Genomic imprinting in mammals: its life cycle, molecular mechanisms and reprogramming

Li, Yufeng; Sasaki, Hidetada

doi:10.1038/cr.2011.15

Cited by 125 publications

(91 citation statements)

References 73 publications

(96 reference statements)

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“…16 However, the differential methylation is erased in primordial germ cells in each generation before the new imprints are set. [17][18][19] THE MECHANISM OF IMPRINT ESTABLISHMENT IN THE GERMLINE The first step of the imprinting cycle, imprint establishment, occurs in male and female gametogenesis. Imprint establishment takes place in growing oocytes in females and prospermatogonia in males.…”

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Genomic imprinting and its relevance to congenital disease, infertility, molar pregnancy and induced pluripotent stem cell

Tomizawa

Sasaki

2012

J Hum Genet

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Genomic imprinting is an epigenetic gene-marking phenomenon that occurs in the germline, whereby genes are expressed from only one of the two parental copies in embryos and adults. Imprinting is essential for normal mammalian development and its disruption can cause various developmental defects and diseases. The process of imprinting in the germline involves DNA methylation of the imprint control regions (ICRs), and resulting parental-specific methylation imprints are maintained in the zygote and act as the marks controlling imprinted gene expression. Recent studies in mice have revealed new factors involved in imprint establishment during gametogenesis and maintenance during early development. Clinical studies have identified cases of imprinting disorders where involvement of factors shared by multiple ICRs for establishment or maintenance is suspected. These include Beckwith-Wiedemann syndrome, transient neonatal diabetes, Silver-Russell syndrome and others. More severe disruptions can lead to recurrent molar pregnancy, miscarriage or infertility. Imprinting defects may also occur during assisted reproductive technology or cell reprogramming. In this review, we summarize our current knowledge on the mechanisms of imprint establishment and maintenance, and discuss the relationship with various human disorders.

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Genomic imprinting and its relevance to congenital disease, infertility, molar pregnancy and induced pluripotent stem cell

Tomizawa

Sasaki

2012

J Hum Genet

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“…In addition to DNA methylation, imprinting in both plants and animals is also regulated by histone methylation (50,52,79,80). The Polycomb Repressive Complex 2 (PRC2) catalyzes trimethylation of histone H3 at lysine 27 (H3K27me3), a repressive mark associated with gene silencing.…”

Section: Polycomb and Histone Methylationmentioning

confidence: 99%

Seed evolution: parental conflicts in a multi-generational household

Pires

2014

BioMolecular Concepts

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Seeds are multi-generational structures containing a small embryonic plant enclosed in layers of diverse parental origins. The evolution of seeds was a pinnacle in an evolutionary trend towards a progressive retention of embryos and gametes within parental tissue. This strategy, which dates back to the first land plants, allowed an increased protection and nourishing of the developing embryo. Flowering plants took parental control one step further with the evolution of a biparental endosperm that derives from a second parallel fertilization event. The endosperm directly nourishes the developing embryo and allows not only the maternal genes, but also paternal genes, to play an active role during seed development. The appearance of an endosperm set the conditions for the manifestation of conflicts of interest between maternal and paternal genomes over the allocation of resources to the developing embryos. As a consequence, a dynamic balance was established between maternal and paternal gene dosage in the endosperm, and maintaining a correct balance became essential to ensure a correct seed development. This balance was achieved in part by changes in the genetic constitution of the endosperm and through epigenetic mechanisms that allow a differential expression of alleles depending on their parental origin. This review discusses the evolutionary steps that resulted in the appearance of seeds and endosperm, and the epigenetic and genetic mechanisms that allow a harmonious coinhabitance of multiple generations within a single seed.

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“…[43][44][45][46][47] The parental-specific methylation at DMRs is maintained in somatic cells during the life of the individual, but is reset (erased and reestablished) in the germ line between generations. 48 Part of this imprint resetting occurs in the embryonic and fetal germ cells, which undergo global epigenetic remodeling. 49 Because imprinted genes are functionally haploid, a single epigenetic hit by EDs could have serious consequences to development and health.…”

Section: Effects Of Endocrine Disruptors On Imprinted Gene Expressionmentioning

confidence: 99%

Effects of endocrine disruptors on imprinted gene expression in the mouse embryo

Kang¹,

Iqbal²,

Tran³

et al. 2011

Epigenetics

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Genomic imprinting in mammals: its life cycle, molecular mechanisms and reprogramming

Cited by 125 publications

References 73 publications

Genomic imprinting and its relevance to congenital disease, infertility, molar pregnancy and induced pluripotent stem cell

Genomic imprinting and its relevance to congenital disease, infertility, molar pregnancy and induced pluripotent stem cell

Seed evolution: parental conflicts in a multi-generational household

Effects of endocrine disruptors on imprinted gene expression in the mouse embryo

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