Epigenetic homogeneity in histone methylation underlies sperm programming for embryonic transcription

Abstract: Sperm contributes genetic and epigenetic information to the embryo to efficiently support development. However, the mechanism underlying such developmental competence remains elusive. Here, we investigated whether all sperm cells have a common epigenetic configuration that primes transcriptional program for embryonic development. Using calibrated ChIP-seq, we show that remodelling of histones during spermiogenesis results in the retention of methylated histone H3 at the same genomic location in most sperm cell. This homogeneously methylated fraction of histone H3 in the sperm genome is maintained during early embryonic replication. Such methylated histone fraction resisting post-fertilisation reprogramming marks developmental genes whose expression is perturbed upon experimental reduction of histone methylation. A similar homogeneously methylated histone H3 fraction is detected in human sperm. Altogether, we uncover a conserved mechanism of paternal epigenetic information transmission to the embryo through the homogeneous retention of methylated histone in a sperm cells population

Do pain, anxiety and depression influence quality of life for people with amyotrophic lateral sclerosis/motor neuron disease? A national study reconciling previous conflicting literature

The original version of this article unfortunately contained a mistake. Oliver Hanemann name was incorrect in the in the acknowledgements section of this paper

Effect of chitooligosaccharide on the de-methylation three CpG sites in the <i>LEP</i> promoter.

<p>Extent of methylation at CpG_52 (A), CpG_62 (B) and CpG_95 (C) of the mouse <i>LEP</i> promoter at days 6 post-induction of differentiation are presented as mean ± standard error from two independent replicate experiments.</p

Effect of chitooligosaccharide on mouse <i>LEP</i> gene expression at day 6 post-induction of differentiation.

<p>Mouse 33-L1 pre-adipocytes were induced to differentiate in absence or presence of chitooligosaccharide and cells were harvested for RNA isolation and quantitative expression of <i>LEP</i> gene on day 6 post-induction of differentiation. Data represents mean ± standard error from three independent replicate experiments.</p

Transcriptional activities of an un-methylated and chemically methylated human <i>LEP</i> promoter in mouse 3T3-L1 pre-adipocytes.

<p>Transcriptional activities of an un-methylated and chemically methylated human <i>LEP</i> promoter in mouse 3T3-L1 pre-adipocytes.</p

Effect of chitooligosaccharide (COS) on the production of leptin by 3T3-L1 pre-adipocytes during adipogenesis.

<p>Mouse 33-L1 pre-adipocytes were induced to differentiate in the absence or presence of chitooligosaccharide and cell culture media was harvested for quantification of leptin production on days 2–4 post-induction of differentiation (A) and days 4–6 post-induction of differentiation (B) Data represents mean ± standard error from three independent replicate experiments. Note the differences in the scale of Y-axis representing the leptin concentration (pg/ml) in the media for different figures.</p

Abundance of mouse <i>LEP</i> mRNA transcripts (A) and protein (B) during adipogenesis.

<p>Mouse 33-L1 pre-adipocytes were induced to differentiate and cells were harvested for RNA isolation and quantitative expression of <i>LEP</i> gene on days 0, 2, 4 and 6 post-induction of differentiation. Cell culture media was harvested for quantification of leptin production on days 2, 4 and 6 post-induction of differentiation. Day 0 and day 6 correspond to pre-adipocyte and mature adipocytes, respectively. Day 2 and day 4 correspond to a phase where the cells were actively involved in the differentiating process. Data represents mean ± standard error from three independent replicate experiments.</p

Genomic imprinting effects on complex traits in domesticated animal species

Monoallelically expressed genes that exert their phenotypic effect in a parent-of-origin specific manner are considered to be subject to genomic imprinting, the most well understood form of epigenetic regulation of gene expression in mammals. The observed differences in allele specific gene expression for imprinted genes are not attributable to differences in DNA sequence information, but to specific chemical modifications of DNA and chromatin proteins. Since the discovery of genomic imprinting some three decades ago, over 100 imprinted mammalian genes have been identified and considerable advances have been made in uncovering the molecular mechanisms regulating imprinted gene expression. While most genomic imprinting studies have focused on mouse models and human biomedical disorders, recent work has highlighted the contributions of imprinted genes to complex trait variation in domestic livestock species. Consequently, greater understanding of genomic imprinting and its effect on agriculturally important traits is predicted to have major implications for the future of animal breeding and husbandry. In this review, we discuss genomic imprinting in mammals with particular emphasis on domestic livestock species and consider how this information can be used in animal breeding research and genetic improvement programs