Mus musculus strain:C57BL/6N
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ABSTRACT:
PROVIDER: PRJDB13467 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:In recent years considerable effort has been devoted to understanding the epigenetic control of sperm development leading to an increased appreciation of the importance of RNA interference pathways, and in particular microRNAs (miRNAs), as key regulators of spermatogenesis and epididymal maturation. It has also been shown that sperm are endowed with an impressive array of miRNA that have been implicated in various aspects of fertilization and embryo development. However, to date there have been no reports on whether the sperm miRNA signature is static or whether it is influenced by their prolonged maturation within the male reproductive tract. To investigate this phenomenon we employed next generation sequencing to systematically profile the miRNA signature of maturing mouse spermatozoa. In so doing we have provided the first evidence for the dynamic post-testicular modification of the sperm miRNA profile under normal physiological conditions. Such modifications include the apparent loss and acquisition of an impressive cohort of some 113 and 115 miRNAs, respectively between the proximal and distal epididymal segments. Interestingly, the majority of these changes occur late in maturation and include the uptake of novel miRNA species in addition to a significant increase in many miRNAs natively expressed in immature sperm. Since sperm are not capable of de novo transcription these findings identify the epididymis as an important site in establishing the sperm epigenome with the potential to condition the peri-conceptual environment of the female reproductive tract, contribute to the inheritance of acquired characteristics, and/or alter the developmental trajectory of the resulting offspring. Examination of the microRNA expression profile in sperm thoughout the mouse epididymis and mouse using next generation sequencing in duplicate.
2015-08-05 | E-GEOD-70198 | biostudies-arrayexpress
Project description: Not available
| S-EPMC6829871 | biostudies-literature
Project description: Not available
| S-EPMC4053787 | biostudies-other
Project description:Epigenetic marks are reprogrammed in the gametes to reset genomic potential in the next generation. In mammals, paternal chromatin is extensively reprogrammed through the global erasure of DNA methylation and the exchange of histones with protamines1,2. Precisely how the paternal epigenome is reprogrammed in flowering plants remains unclear since DNA is not demethylated in sperm and histones are retained3,4. Here, we describe a multi-layered mechanism by which H3K27me3 is globally lost from histone-based sperm chromatin in Arabidopsis. This mechanism involves silencing of H3K27me3 ‘writers’, the activity of H3K27me3 ‘erasers’ and deposition of a sperm-specific histone, H3.105, which we show is immune to lysine 27 methylation. The loss of H3K27me3 facilitates transcription of genes essential for spermatogenesis and pre-configures sperm with a chromatin state that forecasts gene expression in the next generation. Thus, plants have evolved a specific mechanism to simultaneously differentiate male gametes and reprogram the paternal epigenome.
2020-03-17 | GSE144900 | GEO
Project description:Epigenetic marks are reprogrammed in the gametes to reset genomic potential in the next generation. In mammals, paternal chromatin is extensively reprogrammed through the global erasure of DNA methylation and the exchange of histones with protamines1,2. Precisely how the paternal epigenome is reprogrammed in flowering plants remains unclear since DNA is not demethylated in sperm and histones are retained3,4. Here, we describe a multi-layered mechanism by which H3K27me3 is globally lost from histone-based sperm chromatin in Arabidopsis. This mechanism involves silencing of H3K27me3 ‘writers’, the activity of H3K27me3 ‘erasers’ and deposition of a sperm-specific histone, H3.105, which we show is immune to lysine 27 methylation. The loss of H3K27me3 facilitates transcription of genes essential for spermatogenesis and pre-configures sperm with a chromatin state that forecasts gene expression in the next generation. Thus, plants have evolved a specific mechanism to simultaneously differentiate male gametes and reprogram the paternal epigenome.
2020-03-17 | GSE144899 | GEO
Project description: Not available
| S-EPMC3555078 | biostudies-literature
Project description: Not available
| S-EPMC4329520 | biostudies-other
Project description:Epigenetic marks are reprogrammed in the gametes to reset genomic potential in the next generation. In most animal species, paternal chromatin is extensively reprogrammed through the global erasure of DNA methylation and the exchange of histones with protamine. Precisely how the paternal epigenome is reprogrammed in flowering plants remains unclear since sperm chromatin is not demethylated and histones are retained. Here, we show that the sperm-specific histone, H3.10, is immune to lysine 27 methylation and that its deposition in sperm contributes to the global and specific resetting of the epigenetic mark H3K27me3 by uncoupling its inheritance during DNA replication. The loss of H3K27me3 facilitates transcription of genes essential for spermatogenesis and pre-configures sperm with a chromatin state that forecasts gene expression in the next generation, revealing a global wave of epigenetic resetting that coordinates with early plant life. Thus, in contrast to the indiscriminate removal of epigenetic marks in animal sperm, plants have evolved a specific mechanism to simultaneously differentiate male gametes and reprogram the paternal epigenome.
2020-03-17 | GSE137887 | GEO
Project description:Epigenetic marks are reprogrammed in the gametes to reset genomic potential in the next generation. In most animal species, paternal chromatin is extensively reprogrammed through the global erasure of DNA methylation and the exchange of histones with protamine. Precisely how the paternal epigenome is reprogrammed in flowering plants remains unclear since sperm chromatin is not demethylated and histones are retained. Here, we show that the sperm-specific histone, H3.10, is immune to lysine 27 methylation and that its deposition in sperm contributes to the global and specific resetting of the epigenetic mark H3K27me3 by uncoupling its inheritance during DNA replication. The loss of H3K27me3 facilitates transcription of genes essential for spermatogenesis and pre-configures sperm with a chromatin state that forecasts gene expression in the next generation, revealing a global wave of epigenetic resetting that coordinates with early plant life. Thus, in contrast to the indiscriminate removal of epigenetic marks in animal sperm, plants have evolved a specific mechanism to simultaneously differentiate male gametes and reprogram the paternal epigenome.
2020-03-17 | GSE120668 | GEO
Project description:Epigenetic marks are reprogrammed in the gametes to reset genomic potential in the next generation. In most animal species, paternal chromatin is extensively reprogrammed through the global erasure of DNA methylation and the exchange of histones with protamine. Precisely how the paternal epigenome is reprogrammed in flowering plants remains unclear since sperm chromatin is not demethylated and histones are retained. Here, we show that the sperm-specific histone, H3.10, is immune to lysine 27 methylation and that its deposition in sperm contributes to the global and specific resetting of the epigenetic mark H3K27me3 by uncoupling its inheritance during DNA replication. The loss of H3K27me3 facilitates transcription of genes essential for spermatogenesis and pre-configures sperm with a chromatin state that forecasts gene expression in the next generation, revealing a global wave of epigenetic resetting that coordinates with early plant life. Thus, in contrast to the indiscriminate removal of epigenetic marks in animal sperm, plants have evolved a specific mechanism to simultaneously differentiate male gametes and reprogram the paternal epigenome.
2020-03-17 | GSE120664 | GEO