and OsFIE2. OsFIE1 is expressed only in endosperm; the maternal copy is expressed while the paternal copy is not active. Other rice PcG genes are expressed in a wide range of tissues and are not imprinted in the endosperm. The two E（z）-Iike genes appear to have duplicated before the separation of the dicots and monocots; the two homologs of Su（z）12 possibly duplicated during the evolution of the Gramineae and the two ESC- like genes are likely to have duplicated in the ancestor of the grasses. No homologs of the Arabidopsis seed-expressed PcG genes MEA and FIS2 were identified in the rice genome. We have isolated T-DNA insertion lines in the rice homologs of three PcG genes. There is no autonomous endosperm development in these T-DNA insertion lines. One line with a T-DNA insertion in OsEMF2b displays pleiotropic phenotypes including altered flowering time and abnormal flower organs, suggesting important roles in rice development for this gene.展开更多
Sexual imprinting is a common mechanism of mate preference learning. It is thought to influence how traits evolve and in some cases to promote speciation. Recently there has been increasing interest in how sexual impr...Sexual imprinting is a common mechanism of mate preference learning. It is thought to influence how traits evolve and in some cases to promote speciation. Recently there has been increasing interest in how sexual imprinting itself evolves. Theoretical work on polygynous mating systems predicts that females will evolve paternal imprinting, which means they learn to prefer phenotypes expressed by their fathers. In nature however, females of some species learn to prefer phenotypes expressed by their mothers instead. We used a dynamical systems model and tools from adaptive dynamics to study how sexual imprinting evolves in species with socially monogamous mating systems. We considered cases in which the target trait for imprinting is un- der viability selection but is not a reliable signal of paternal investment. Thus, the target trait signals the genetic benefits rather than the parental care benefits of mate choice. When mating is socially monogamous and there is some extra-pair patemity, we show that maternal imprinting can be favored over paternal imprinting. Counterintuitively, females often become choosier when selecting social partners in systems where extra-pair mating is more frequent. That is, females may be more selective when choosing social partners that will sire a smaller percentage of their offspring. Our results offer new testable hypotheses, and ad- vance our understanding of the mechanisms that drive the evolution of mate choice strategies in nature .展开更多
In mammals,genomic imprinting confers developmental asymmetry and complementation on the parental genomes and makes both parental genomes essential for complete development.Genomic imprinting is,therefore,the first re...In mammals,genomic imprinting confers developmental asymmetry and complementation on the parental genomes and makes both parental genomes essential for complete development.Genomic imprinting is,therefore,the first regulatory step of genome-wide gene expression of embryogenesis and thought to be the epigenetic foundation of bisexual reproduction.However,how the genomic imprinting is originated,established and maintained during vertebrate evolution remains unknown.Because no endogenous imprinting gene has been identified in non-mammalian vertebrates,genomic imprinting is thought to be a unique evolutionary event of mammals.Here,in order to study the evolutionary origin of genomic imprinting in vertebrates,we examined whether parent-specific methylation occurred in the teleost homologue of mammalian imprinting gene during gametogenesis.Bisulfate sequencing analy-sis showed that,as mammalian Igf2 CpG island,goldfish Igf2 CpG island was a parental differentially methylated region(DMR) that was hypermethylated in sperm but unmethylated in eggs.Unlike mam-malian imprinting gene DMR,however,the parent-specific methylation pattern of goldfish Igf2 DMR was not maintained during embryogenesis,suggesting that the parent-specific methylation of goldfish Igf2 DMR might be a primitive genomic imprinting in the early period of vertebrate evolution.These results indicate that the evolutionary foundation of genomic imprinting exists in lower vertebrates and genomic imprinting should not be considered as a unique evolutionary event of mammals.展开更多
