Imprinting of Genes and the Barker Hypothesis

Young, Lorraine

doi:10.1375/1369052012632

Cited by 58 publications

(15 citation statements)

References 61 publications

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“…Imprint status and specificity of allele expression can also vary with species. Some genes are reciprocally imprinted in mice and humans, while others are imprinted in mice but not in humans at equivalent stages of development [4, 13]. In the germ line, all imprint marks are erased during early development by genome-wide demethylation and are then re-established during late fetal and early postnatal life [14].…”

Section: Imprinted Genesmentioning

confidence: 99%

“…When mouse blastocysts cultured with serum are transferred to recipient mothers, the fetuses are small at day 14 and have reduced H19 and Igf2 expression as a result of increased ICR methylation [33]. In contrast, culturing sheep zygotes with serum before implantation leads to fetal overgrowth associated with altered DNA methylation at the imprinted IGF2R locus [13]. Less is known about the nutritional regulation of placental DNA methylation but both under- and overnutrition alter placental development and Igf2 gene expression [10].…”

Section: Epigenetic Regulation Of the Igf2 Genementioning

confidence: 99%

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Imprinted Genes, Placental Development and Fetal Growth

Fowden

Sibley²,

Reik³

et al. 2006

Horm Res Paediatr

223

176

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In mammals, imprinted genes have an important role in feto-placental development. They affect the growth, morphology and nutrient transfer capacity of the placenta and, thereby, control the nutrient supply for fetal growth. In particular, the reciprocally imprinted Igf2–H19 gene complex has a central role in these processes and matches the placental nutrient supply to the fetal nutrient demands for growth. Comparison of Igf2P0 and complete Igf2 null mice has shown that interplay between placental and fetal Igf2 regulates both placental growth and nutrient transporter abundance. In turn, epigenetic modification of imprinted genes via changes in DNA methylation may provide a mechanism linking environmental cues to placental phenotype, with consequences for development both before and after birth. Changes in expression of imprinted genes, therefore, have major implications for developmental programming and may explain the poor prognosis of the infant born small for gestational age and the wide spectrum of adult-onset diseases that originate in utero.

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Section: Imprinted Genesmentioning

confidence: 99%

Section: Epigenetic Regulation Of the Igf2 Genementioning

confidence: 99%

Imprinted Genes, Placental Development and Fetal Growth

Fowden

Sibley²,

Reik³

et al. 2006

Horm Res Paediatr

223

176

View full text Add to dashboard Cite

show abstract

“…(10,66) This can bind to several receptors (insulin-like growth factor receptor 1, insulin receptor, and the IGF 2 receptor/mannose-6 phosphate), and the growth factor is subject to imprinting, such that only the male allele is expressed in most tissues of mouse, sheep and human. (67) Imprinted genes are more easily disrupted by environmental factors. It has been shown that hyperglycaemia can impair nephrogenesis (68) and that this is associated with increased expression of the IGF II/mannose-6-phosphate receptor, which could then clear IGF II.…”

Section: How Does Glucocorticoid Exposure Affect Fetal Metanephric Dementioning

confidence: 99%

Kidney development and the fetal programming of adult disease

2003

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Recent evidence, from both epidemiological and animal experimental studies, suggest that the very first environment, the intrauterine, is extremely important in determining the future health of the individual. Genetic and 'lifestyle' factors impinge on, and can exacerbate, a 'programming' effect of an adverse fetal environment. In this review, we present compelling evidence to suggest that one of the major organs affected by an unfavourable prenatal environment is the kidney. Many of the factors that can affect fetal renal development (i.e. exposure to excess glucocorticoids, insufficient vitamin A, protein/calorie malnutrition (in rats) and alterations in the intrarenal renin angiotensinogen system), also produce hypertension in the adult animal. When nephron number is compromised during kidney development, maladaptive functional changes occur and can lead, eventually, to hypertension and/or renal disease. Surprisingly, it is during the very earliest stages of kidney development that the vulnerability to these effects occurs.

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“…Deregulation of imprinted loci has previously been associated with malformed offspring including disruption of the Igf2 imprinted region in mice. Disruption of this imprinted region in mice results in their offspring being retarded [86] and loss of imprinting (LOI) of this same region results in them having Beckwith-Wiedemann syndrome (BWS) [87]. Long-term cohort studies looking at the incidence of imprinting disorders and the use of ART have failed to draw a significant relation between the two [88, 89].…”

Section: Epigenetic Modifications Affecting Reproductive Outcomementioning

confidence: 99%

Epigenetic Regulatory Mechanisms Associated with Infertility

Minocherhomji

Madon

Parikh

2010

Obstetrics and Gynecology International

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Infertility is a complex human condition and is known to be caused by numerous factors including genetic alterations and abnormalities. Increasing evidence from studies has associated perturbed epigenetic mechanisms with spermatogenesis and infertility. However, there has been no consensus on whether one or a collective of these altered states is responsible for the onset of infertility. Epigenetic alterations involve changes in factors that regulate gene expression without altering the physical sequence of DNA. Understanding these altered epigenetic states at the genomic level along with higher order organisation of chromatin in genes associated with infertility and pericentromeric regions of chromosomes, particularly 9 and Y, could further identify causes of idiopathic infertility. Determining the association between DNA methylation, chromatin state, and noncoding RNAs with the phenotype could further determine what possible mechanisms are involved. This paper reviews certain mechanisms of epigenetic regulation with particular emphasis on their possible role in infertility.

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Imprinting of Genes and the Barker Hypothesis

Cited by 58 publications

References 61 publications

Imprinted Genes, Placental Development and Fetal Growth

Imprinted Genes, Placental Development and Fetal Growth

Kidney development and the fetal programming of adult disease

Epigenetic Regulatory Mechanisms Associated with Infertility

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