clustered in 25 genomic regions, have been identified elements and the specification of chromosomal domains, mice and humans. Hudson, Kulinski, Huetter and the review focuses mainly on the less obvious effects of Barlow show that the different patterns of imprinted ATP-dependent nucleosome remodeling enzymes. These gene expression observed in embryonic tissues and extra- enzymes have been shown to disrupt the ionic associa- xplained by differences in DNA methylation and Can be tion of DNA with histones in nucleosomes or nucleo- ive histone modifications. They conclude that genes with flexibility, allowing it to respond to environmental displaying imprinted expression only in extra-embryonic clues. Finding out how an organism integrates such isms than genes with widespread expression. As Koehler new insights into genotype-environment interactions eld tissues may be regulate pigenetic mechan es into its development promises to yie and Weinhofer-Molisch describe, plants are known to One important clue to the nature of epigenetic not restricted to th printing in the endosperm, which is phenomena is that they seem to involve TEs. Indeed, contribute to the next generation. The authors then as TEs, and by recruiting the epigenetic machinery, these ummarize the roles of histone methylation and of the sequences could mark the ICRs defined above, thus lycomb group proteins. They suggest mechanisms that determining the epigenetic status of the affected alleles could explain how epigenetic marks are reprogrammed in Moreover, epigenetic processes involving DNA methyla gametes. Although this discussion clearly shows that tion-demethylation, histone modifications and RNA imprinted genes have an important role in the develop- interference, are all known to influence the expression mental process, recent studies have also reported differ- of various TEs during development. Because TEs are ential DNA methylation between alleles at nonimprinted known to be able to activate-deactivate various genes loci in human autosomes, which seems to involve about and to regulate host genes differentially during embry 10% of all genes( Schilling et al., 2009; Zhang et al., 2009). nic development, as reported in the mouse(Peaston et al processes, which often involve the decrease in DNA It is well known that early in female development, in methylation 1(DDM1)chromatin remodeling protein mammals, one of the two X chromosomes is transcription- that controls TE expression, may contribute to loss of ally silenced, which compe fitness in Arabidopsis and to meiotic failure in mouse Wutz summarize the mechanistic concepts in X inactivation evelated tes It is thus believed that organisms have that underlie this dosage compensation in mammals. fering RNAs as discussed by Teixeira and Colot, Random X inactivation depends on the noncoding Xist intended to thwart the effects of TEs. Because the RNA in the inactive X chromosome (Xi)and seems to be conserved among placental mammals, but seems to differ developing germline, TEs may take this opportunity to in other mammals. The silencing of genes on the Xi is transpose at a high rate and thus invade the host mediated by various epigenetic factors, such as the histone genome. Why then are TEs not entirely repressed in the variant macroH2A, which are associated with silent germline? Zamudio and Bourchis give support to the hromatin. Leeb and Wutz conclude that genes and idea that this time-limited loss of repression allows the ongenic sequences undergo similar epigenetic modifica- genome to detect rogue elements and force them into ions on the Xi. The authors then show how the cell counts repression. The germline can therefore be seen as playing and chooses the appropriate number of X chromosomes to an insidious trick on the tEs by forcing them to revea inactivate, how chromosome-wide gene repression is their existence and their capacity to injure the genome coordinated and how a stable inactive x chromosome and subsequent generations. However, the alternative established. They detail the conservation and divergence of hypothesis that TEs simply exploit the open chromatin to this mechanism in different mammalian species. It is not transpose cannot be entirely ruled out. clear whether the mechanism underlying X inactivation is By their effects modifying the genomic methylation specific to mammal or also occurs in other species and this state and changing the structure of chromatin, the warrants further investigation environmental conditions encountered during the devele DNA methylation, DNA-associated protein modifica- ment and lifetime of an organism have been reported to tions and RNA interference, are all epigenetic processes have a major impact on the expression of various genes, that are closely connected to chromatin structure. In their including TEs, and their effects have even been observed review, Chioda and Becker summarize the role of even in subsequent generations(see Kristensen et al., 2009) nucleosome remodeling factors in regulating dna Diets or exposure to chemicals that interfere with the dnA accessibility within chromatin, notably during transcrip- methylating enzymes involved may have major effects tion initiation, and explore the impact of the newly both on normal physiology and on the manifestation of emerging ideas, suggesting that remodeling complexes diseases such as cancers. In their review, Bollati and shape the epigenome during development and stem cell Baccarelli identify a number of environmental toxicants, differentiation; Desvoyes, de la Paz Sanchez, Ramirez- such as metals, phytoestrogens, hydrocarbons, dioxin Parra and Gutierrez (2010)then review the impact of biphenyls, phthalates and several classes of pesticide that nucleosome dynamics and histone modifications on cell can alter epigenetic states and may therefore have health- proliferation during Arabidopsis development. Because related effects. They therefore. discuss the available aspects such as posttranslational modifications of his- evidence of transgenerational environmental effects, which tones and the constituents of nucleosomes are known for have been clearly shown to occur in mouse and plants, but to affect DNA accessibility in genes and regulatory which are still contentious in human beings, even though Heredityclustered in 25 genomic regions, have been identified in mice and humans. Hudson, Kulinski, Huetter and Barlow show that the different patterns of imprinted gene expression observed in embryonic tissues and extra￾embryonic tissues, such as the placenta in mammals, can be explained by differences in DNA methylation and repres￾sive histone modifications. They