DNA methylation is an epigenetic modification that plays a crucial role in various regulatory processes,including gene expression regulation,transposable element repression,and genomic imprinting.However,most studies ...DNA methylation is an epigenetic modification that plays a crucial role in various regulatory processes,including gene expression regulation,transposable element repression,and genomic imprinting.However,most studies on DNA methylation have been conducted in humans and other model species,whereas the dynamics of DNA methylation across mammals remain poorly explored,limiting our understanding of epigenomic evolution in mammals and the evolutionary impacts of conserved and lineage-specific DNA methylation.Here,we generated and gathered comparative epigenomic data from 13 mammalian species,including two marsupial species,to demonstrate that DNA methylation plays critical roles in several aspects of gene evolution and species trait evolution.We found that the species-specific DNA methylation of promoters and noncoding elements correlates with species-specific traits such as body patterning,indicating that DNA methylation might help establish or maintain interspecies differences in gene regulation that shape phenotypes.For a broader view,we investigated the evolutionary histories of 88 known imprinting control regions across mammals to identify their evolutionary origins.By analyzing the features of known and newly identified potential imprints in all studied mammals,we found that genomic imprinting may function in embryonic development through the binding of specific transcription factors.Our findings show that DNA methylation and the complex interaction between the genome and epigenome have a significant impact on mammalian evolution,suggesting that evolutionary epigenomics should be incorporated to develop a unified evolutionary theory.展开更多
文摘G-enomic imprinting is an epigenetic mechanism that produces functional differences between the paternal and mammal genomes and plays an essential role in mammalian development and growth. There are a number of genes in our genomes that are subject to genomic imprinting where one parent＇s copy of the gene is expressed while the other is silent. Silencing of one allele predetermines that any function ascribed to that gene are now dependant on the single active copy. Possession of only a single active allele can lead to deleterious health consequences in humans. If imprinted genes are crucial in mammalian development, one would also expect mutations in these genes to cause diseases. Since imprinting is an epigenetic mechanism, mistakes in maintaining epigenetic mark also cause imprinting disorders. Here we in this review focus on the current understanding of this unique genetic mechanism more than two decades after the first description of the imprinting phenomenon was given by McGrath and Solter. Although the possible molecular mechanisms by which imprinting is imposed and maintained are being identified, we have a long way to go in understanding the molecular mechanisms that regulate the expression of these oddly behaving genes, the function of imprinting and the evolution. Post genomic technologies might ultimately lead to a better understanding of the ＇imprinting effects＇.
文摘Polycomb group proteins （PcG） play important roles in epigenetic regulation of gene expression. Some core PeG proteins, such as Enhancer of Zeste （E（z））, Suppressor of Zeste （12） （Su（z）12）, and Extra Sex Combs （ESC）, are conserved in plants. The rice genome contains two E（z）-Iike genes, OsiEZ1 and OsCLF, two homologs of Su（z）12, OsEMF2a and OsEMF2b, and two ESC-like genes, OsFIE1 and OsFIE2. OsFIE1 is expressed only in endosperm; the maternal copy is expressed while the paternal copy is not active. Other rice PcG genes are expressed in a wide range of tissues and are not imprinted in the endosperm. The two E（z）-Iike genes appear to have duplicated before the separation of the dicots and monocots; the two homologs of Su（z）12 possibly duplicated during the evolution of the Gramineae and the two ESC- like genes are likely to have duplicated in the ancestor of the grasses. No homologs of the Arabidopsis seed-expressed PcG genes MEA and FIS2 were identified in the rice genome. We have isolated T-DNA insertion lines in the rice homologs of three PcG genes. There is no autonomous endosperm development in these T-DNA insertion lines. One line with a T-DNA insertion in OsEMF2b displays pleiotropic phenotypes including altered flowering time and abnormal flower organs, suggesting important roles in rice development for this gene.