conclude that genes displaying imprinted expression only in extra-embryonic tissues may be regulated by different epigenetic mechan￾isms than genes with widespread expression. As Koehler and Weinhofer-Molisch describe, plants are known to display genomic imprinting in the endosperm, which is not restricted to this tissue but extends to tissues that contribute to the next generation. The authors then summarize the roles of histone methylation and of the polycomb group proteins. They suggest mechanisms that could explain how epigenetic marks are reprogrammed in gametes. Although this discussion clearly shows that imprinted genes have an important role in the develop￾mental process, recent studies have also reported differ￾ential DNA methylation between alleles at nonimprinted loci in human autosomes, which seems to involve about 10% of all genes (Schilling et al., 2009; Zhang et al., 2009). Understanding the exact role of these genes is likely to be of the utmost relevance for our understanding of how genomes are regulated. It is well known that early in female development, in mammals, one of the two X chromosomes is transcription￾ally silenced, which compensates for the unequal copy number of X-linked genes in males and females. Leeb and Wutz summarize the mechanistic concepts in X inactivation that underlie this dosage compensation in mammals. Random X inactivation depends on the noncoding Xist RNA in the inactive X chromosome (Xi) and seems to be conserved among placental mammals, but seems to differ in other mammals. The silencing of genes on the Xi is mediated by various epigenetic factors, such as the histone variant macroH2A, which are associated with silent chromatin. Leeb and Wutz conclude that genes and nongenic sequences undergo similar epigenetic modifica￾tions on the Xi. The authors then show how the cell counts and chooses the appropriate number of X chromosomes to inactivate, how chromosome-wide gene repression is coordinated and how a stable inactive X chromosome is established. They detail the conservation and divergence of this mechanism in different mammalian species. It is not clear whether the mechanism underlying X inactivation is specific to mammal or also occurs in other species and this warrants further investigation. DNA methylation, DNA-associated protein modifica￾tions and RNA interference, are all epigenetic processes that are closely connected to chromatin structure. In their review, Chioda and Becker summarize the role of nucleosome remodeling factors in regulating DNA accessibility within chromatin, notably during transcrip￾tion initiation, and explore the impact of the newly emerging ideas, suggesting that remodeling complexes shape the epigenome during development and stem cell differentiation; Desvoyes, de la Paz Sanchez, Ramirez￾Parra and Gutierrez (2010) then review the impact of nucleosome dynamics and histone modifications on cell proliferation during Arabidopsis development. Because aspects such as posttranslational modifications of his￾tones and the constituents of nucleosomes are known for to affect DNA accessibility in genes and regulatory elements and the specification of chromosomal domains, the review focuses mainly on the less obvious effects of ATP-dependent nucleosome remodeling enzymes. These enzymes have been shown to disrupt the ionic associa￾tion of DNA with histones in nucleosomes or nucleo￾some assembly intermediates and to endow chromatin with flexibility, allowing it to respond to environmental clues. Finding out how an organism integrates such chromatin changes into its development promises to yield new insights into genotype–environment interactions. One important clue to the nature of epigenetic phenomena is that they seem to involve TEs. Indeed, imprinted genes often contain repeated sequences, such as TEs, and by recruiting the epigenetic machinery, these sequences could mark the ICRs defined above, thus determining the epigenetic status of the affected alleles. Moreover, epigenetic processes involving DNA methyla￾tion–demethylation, histone modifications and RNA interference, are all known to influence the expression of various TEs during development. Because TEs are known to be able to activate–deactivate various genes and to regulate host genes differentially during embryo￾nic development, as reported in the mouse (Peaston et al., 2004), many changes in individual phenotypes are expected. This is consistent with reports that epigenetic processes, which often involve the decrease in DNA methylation 1 (DDM1) chromatin remodeling protein that controls TE expression, may contribute to loss of fitness in Arabidopsis and to meiotic failure in mouse spermatocytes. It is thus believed that organisms have developed defense mechanisms, mostly based on inter￾fering RNAs as discussed by Teixeira and Colot, intended to thwart the effects of TEs. Because the epigenetic repression of TEs is relaxed in the early￾developing germline, TEs may take this opportunity to transpose at a high rate and thus invade the host genome. Why then are TEs not entirely repressed in the germline? Zamudio and Bourc’his give support to the idea that this time-limited loss of repression allows the genome to detect rogue elements and force them into repression. The germline can therefore be seen as playing an insidious trick on the TEs by forcing them to reveal their existence and their capacity to injure the genome and subsequent generations. However, the alternative hypothesis that TEs simply exploit the open chromatin to transpose cannot be entirely ruled out. By their effects modifying the genomic methylation state and changing the structure of chromatin, the environmental conditions encountered during the develop￾ment and lifetime of an organism have been reported to have a major impact on the expression of various genes, including TEs, and their effects have even been observed even in subsequent generations (see Kristensen et al., 2009). Diets or exposure to chemicals that interfere with the DNA￾methylating enzymes involved may have major effects both on normal physiology and on the manifestation of diseases such as cancers. In their review, Bollati and Baccarelli identify a number of environmental toxicants, such as metals, phytoestrogens, hydrocarbons, dioxin, biphenyls, phthalates and several classes of pesticide that can alter epigenetic states and may therefore have health￾related effects. They therefore discuss the available evidence of transgenerational environmental effects, which have been clearly shown to occur in mouse and plants, but which are still contentious in human beings, even though Editorial 2 Heredity