文摘Sexual imprinting is a common mechanism of mate preference learning. It is thought to influence how traits evolve and in some cases to promote speciation. Recently there has been increasing interest in how sexual imprinting itself evolves. Theoretical work on polygynous mating systems predicts that females will evolve paternal imprinting, which means they learn to prefer phenotypes expressed by their fathers. In nature however, females of some species learn to prefer phenotypes expressed by their mothers instead. We used a dynamical systems model and tools from adaptive dynamics to study how sexual imprinting evolves in species with socially monogamous mating systems. We considered cases in which the target trait for imprinting is un- der viability selection but is not a reliable signal of paternal investment. Thus, the target trait signals the genetic benefits rather than the parental care benefits of mate choice. When mating is socially monogamous and there is some extra-pair patemity, we show that maternal imprinting can be favored over paternal imprinting. Counterintuitively, females often become choosier when selecting social partners in systems where extra-pair mating is more frequent. That is, females may be more selective when choosing social partners that will sire a smaller percentage of their offspring. Our results offer new testable hypotheses, and ad- vance our understanding of the mechanisms that drive the evolution of mate choice strategies in nature .
基金Supported by National Natural Science Foundation of China (Grant No.30430370)National Key Basic Research Development Program of China (Grant No.2004CB117401)
文摘In mammals,genomic imprinting confers developmental asymmetry and complementation on the parental genomes and makes both parental genomes essential for complete development.Genomic imprinting is,therefore,the first regulatory step of genome-wide gene expression of embryogenesis and thought to be the epigenetic foundation of bisexual reproduction.However,how the genomic imprinting is originated,established and maintained during vertebrate evolution remains unknown.Because no endogenous imprinting gene has been identified in non-mammalian vertebrates,genomic imprinting is thought to be a unique evolutionary event of mammals.Here,in order to study the evolutionary origin of genomic imprinting in vertebrates,we examined whether parent-specific methylation occurred in the teleost homologue of mammalian imprinting gene during gametogenesis.Bisulfate sequencing analy-sis showed that,as mammalian Igf2 CpG island,goldfish Igf2 CpG island was a parental differentially methylated region(DMR) that was hypermethylated in sperm but unmethylated in eggs.Unlike mam-malian imprinting gene DMR,however,the parent-specific methylation pattern of goldfish Igf2 DMR was not maintained during embryogenesis,suggesting that the parent-specific methylation of goldfish Igf2 DMR might be a primitive genomic imprinting in the early period of vertebrate evolution.These results indicate that the evolutionary foundation of genomic imprinting exists in lower vertebrates and genomic imprinting should not be considered as a unique evolutionary event of mammals.
基金funded by National Natural Science Foundation of China(31821001)the Strategic Priority Research Program of the Chinese Academy of Sciences(XDB31000000)the PI Project of Southern Marine Science and Engineering Guangdong Laboratory(Guangzhou)(GML2020GD0804).
文摘DNA methylation is an epigenetic modification that plays a crucial role in various regulatory processes,including gene expression regulation,transposable element repression,and genomic imprinting.However,most studies on DNA methylation have been conducted in humans and other model species,whereas the dynamics of DNA methylation across mammals remain poorly explored,limiting our understanding of epigenomic evolution in mammals and the evolutionary impacts of conserved and lineage-specific DNA methylation.Here,we generated and gathered comparative epigenomic data from 13 mammalian species,including two marsupial species,to demonstrate that DNA methylation plays critical roles in several aspects of gene evolution and species trait evolution.We found that the species-specific DNA methylation of promoters and noncoding elements correlates with species-specific traits such as body patterning,indicating that DNA methylation might help establish or maintain interspecies differences in gene regulation that shape phenotypes.For a broader view,we investigated the evolutionary histories of 88 known imprinting control regions across mammals to identify their evolutionary origins.By analyzing the features of known and newly identified potential imprints in all studied mammals,we found that genomic imprinting may function in embryonic development through the binding of specific transcription factors.Our findings show that DNA methylation and the complex interaction between the genome and epigenome have a significant impact on mammalian evolution,suggesting that evolutionary epigenomics should be incorporated to develop a unified evolutionary theory.
